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^^^^^^^^^^^^^^^^^^1 REDDISH 

^^^^^^^^^^^^^^^^^^H BROWNISH 

Scale of Urinary Colors, according to Vogel. 

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G* A. DeSantos Saxe, M^a 

Instructor in Genito-urinary Surgery, New York Post-graduate Medical School and 
Hospital ; Assistant Genito-urinary Surgeon, Bellevue Hospital, Out-patient 
Department ; formerly Assistant Pathologist to the Columbus Hospi- 
tal ; Member of the American Urological Association ; 
Fellow of the New York Academy of Medicine, Etc. 

Second Edition, Revised 

With Text Illustrations and Colored Plates, a 
Number of Them Original 



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r. -^/g. \^0-\.\ 

Set up, electrotyped, printed, and copyrighted September, 1904. Reprinted 

April, 1906. Revised, reset, electrotyped, printed, and 

recopyrighted October, 1909 

Copyright, 1909, by W. B. Saunders Company 





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The object of this manual is to furnish a concise 
guide to the examination of urine for the prac- 
titioner in his daily work and for the student in 
his laboratory course, as well as in his study for 

In accordance with this aim, an effort has been 
made to treat the important and practical parts of 
the subject as fully as possible, while theory, dis- 
cussion of moot-points, and cumbersome analytic 
details have been either omitted or treated in the 
briefest possible manner. 

The theory of urinary secretion and the methods 
of functional examination of the kidneys have been 
given a rather more prominent place than has been 
done in other text-books, for the reason that a 
knowledge of these themes, while still of little prac- 
tical use, adds materially to a grasp of the modem 
status of uranalysis and of the directions in which 
advances may be expected in this science. 

Special attention has been paid to technics and to 
the interpretation of findings. In this connection 
some hints as to the methods of working that devel- 
oped in my own experience have been inserted, which 
I trust may prove helpful to the beginner. 

In a text-book of this scope, it is not necessary to 


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mention in detail the authorities consulted, and this 
has not been done here, except in a few instances. 
I take occasion, however, to acknowledge my espe- 
cial indebtedness for material to the works of Neu- 
bauer and Vogel, Hammarsten, Von Jaksch, Ogden, 
F. C. Wood, Simon, Purdy, Heitzmann, and Tyson, 
and to express my sincere thanks to Dr. Henry T. 
Brooks, Pathologist to the Postgraduate Hospital, 
for many valuable hints in the preparation of this 

The metric system is used in the greater part of 
the book, but the old system of weights and measures 
has been retained in some places for the sake of 
convenience in working, and in order to keep intact 
the original formulas of certain authorities. 

Unless otherwise specified, the reagents and solu- 
tions are supposed to correspond to the standard 
of the United States Pharmacopoeia. 

If this little volume will contribute towards a 
clearer and more precise understanding of the sub- 
ject of uranalysis on the part of the student or prac- 
titioner, my task shall not have been fruitless. 

G. A. DeS. S. 

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Time was when those engaged in laboratory work 
were bidden to '* stick to their lasts" when they at- 
tempted to come into contact with patients. To-day 
we see on every hand a clearly defined change in the 
relations of the laboratory man and the bedside man. 
In fact, to attain the highest standing in clinical 
medicine, in surgery, or in any of the specialties, it 
is now necessary for a physician to be thoroughly 
trained in laboratory work and to be able to apply 
laboratory methods in his daily routine, as well as in 
his search for the unknown in the particular branch 
in which he is interested. The highest places in the 
gift of our great universities in the department of 
clinical medicine and in some of the specialties are 
now given to men who have made reputations in 
laboratory research as well as in clinical study. As 
was well said recently by Dr. Christian, Dean of the 
Harvard Medical School, **The future of medicine in 
this country lies in a perfect co-ordination of the 
laboratory and the ward, both of which should be 
under the same head. ' ' ^ 

Written by one who is primarily devoted to clinical 
work in a branch of surgery in which the greatest de- 
pendence is placed upon urine examinations, this book 
is, therefore, addressed to the clinical worker, the 
practitioner, who aims to make the laboratory his 

1 Quoted from memory by the author. 


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daily guide and counselor. Whether he himself ex- 
amines the specimens, or whether he is fortunate 
enough to have this work done for him, the practitioner 
will require a thorough knowledge of the urine when 
he comes to interpret the findings of the microscope 
or of the test-tube. 

In the new edition the clinical side of urine analysis 
has been still more markedly emphasized than in the 
first. The book has not only been revised and ampli- 
fied, but many of the chapters have been entirely 
rewritten, to meet the important advances in the field 
of physiologic chemistry and chemical pathology in 
the midst of which we live to-day. In many respects 
this second edition also represents the fruits of indi- 
vidual experience in urinalysis and in clinical work 
in urinary diseases, covering now a period of ten years, 
as well as the results of the author's published re- 
searches on urethral shreds, prostatic and vesicular 
elements in the urine, etc. 

Among the chapters which have been practically 
rewritten are those on acidity, albuminuria, albumoses, 
mucin, nucleo-albumin, indican, phosphates, sulphates, 
and the nitrogenous bodies, inchiding uric acid. A 
number of new subjects have been introduced — e, g,^ 
a short section on the pentoses, a brief account of 
Cammidge's reaction, a detailed description of the 
methods of preserving and staining urinary sediments 
and of preparing sediments for bacteriologic examina- 
tions. New chapters have also been inserted on 
urethral shreds, vesicular sago-bodies, etc. ; on dia- 
betes, and on the toxemias of pregnancy. A complete 
yet concise account of the present-day methods of 
functional renal diagnosis has been incorporated. 

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In every instance tests which have proved valueless 
have been dropped. Few new tests have been ad- 
mitted, and only such as have proved useful in the 
author's own work. A number of new and original 
illustrations have been added. In order to make the 
volume compact, in spite of the numerous additions, 
smaller type has been used for the parts that are not 
apt to be required for daily reference. 

The favorable reception of the first edition and its 
adoption as a text-book in a number of the medical 
schools of this country leads the author to hope that 
this edition will prove even more useful than its prede- 
cessor to the student and the practitioner. 

G. A. DeS. S. 

130 West 71ST St., New York City. 
October,, 1909. 

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I. Introduction. Composition of Urine in Health 17 

II. Selection of a Specimen of Urine 21 

III. Physical Properties of the Urine 25 




IV. Serum-albumin 50 

Methods of Testing for Albumin 56 

Quantitative Tests for Albumin 70 

Approximate Clinical Estimation 70 

V. Other Proteids in the Urine 77 

Serum-globulin 77 

Fibrin 79 

Albumoses 80 

Mucin (Moerner's Mucoid) 87 

Substances Formerly Taken for " Nucleo-albumin "... 89 

Nucleoproteid 92 


VI. Glucose 96 

Detection of Sugar in the Urine 97 

Quantitative Determination of Sugar iii 

VII. Other Carbohydrates in the Urine 122 

Lactose 122 

Levulose 1 23 

Laiose 123 

Pentoses 124 

Other Substances Allied to Glucose 125 

Cammidge*s Reaction 128 


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VIII. The Excretion of Nitrogen in the Urine 131 

Urea 133 

IX. The Purin Bodies — Uric Acid and its Chemical Con- 
geners 145 

Uric Acid 146 

Urates 154 

Purin (Xanthin or AUoxur) Bases 155 

Quantitative Test for Purin Bodies (Uric Acid + Purin 

Bases) 157 

Ammonia 159 

Creatin and Creatinin 160 

Allantoin 161 

Nucleic Acid 161 

Hippuric Acid 162 


X. Acetone and Diacetic Acid 165 

Acetone. 165 

Diacetic Acid 170 

Beta-oxybutyric Acid 172 

XI. Indican and Other Ethereal Sulphates; Diazo- 

REACTioN 174 

Indican 174 

Other Ethereal Sulphates 181 

Ehrlich's Diazo-reaction 182 


XII. Urinary Coloring-matters 186 

Normal Coloring-matters 186 

Biliary Pigments and Acids 189 

Bile-pigments 189 

Bile-acids 191 

Blood Pigments 193 

XIII. Leucin, Tyrosin, Fatty Matter, and Other Organic 

Constituents 201 

Leucin and Tyrosin 201 

Fat and Cholesterin in the Urine 203 

Other Organic Constituents of Minor Importance 204 

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XIV. Chlorids 208 

XV. Phosphates 215 

XVI. Sulphates, Carbonates, and Less Important Inorganic 

Constituents 223 

Sulphates 223 

Carbonates 229 

Inorganic Constituents of Minor Importance 229 

Accidental Inorganic Constituents 231 

XVII. Urinary Concretions 232 


XVIII. General Considerations 235 

Methods of Obtaining Sediments 235 

Methods of Examining Sediments 239 

Preservation and Mounting of Sediments 242 

Staining of Sediments 244 

Extraneous Materials in Sediments 245 

Classification of Sediments 250 

Sediments in Acid and Alkaline Urines 251 

XIX. Unorganized Sediments 255 

XX. Organized Sediments 274 

Blood 274 

Pus 281 

Connective-tissue Shreds 284 

Epithelium 285 

Casts 298 

False Casts or Cylindroids 309 

Mucous Threads 310 

Prostatic Plugs 311 

Amyloid Bodies 312 

Spermatozoa 313 

Sago Bodies and Other Vesicular Elements in Massage- 
urine 314 

Urethral Shreds 319 

Micro-organisms 237 

Parasites 337 

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XXI. Characters of the Urine in Diseases of the Kidney 

AND Renal Pelvis 342 

Acute Congestion 343 

Chronic Congestion i . . . . 345 

Acute Diffuse Nephritis 346 

Chronic Diffuse Nephritis 349 

Chronic Parenchymatous Nephritis 351 

Chronic Interstitial Nephritis 353 

Amyloid Kidney 356 

Tuberculosis of the Kidney 358 

Stone in the Kidney 360 

Tumors of the Kidney 362 

Cysts and Cystic Degeneration of the Kidney 364 

Abscess of the Kidney 364 

Embolism of the Kidney 365 

Acute Pyelitis and Pyelonephritis 365 

Chronic Pyelitis and Pyelonephritis 366 

Hydronephrosis 366 

Pyonephrosis 367 

Ureteritis 368 

XXII. Characters of the Urine in Diseases of the Lower 

Urinary Tract and of the Genital Organs.. 369 

Cystitis 369 

Tuberculous Cystitis 371 

Tumors of the Bladder 373 

Stone in the Bladder 373 

Prostatitis 373 

Tuberculosis and Cancer of the Prostate 375 

Seminal Vesiculitis 376 

Spermatorrhea 377 

Urethritis 377 

XXIII. The Urine in Abdominal States of Metabolism 380 

Diabetes Mellitus 380 

Diabetes Insipidus 385 

The Toxemias of Pregnancy 386 

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XXIV. General Considerations; The Secretion of Urine.. 389 

The Objects of Determining the Renal Function 389 

Theories of Renal Secretion 391 

XXV. Methods of Determining the Functional Efficiency 

OF the Kidneys 395 

Determining the Freezing-point of the Urine (Cryoscopy) 395 
Determining the Electric Conductivity of the Urine .... 400 

The Methylene-blue Test 401 

The Indigo-carmin Test 403 

The Phloridzin Test 404 

Experimental Polyuria 408 

XXVI. The Toxicity of the Urine 410 

Ptomains 412 

Leukomains 412 


Routine Examination, Reagents, Apparatus, etc 414 

Routine of Examination 416 

Lists of Reagents, Apparatus, Etc 421 

Liquid Reagents 422 

Solid Reagents 423 

Bacterial Stains 423 

Apparatus 424 

Thermometric Equivalents 425 

Relations of English to Metric Systems 425 

Index 427 

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Examination of the Urine 





A KNOWLEDGE of the characters of the urine in health 
and disease is of the greatest importance to the physician, 
inasmuch as this fluid constitutes one of the most valuable 
aids to both medical and surgical diagnosis. Next to the 
pulse and the temperature, the urine offers the greatest 
possibility for an insight into the workings of the human 
system. Aside from its purely clinical value, urinalysis 
is essential to the study of the physiologic processes of the 
body and the determination of changes in its metabolism 
produced through normal or abnormal influences. 

The urine is a watery fluid secreted by the kidneys, 
and in health contains a large variety of constituents which 
are derived from the wasting and decomposition of the 
fluids and tissues of the body and from certain elements 
of the food. 

The constituents of normal urine are difl&cult to classify 
2 17 

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systematically on account of their complexity, but a useful 
division of the dissolved elements of the urine (modified 
from Hoppe-Seyler) is as follows: 

1. Gases 

2. Inorganic salts 

3. Urea and its congeners 

4. Aromatic substances 

5. Fatty and other non-nitrog- 

enous substances 

6. Other organic substances. . . . 

Oxygen, nitrogen, and carbonic acid 
(very small quantities; dis- 
' (a) Chlorids of sodium and potas- 

(b) Potassium sulphate. 

(c) Sodium, calcium, and magnesium 


(d) Calcium carbonate. 

(e) Silicic acid. 

(/) Ammonium compounds. 
Urea, uric acid, xanthin, creatinin, 
allantoin, oxaluric acid, sulpho- 
cyanic acid, etc. 
'The ethereal sulphates of phenol, 
cresol, pyrocatechin, indoxyl, 
and skatoxyl; hippuric acid 
and aromatic oxyacids. 
Fatty acids; oxalic, lactic, glycero- 
phosphoric acids, and a very 
minute amount of certain car- 
/Pigments; ferments, especially pepsin; 
\ mucoid substances. 

The following table (Parkes) gives an idea as to the char- 
acter and general quantitative relations of the urinary con- 
stituents, but it cannot serve as a clinical guide for the 
interpretation of urinary analyses. For this reason other 
tables (pp. 19, 20) have been compiled by the author, 
as exhibiting the chief points necessary for judging the 
results of quantitative estimations in urine. The figures 
given in these tables correspond with results of analyses 
carried on in the author's laboratory, and in the main 
are in accordance with the figures given by other writers 
on urine analysis. 

The composition of normal urine, according to Parkes, 
is as follows: 

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Amount of Urinary Constituents Passed in Twenty-four 
Hours (Parkes) 



total solids 


Uric acid 

Hippuric acid 


Pigments and other organic matters. 

Sulphuric acid 

Phosphoric acid 

Chlorin , 






Average Man, 

66 Kilograms. 





















Per Kilogram 
OF Body- 

23.000 grams 
1. 100 " 
0.500 gram 


I. General Characters of Normal Urine 

Transparency. — Clear or faintly cloudy. 

Color. — Amber-yellow. 

Specific Gravity. — 10 15 to 1020 at 15° C. 

Reaction. — Acid (depending on diet, etc.). 

Acidity (total) may be expressed in one of the following ways (see p. 


1. Equivalent to from 3 to 5 cc. rV-normal NaOH in 10 cc. of urine. 

2. Equivalent to from 2 to 4 gm. of oxalic acid in twenty-four hours. 

3. Equivalent to from 1.15 to 2.3 gm. of HCl. 

4. Equivalent to from 0.4 to 20 parts per thousand of acid phos- 

Amount voided in twenty-four hours (average) : 
1200 to 1500 cc. (50 fluidounces). 

24.0 cc. of urine in twenty-four hours per each kilo of body-weight; 
a kilo being equivalent to 2.3 pounds, 

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II. Normal Constituents of Urine 

Total solids. 

Chlorids (NaCl) 

Phosphates (PaOg) 

f § earthy 

\ § alkaline 



Uric acid 

Indican . 

Per Cent. 







Parts in iooo 

(Grams in 




Grams in 








(average 0.7) 


Grains per 






III. Graphic Expression of Quantities in Urine 
For comparing normal and abnormal conditions of 
excretion, there is nothing more convincing than the 
graphic method. A simple chart for this purpose is shown 
herewith. The solid line shows the proportions of urea, 
chlorids, phosphates (phosphoric acid), and the specific 
gravity in normal urine. The dotted line shows an abnor- 
mal urine plotted in the same way (a case of cancerous 
cachexia). (See Plate 2.) 

The urea, chlorids, phosphates, sulphates, and uric 
acid are expressed in grams per twenty-four hours; the 
specific gravity is shown by the two last figures of the 
hydrometer reading, the normal average being taken as 
1020. The quantity voided in twenty-four hours is indi- 
cated " in terms of 100 cc." — i. e., by the number of 
times 100 cc. are voided. 

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Plate 2 


GhAUri m 34 Hoiifts 

3 5 * > J. 










< ■ 

Graphic Expression of Quantities in the Urine. 

Solid line, normal urine; dotted line, an example of pathologic urine 

in a case of cancerous cachexia. 

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For accurate quantitative work it is absolutely necessary 
to obtain the total amount of urine passed in twenty-four 
hours or, at least, a sample obtained after mixing thor- 
oughly the entire quantity so collected. In the latter case 
the quantity eliminated in twenty-four hours must be 
measured and made known to the examiner. A perfectly 
clean bottle, holding about § gallon, should be used 
for collecting the twenty-four-hour quantity. It should 
be well corked after each addition, and should be kept 
in a cool, dry room to avoid decomposition. It is important 
that no foreign matter whatever, such as dust, feces, spu- 
tiun, etc., be introduced into the sample, and the urine 
should never be allowed to stand in open or dirty vessels. 

The reason for collecting the twenty=f our-hour quan- 
tity is that the proportion of the constituents and the 
amount of albumin, etc., vary a good deal at different 
hours of the day and night, and that the object should 
be to obtain the average composition of the urine in the 
twenty- four hours. 

The best time to obtain a sample of urine when we do 
not want the twenty-four-hour quantity, but merely wish 
to test qualitatively for sugar, albumin, etc., is during the 
day, about three hours after a meal. It is a mistake to 
take the morning urine, as is so commonly done; for in 
slight albuminuria the urine passed in the morning is the 
least likely to contain albumin, and the same is true of 


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sugar in glycosuria. Sometimes, when a case requires 
careful study, a comparison of the day urine and the night 
urine is desired; in that case we collect the urine from 
7 A. M. to 7 p. M. in one bottle, and from 7 p. m. to 7 A. m. 
in another bottle, each being appropriately marked. 

If a more concentrated urine is desired than is obtained 
in a given case with ordinary diet, it may be advisable to 

Fig. I. — Stoppered graduate . 

Fig. 2. — Cylindric graduate. 

reduce the amount of water and other fluids ingested for 
a day or so, and thus a urine with greater concentration 
and more abundant sediment may be obtained for micro- 
scopic examination. 

The urine is subject to rapid decomposition after 
being voided, as the result of the action of molds and 
other micro-organisms, and also as the result of reactions 
between its various constituents. On standing, a normal 
urine precipitates, as a rule, first, some amorphous urates, 

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then some uric-acid crystals, and sometimes calcium 
oxalate. If allowed to stand open, and if exposed to high 
temperature, as in hot weather, the urine becomes clouded 
from a large number of bacteria and fimgi. At the end of a 
few days it becomes ammoniacal — that is, the urea is 
gradually transformed into ammonium carbonate, accord- 
ing to the following formula: 

CH,N,0 + 2H,0 = (NHJjCOj. 

In consequence of this the urine grows alkaline and the 
sediment contains ammonium urate, triple phosphate, 
and amorphous masses of calcium phosphate. Urines of 
normal concentration and acidity do not decompose so 
rapidly as urines of low density and slight acidity. 

While this series of changes is known as alkaline fer- 
mentation^ there is another form that has been known as 
acid fermentation. This change is sometimes seen as a 
preliminary stage of alkaline fermentation. It consists 
of an increase in acidity, a darkening in color, and the 
deposition of uric acid and urates, and occasionally of 
calcium-oxalate crystals, together with many yeast fungi 
and bacteria. This change is probably caused by the 
mucus, which acts as a ferment and induces an acetic-acid 
or lactic-acid fermentation. The reason for this increase 
of acidity has been also attributed to a reaction between 
the biurates and MH2PO4, dihydrogen phosphate (Ham- 

Preservation. — It is very important, therefore, that 
the urine be examined in as fresh a state as possible. In 
order to preserve it during the collection of the specimen 
or during the transportation to the laboratory, etc., a num- 
ber of substances have been used as antiseptics. The 
most practical is the addition of a crystal or two of thymol, 

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or an ounce of cold saturated solution of boric acid to the 
quart of urine. With thymol, however, the urine may give 
a test suggesting the presence of bile. Chloroform (a few 
drops) will preserve urine well for chemic analysis (save 
that it gives a deceptive precipitate with Fehling's solution), 
but it makes the sediment unfit for microscopic examina- 
tion. The use of formalin, of which 2 or 3 drops are added 
to the urine, has been advocated of late, but it is apt to 
cause a reduction of Fehling's solution which may be 
taken for glucose; besides, it is apt to affect the organized 
sediment, shrinking the cells and distorting the casts. The 
addition of formalin to urine also obscured the microscopic 
examination, in the author's experience, by the production 
of innumerable gas-bubbles if the urine was allowed to 
stand for any length of time. The addition of 5 grains 
of salicylic acid to 4 ounces of urine is favored by some, and 
is said to be very efficient. In warm weather urines should 
be kept on ice. 


Name the principal groups of constituents in the normal urine. 

What gases are found in it? 

What inorganic salts? What organic substances? 

What is the average amount of total solids in urine in twenty-four 
hours? The average amount of chlorids, phosphates, sulphates, urea, 
uric acid? Describe a graphic method for recording quantitatively the 
constituents of urine. 

Give the rules in selecting a specimen of urine. 

How is the specimen collected? 

Why do we insist upon the twenty-four-hour quantity ? 

At what time should urine be taken if it is not possible to obtain the 
twenty-four-hour quantity, and why? 

Describe the processes of decomposition occurring in urine on standing. 

What constitutes alkaline fermentation? 

What is known as acid fermentation ? 

How should urine be preserved from decomposition? 

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Amount. — Th e amount of urine passed during twen ty- 
four hou rs by a healthy adult is from 1200 to 1600 cc , 
the average being about 1500 cc. or about 50 fluidounces. 
Women pass smaller quantities than men, and small- 
sized persons void less than large-sized individuals. One 
kilogram of body-weight produces on the average i cc. 
of urine in the course of one hour. The average amount 
is obtained by multiplying the body-weight in kilos by 24 
(60X24 = 1440 cc). Children eliminate 28.0 cc. per 5 
kilograms per hour. The drinking of large quantities of 
liquids increases, while the taking of violent exe rcise, 
through tree perspiration, diminishes, the average amount. 
The phy si ologic limits are 800 to .^000 cc. I n health the 
largest amount is usually passed in the afternoon, a moder- 
ate amount in the forenoon, and the smallest amount 
during the night. 

In warm weather considerably smaller quantities are 
passed than during the cold months. In disease the quan- 
tity of urine may be diminished or increased, or the urine 
may be suppressed through obstruction, or retained in 
the bladder through an impediment in the region of its 
neck or in the urethra. 

Oliguria is a term used for diminished quaq titv of nrinp 
(below 800 cc. in twenty-four hours). Anuria is used to 
designate cases in which no urine, or a very small quantity , 
is passed — i, e., when tnere is a partial or complete sup- 

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pression of urine. Polyuria is a term iiseH for a. ma rkedly 
i ncreased quantity of urin e (over 3000 cc). 

The increase or decrease must, however, be constant, 
as attested by several examinations, and must be inde- 
pendent of ingested fluids to justify the terms polyuria or 
oliguria. Polyuria must be distinguished from pollakuria 
(frequent urination) and refers only to the quantity passed, 
not the frequency of voiding the bladder. 

Diminution in quantity is noted in fever s; in shock 
after anesthesia or a fter operation s on the genito-urinary 
organs; in stasis in the kidney due to heart disease, etc.; 
in acute congestion o f the kidney; in acute nephri tis and 
in the acute phases of chronic nephritis; in diseases ac- 
c ompanied by diarrhea and vomitin p r . such as cholera or 
yellow fever, and in all diseases in the last stages before 

Increased quantit y is observed in diabetes mellit us 
and insipidus , in some diseases of the nervous system , 
such as hysteria and convulsions, and in cerebral hemor- 
rhage; in convalescence from acut e and inflam matory 
diseases; in convalescence from acute conges tion and from 
acute diffuse nephritis; in jrhronic nephrit is, both inter- 
stitial and diffuse, and in amyloid kidney; in hypertrophy 
of the heart and in all conditions causing increased blood- 
pressure; also i n cases in which d iureti cs have been fr eely 
used or a large amount of water dr uri¥! 

With the exception of the chronic diffuse and interstitial 
varieties of nephritis, in which there is an increase, there 
is a tendency to diminution in all forms of Bright's disease. 
A marked diminution in the urine in chronic nephritis, 
if accompanied by low specific gravity, is a very grave 
sign and usually precedes death. 

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Color. — The normal color of urine is of a pale -vellow. 
straw, or a mber tint, b ut even in health it may vary con- 
siderabiy according to the a mount ot water dru nk, etc. 
jjiluie urmes are usually pale; concentrated urines are 
deeply colored. The action of the skin in perspiration, 
the quantity of water drunk, and sometimes the quality 
of the food may have to do with changing the color of the 
urine in health. Color is not a very trustworthy sign in 
urine examinations. 

In disease the color of urine may be changed, owing 
to the increase or diminution of the normal coloring- 
matters or the addition of abnormal pigments. The 
general rule, stated before, about the proportion of color 
to concentration usually holds good in disease. An excep- 
tion, however, is the urine of diabetes mellitus, which is 
characteristically pale, but has a high specific gravity 
owing to the presence of sugar. Very pale-colored urine 
occurs in diabetes insipidus, hysteria, interstitial nephritis, 
etc. Hi ghly colored urine occurs in acute fevers and in 
inflammations, and is due to concentration and also to the 
presence of uroery thrift (see p. i86). Reddish urine 
is always due to the presence of abnormal coloring-matters, 
usually blood. A brown or reddish color is seen in urines 
after ingestion of rhubarb and senna; a yellow color, after 
santonin. A dark-brown urine may be a sign of hemor- 
rhage from the kidney, and be due to the presence of 
methemoglobin or hematin. Smoky an d dark urine is often 
seen after carbolic acid has been used mternally or some- 
times after its external use, as well as after the taking of 
large doses of salol or guaiacol. These urines show the 
black color, especially on standing, owing to the formation 
of hydroquinon as the result of decomposition of the 

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phenol (see Phenol, p. i8i). A dark urine is also seen 
in the presence of alkapton (see p. 127). 

Bile-pigmen tSy when present in excess, give a dark color 
with a yellowish-green foam, and on standing the urine 
becomes greenish. In cholera and typhus the urine may 
be bliie. In melanotic cancer the urine is almost bldcky 
especially after standing, owing to the presence of melanin. 
A ^reenish-bltce urine is eliminated after methylene-blue 
has been taken. A greenish tint is also sometimes seen 
after the use of a large quantity of milk, also in chronic 
Bright's disease and in diabetes with large amounts of 

Odor . — ^The odor of normal urine is pem lj^j, flrnmfltir. 
sometimes styled "urinou s." It is due to the presence 
of volatile acids — phenyljc, taurylic, and damaluric — 
in very minute quantities, and partly also to urea. The 
odor is strongest- in concentrated urine. On standing, 
normal urine ac quires a disagreeable odor which is bo th 
putr id and ammoniaca l. The putrid odor is due to 
decomposition of mucus or other organic matters. The 
ammoniacal odor is due to the formation of ammonium 
carbonate. It is important to note the odor of freshly 
passed urine, for if it is putrid or ammoniacal the urine 
must have decomposed within the body — e. g,, in the 
bladder. A urine which contains a large amount of pus 
or albumin may suffer decomposition of its proteid matter 
to such an extent as to evolve an odor of sulphuretted 
hydrogen. A fecal odor is noted when there is con- 
tamination of the urine by the feces through a fistula, etc. 

Certain vegetable foods and certain druf^s, when taken 
internally, very quickly pr oduc e a peculiar odor in_ the 
urin e. Thus, turpentine produces the odor of violets; 

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cubebs, copaiba, sandalwood oil, asparagus, etc., produce 
their characteristic odors in the urine. 

In disease the only abnormal odors to be noted are the 
increased odor, usually styled ^^ strong," in concentrate d 
urine; th e sweet or fruity smell of diabetic urine : th e foul 
odor of cystitis, and the "sulphuretted" odor of urine 
con taming much j^us. A peculiar odor, intense in its^ 
foulness, is noted in pyelitis. A sulphuretted odor is noted 
in the presence of cystin in decomposing urines containing 
this substance. 

Consistence. — Normal urine is always of the consist- 
ence of water. When the urine contains much pus or 
mucus, especially if it has become alkaline, it becomes 
very thick and stringy. Urine containing much sugar 
or albumin tends to froth when shaken. Chylous urine 
which contains fat in fine emulsion is thjckened in con- 

Transparency . — Normal freshly voided urine is always 
perfec tly cl ear, but on stanamg a tew mmutes tnere is 
generally a faint cloud which floats usually in the center 
of the urine or settles at the bottom if the urine is dilute 
enough. Thi s cloud or ^^ nubecula^ ^ consists of mu cus, 
e pithelium, bacteria, and debris of cells. It is much more 
pronounced m women on account of the admixture of 
vaginal mucus, which becomes washed away from the 
genitals in the passage of the urine from the urethra. In 
catarrhal conditions of the genito-urinary tract, especially 
in cystitis, prostatitis, and urethritis, the normal mucous 
cloud is markedly increased, so that the urine appears 
cloudy soon after being voided, and the cloud sinks 
more rapidly to the bottom. The mucous cloud may h6 
distinguished from other causes of turbidity by the fa ct 

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that it tends to float in the center of the fluid, and is pre- 
cipitated on the a ddition of an excess of acetic a cid. 

A cloudy urine may be the result of the presence of 
bacteria, phosphates, urates, or pus. 

Bacteria , when present in large numbers (bacteriuria), 
give rise to a faint cloud which tends to float in the middle 
of the vessel and does not settle, even when the urine stands 
for a long time. This cloud, unlike the mucous cloud, 
remains unchanged on the addition of acetic acid. 

Phosi)hates may give rise to cloudiness when there is 
an excess of the earthy or triple salts and when the acidity 
of the urine is lowered, thus lessening the solubility of the 
phosphatic elements. It is difficult to mistake turbidity 
due to phosphates for anything else, as it does not form a 
cloud, but pervades the urine uniformly, settling slowly 
on standing. A few drops of acetic acid, by correc ting 
the lowered acidity, wil l almost instantly clear up t he 
urine in such ca ses.^ 

C/jjj^, if present in excess in normal acid urines, may 
cause turbidity or may give a sediment of urates — of 
sodium, potassium, calcium, and magnesium — if the urine 
be allowed to stand in the cold. Th is deposit settle s 
qui ckly, is white, pinkish, dirtv-yello^Y ^ or hrirk-red in 
color, and often settles on the sides of the vessel. It is 
well to remember that a sediment occurring in acid urine 
can be composed only of urates or of organized elements 
(pus-cells, casts, etc.). The Hi<;tinprni^|^inpr \e9A for the 
clo udines s d ue to urates consists in heating the urine gentl y 
ove r the flame, which quickly dispels the cloudines s and 
cle g^rs the u rine. 

^ With a deposit of phosphates there usually is a certain amount of car- 
bonates which add to the cloudiness. They are also dissolved on the 
addition of acetic acid. 

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Pus in the urine shows its presence by cloudiness imme- 
diately after passing, and on standing a few minutes by 
the deposit of an opaque, amorphous, yellowsh-white 
sediment, which sinks to the bottom much more rapidly 
than mucus. In the presence of an admixture of pus and 
mucus the opacity of the sediment and the rapidity of its 
sinking grow less as the mucus is increased. In an alkaline 
or ammoniacal urine the pus-deposit occurs as a tenacious, 
gelatinous-looking mass which adheres to the bottom and 
to the sides of the vessel. On repeatedly shaking the 
urine, it is impossible to disintegrate this mass completely, 
and if it be allowed to settle and the urine be then decanted 
into another vessel, the gelatinous pus is often dislodged 
in a lump and precipitated into the second vessel. 

To test a cloudy urine for pus, as distinguished from 
mucus, urates, etc., Dannies reaction is of value. It con- 
sists of allowing the sediment to settle in a conic glass, 
decanting the urine which floats over it, and adding a 
solution of potassium hydrate drop by drop until the 
gelatinous, glairy mass described above is formed, adheres 
to the bottom of the vessel, and slips out from it in a lump. 
This same mass is formed spontaneously in purulent urine 
by alkaline fermentation. The same test m ay be performe d 
more rapidly b y adding equal parts of the KOH solutio n 
to tne urme and olbserviny the appearance of the gelat inous 
precipit ate. 

Donne's test is conclusive only in acid urines. If the 
urine is alkaline, it may fail to show pus, which is then 
best looked for with the microscope. According to 
Goldberg, Donne's test is sensitive to 1000 pus cells per 
cubic millimeter of urine. 

The table on page 32 shows in a condensed form how 

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2 ^ 


•2 II 



• . 8 
^ •■a 

I ^ . 

1 "f^ 

"3 3 











H-l G 





■5 S 

*^ CO 

•a S 



^ o 

•5 « 


o 5 

■^ 5 



3 t § 


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the source of turbidity may be detected in a few seconds 
in a urine with the use of only two reagents and heat. 

Chyluria may be mistaken for pyuria. The former 
depends upon the presence of a parasite — Filaria sanguinis 
hominis — in the blood, and is characterized by urine which 
is a fat-emulsion and is milky in appearance. This urine 
will stand for days without settling, is milky, yellowish- 
white in color, and shows a film of fat or of creamy flakes 
on the surface. The fat is dissolved on shaking with 
ether and the urine is cleared. When there is much fat, 
chylous urine may coagulate on standing. 

Reactio n, — The reaction of normal urine is faindv 
acid to blue litmu s- paper, but occasionally it is faintly 
alkaline to red litmus and faintly acid to blue litm us— 
in other words, amphoteric . The mixed quantity of 
twenty-four hours is always acid normally. The acidity 
is due to the presence of acid sodium phosphate (monosodic 
acid phosphate — NaH2P04) and not to free acid. The 
degree of acidity of the urine depends upon the amount 
of the acid phosphate as compared with that of the di- 
sodium or alkaline phosphate. The urine is neutral or 
amphoteric when the disodium salt is present in a larger 
quantity, although not enough to neutralize the mono- 
sodium or acid salt, so that both blue and red litmus-papers 
give a reaction (Huppert). 

In testing the reaction of urine strips of litmus-paper are 
used — the blue paper turns red in acid urine; the red paper 
turns blue in alkaline urine, and if the urine be amphoteric, 
both reactions take place. In testing, the paper should be 
dipped to about half its length into the urine. 

Real and Apparent Acidity. — A great deal of work has been done during 
the past few years by both physiologists and chemists in solving the numer- 


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ous problems arising from the peculiar behavior of the urine toward litmus- 
paper and other indicators. The question was asked for a long time how 
it was possible that an acid fluid could be excreted from the alkaline blood. 
Heidenhain and other physiologists attributed the change in reaction to 
some vital process which goes on in the cells of the kidney. Experiments 
showed, however, that no mysterious vital process was necessary to pro- 
duce an acid fluid from an alkaline. As early as 1876, Maly and Posch 
showed that when a solution of disodic phosphate (Na^HPOJ, com- 
monly known as "alkaline phosphate," and a solution of monosodic 
phosphate (NaHjPOJ, commonly known as " acid phosphate, " were 
mixed and dialysed through parchment, the resultant dialysed fluid had 
an acid reaction. As both of these salts occur in the blood, it is easily 
seen that no vital phenomena are necessary to effect the change from 
alkalinity to acidity during the process of urinary excretion. Analogous 
experiments with other sets of alkaline salts by Koeppe (1901) showed 
that by mixing a solution of neutral salts with a solution of alkaline salts 
an acid fluid could be produced. The explanation of this phenomenon 
is based upon the fact that the molecules in the mixture of salts become 
dissociated and that during the process of solution new combinations may 
form, resulting in the formation of acid salts. 

According to modem physical chemistry an alkaline reaction is due to 
the presence of the ions OH, while an acid reaction is due to the presence 
of the ion H. Titration, no matter how accurate, cannot determine the 
actual number of OH ions^ on the one hand, or of H ions on the other, 
which may be formed in a solution. In other words, while formerly 
chemists understood by " degree of acidity" the amount of hydrogen that 
could be replaced by the sodium of the sodium hydrate solution, regardless 
of whether these hydrogen ions were already dissociated or not, modern 
physical chemistry regards as acidity the number of dissociated hydrogen 
ions in a given volume of fluid.. The most accurate way to estimate the 
dissociated ions is by electrochemic measurements. Thus Rohrer ^ 
found by this method that the presence of the hydrogen ions in the 
normal urine is exceedingly low. The actual acidity of tJie urine by 
accurate methods is about -foooo" ^^ ^^^ indicated by titration. 

The most difficult problem in titrating the urine for total acidity is the 
choice of an indicator. The reason of this is that the acidity of the urine 
(in the ordinary sense of the word) depends upon a variety of acid salts. 
Each of these has a separate end-reaction point. Litmus-paper, which 
was formerly used as an indicator, is the poorest of all acid-detecting sub- 
stances for this purpose. As there is no phosphate neutral to litmus- 

* Archiv. fiir die gesammte Physiologie, vol. Ixxxvi, p. 586, 1901. 

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paper (the acid phosphates give an acid reaction; while the normal or 
monacid phosphate is alkaline), litmus is worthless as an indicator in 
urine (see Oxalic Acid Method). 

The difficulty with other indicators is that it is impossible to watch 
accurately the end reaction. Phenolphthalein is preferred in acidimetry 
on account of the sharpness of the end reaction which it gives, and 
because it is in itself but very feebly acid as compared to other indi- 
cators. The presence of ammonium salts, however, materially inter- 
feres with its action. For clinical purposes, however, phenolphthalein 
is sufficiently accurate, at least, for comparison. 

Finally, according to Lieblein, there is still another source of error, 
namely, the fact that the addition of an alkaline solution, such as is used 
in titration, induces a combination of the alkaline phosphates with the 
calcium chlorid of the urine, resulting in a calcium phosphate of variable 
constitution. The phosphoric acid is not neutralized in constant propor- 
tion, therefore, in any of the titration methods with sodium hydrate solu- 
tion. The amount of phosphoric acid remaining non-neutralized will 
depend upon the amount of calcium and magniesum salts in the urine. 
For these reasons Folin's method (see p. 37) is the most accurate of the 
procedures thus far devised for acidimetry of urine. 

It is questionable whether results obtained by titration are sufficiently 
accurate to repay the time taken in carrying out the method. The results, 
at best, are valuable only as a means of comparison. 

Methods of Determining Total Acidity.^ — The 

^^ Oxalic Acid^^ Method with Litmus. — ^The so-called 
"oxalic acid" method, in which the total acidity is ex- 
pressed "in terms of oxalic acid," is not trustworthy and 
is no longer used by the author. It is as follows: 

Take 100 cc. from a twenty-four-hour specimen, and titrate it in a flask 
or beaker with a decinormal solution of sodium hydrate, using strips of 
sensitive litmus-paper as indicators, until a faintly alkaline reaction is 
produced. The number of cubic centimeters of the sodium hydrate solu- 
tion multiplied by 0.0063 wi^^ g^^e the percentage of acidity in terms of 

^ It is needless to say that the acidity of the urine should always be 
tested in fresh samples of twenty-four-hour urine, for the estimation would 
otherwise be interfered with, both by the possibility of alkaline fermenta- 
tion and by the so-called acid fermentation, which at times precedes al- 
kaline decomposition. 

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oxalic acid. Normally, the total acidity corresponds to 0.189 per cent 
oxalic acid, or 1.9 gm. oxalic acid per liter, or from 2 to 4 gm. of oxalic 
acid daily. 

The Phenolphthahin Method} — ^The solutions required 
are a decinormal sodium hydrate solution and a i per cent, 
alcoholic solution of phenolphthalein. 

Fill the buret with the xV-normal NaOH solution and note the amount 
(reading at lower meniscus, after allowing the fluid in the buret to stand 
for two or three minutes). Place 10 cc. of urine in a beaker and add 2 
drops of phenolphthalein solution. Add NaOH solution from the 
buret drop by drop, until the red color which forms as we approach the 
point of neutralization no longer disappears on shaking. A uniform pale 
red color now tinges the urine, indicating that the acidity is neutralized. 
The number of cubic centimeters of NaOH solution used, multiplied by 
10, will show the acidity in 100 cc. or, in other words, the " percentage of 
total acidity." Normally, from 3 to 5 cc. of xV-normal sodium hydrate 
are used for 10 cc. of urine — i. e., the acidity is from "30 to 40 per cent." 
In the twenty-four-hour quantity (say, 1500 cc.) it is normally from be- 
tween "20 and 30 per cent." According to Emerson, the error is at least 
from 4 to 8 per cent. 

The disadvantage of this method is the uncertainty of 
phenolphthalein as an indicator under the conditions 
which exist in the urine (see above). 

Freund and Topfefs Method. — ^This is somewhat more 
accurate than the preceding, alizarin being used as an 

Ten cc. of urine are placed in a beaker and from 2 to 4 drops of a i 
per cent, alizarin solution are added. In the presence of free acids a 
pure yellow tint is developed, while combined acids give rise to a deep 
violet color. If neither of these colors appear, there are probably com- 
bined acids and disodic (alkaline) phosphates. The amount of deci- 
normal hydrochloric acid solution added to this urine, required to produce 
a pure yellow color, represents the amount of alkaline phosphates present, 

^ Naegeli, Zeitschrift fiir Physiol. Chem., 1900, xxx, 313. 

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while the amount of decinormal NaOH solution required to produce a 
deep violet color represents the amount of acid phosphates. Normally, 
the acidity corresponds to from 4.0 to 20.0 per cent, acid phosphates 
(Serkowski). When over 20 per cent., there is hyperacidity. 

Folin^s Method, — In order to rule out the error which 
arises with phenolphthalein from the presence of ammo- 
nium compounds and of calcium phosphate (see above), 
Folin ^ adds an excess of potassium oxalate. He measures 
with a pipet 25 cc. of urine into a 200-cc. Erlenmeyer flask, 
adds I or 2 drops of 0.5 per cent, phenolphthalein solution, 
and 15 to 20 gms. of potassium oxalate v After shaking 
the flask thoroughly for one minute, the contents is imme- 
diately titrated with the decinormal NaOH solution, the 
shaking being continued. The sodium hydrate is added 
until a faint, yet distinct, color is obtained.^ The calcu- 
lation in " percentage ^' is the same as with the phenol- 
phthalein method of Naegeli (see p. 36). 

Clinical Signifi cance of Reaction and Aridity of 
Urine . — In drawing conclusions from the quantitativ e 
estimation of acidity, the diet should be considered as a 
prime factor. T hg more proteid material is assimilat ed, 
th e higher the acidity will be, while a vegetable diet will 
r educe the acidity or cause the urine to become amph oteric. 

Normally, the acidity of the urine varies at different 
times of the day, there being an ebb and flow of the acidity 
tide corresponding with the meals. The acidity begins 

* American Journal of Physiology, 1903, ix, 265. 

^ To calculate the acidity of the urine, obtained by any of the titration 
methods with sodium hydrate, in terms of hydrochloric acid, multiply 
the number of cubic centimeters of decinormal NaOH used by the coeffi- 
cient 0.00365. One cubic centimeter of the decinormal soda solutions 
corresponds to 0.0365 gm. of hydrochloric acid. Normally, the acidity 
of the twenty-four-hour urine corresponds to about 1.15 to 2.3 gm. HCl. 

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to diminish soon after a meal, and reaches its lowest point 
in about three or four hours, the urine even becoming 
alkaline at such times. The urine is less acid after a 
vegetable diet, and is increased in acidity after a red-meat 
diet. The discharge of hydrochloric acid by vomiting, 
washing out the stomach, or through a fistula, or the 
presence of an excess of HCl in the stomach may cause 
an alkaline reaction. It is on this account that the acidity 
should never be tested in other than twenty-four-hour 
urines. The urine may become alkaline after hot baths and 
free perspiration. Alkalin e salts or vegetable acids give n 
internally as drugs or taken wit h the food in large amou nts 
win decrease the acldlty ot the urme , the acids being con- 
verted into carbonates in the blood, passing into the urine 
as such. The patient should not take any of these drugs 
while under observation for the acidity of his urine. 

An increase of acidity is seen in persons with increased 
proteid exchange. It has been noted that in certain neu- 
roses of the urinary tract there may be an increase of 
acidity, and the same takes place in diabetes mellitus when 
diacetic and oxybutyric acids are present. An increase d 
acidity is also said by some writers to be characteristi c of 
excessive intestinal auto-intoxication. The increase of 
indican and ot the other ethereal sulphates is a better 
measure for the intensity of intestinal putrefaction (see 
p. 174) than is the acidity of the urine. There may be 
increased acidity without indicanuria, in which case it is 
improbable that an increased putrefaction exists in the 
intestine. T^ <;hmi]H bf rf^Tr>f^mK^r|^|^ t hat the so-call ed 
percentage of aci dity varies with the specific gravity ofjj ie 
unne, ana that urine of high specific gravity is usual ly 
fllgl'lly aulU, Wliile by si mpiy maKmg the patient drink more 

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water we can reduce the ^' percenta ge of acidit y." It has 
been claimed lor a long time that the acidity of the urine 
is quantitatively increased in persons with the uric-acid 
diathesis, but at present little importance is attached to 
the question of the reaction of the urine in this clinical 
condition. Uric acid in solution never influences the 
urinary acidity directly, although it may increase the 
acidity indirectly by transforming neutral into acid phos- 
phates (Croftan). There is a limit to the possible in- 
crease in acidity in the urine set by the resistance of the 
body against an acid intoxication. The amount of am- 
monia excreted is increased whenever an acid intoxica- 
tion is present, the body thus protecting itself against loss 
of alkaline mineral material. 

The urinary acidity is always increased in the p resence 
of fe ver, for the reason that febrile conditions are acco m- 
panied by an increased oxidation of pro teids. During 
this process of oxidation sulphuric and phosphoric acids 
become free from the sulphur and the phosphorus which 
form part of the proteid molecule. 

Decreased acidity ma y occur after the absorption of a 
ser ous exudate or transuda te or after the absorption of 
blood into the intestine, the blood salts entering into' the 
c irculation and renderin g the urine alkaline. In some 
cases of pneumonia, in typhoid tever, and in diseases of the 
central nervous system there may be alkaline urine, and a 
marked alkalinity has been noted by Emerson in certain 
cases of nephritis, especially of the chronic parenchyma- 
tous type accompanied by much edema. 

Obstruction and inflammation of the lower portion of 
the urinary tract or in the renal pelvis may also render the 
urine alkaline. The alkalinity of any urine, therefore, js 

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only important when noted in a freshly voided specime n, 
although the rapidity with which a urine grows alkaline 
on standing may be noteworthy in cases of cystitis, stone, 
etc., provided the temperature be kept moderately low 
and protection of the urine against bacterial contamina- 
tion be carefully maintained. 

To test for the presence of volatile alkali, which is present 
in urines which have undergone alkaline fermentation, as 
distinguished from th^ fixed alkali present in urine alkaline 
in virtue of a change of diet, etc., the red litmus-paper 
should be watched while it is drying. When there is fixed 
alkali this litmus-paper retains the blue color where it has 
been dipped into the alkaline urine. Whe n there is volatil e 
alkali, the blue color fades on drying, the paper returnin g 
to a rea color. 

Specific Qravity. — The specific gravity of normal 
unne is oetwe en 1012 and 1024 w hen the amount pass ed 
is norrn aH The standard normal average is 1020 at 60° F. 
(15.5° C). In disease it varies between 1002 and 1060. 
In hot weather it may reach 1035, owing to abundant 
perspiration. The specific gravity is also increased by 
muscular exertion. In children it averages 102 1. Jt 
i s proportionate to the amount of total solids in the u rine, 
a nd th ese in turn vary ac cording[ tn th^ ti fnff p^ ^^^ ^^Yj 
t he meal s, t he amount ot exercise, the amount of fl uid 
drunk, ana tne t otai amount of urine passed d aily. A sci- 
entihc determination of specific gravity cannot be made, 
therefore, without a specimen from the mixed twenty- 
four-hour quantity. Determinations with specimens ob- 
tained at various times may be necessary, but they are of 
no value imless the conditions of diet, exercise, temperature, 
etc., are known. 

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Determination. — The specific gravity of urine is usually 
determined clinically by the use of a special hydrometer 
or urinometer (Fig. 3), which is sufficiently accurate for 
ordinary work. The best type is that of Squibb. The 
urinometer is constructed for a scale from 1000, which is 
marked at the top of the 
stem, to 1060, its principle 
being that the weight of the 
instrument is constant and 
that the denser the fluid the 
less deeply will the instru- 
ment sink in it. A small cyl- 
inder holding about 2 ounces, 
sometimes made with flutings, 
intended to lessen the amount 
of urine required, is supplied 
with each instrument, with a 
thermometer showing the tem- 
perature of the fluid tested. 
Every urinometer must be tested with distilled water at 
60° F. (15.5° C), in which it should sink to 1000, or zero. 
(Squibb's urinometers are standardized at 22.5° C. or 
77° F., a more convenient temperature for clinical work.) 
Carefully made urinometers have accurate division of the 
fractions of degrees, which gradually approach one another 
as they get nearer the bulb, as allowance is made for the 
weight of the stem above the water. The best instruments 
have been tested by the makers and bear the correction for 
variations in temperature on the container. 

In determining the specific gravity a sufficient amount 
of urine is poured into the cylinder, which should not be 
too small in proportion to the urinometer, as the latter must 

Fig. 3. — Squibb's urinometer with 
thermometer and cylinder. 

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not, on any account, be allowed to impinge against the side 
of the cylinder. If this occurs, the influences of friction and 
of capillary attraction tend to prevent the instrument from 

sinking. The urinometer should 
be dried before immersion. The 
foam should be removed from the 
urine by means of filter-paper, 
and the instrument should be 
lowered gently with a slight spin- 
ning turn, which will prevent it 
from being attracted to the sides 
of the vessel. The reading should 
be taken when the instrument is 
completely at rest and is not 
touching the sides of the cylinder 
at any point. The urine will be 
found rising in a small hillock 
around the stem (Fig. 4), over the 
level of the fluid, and in reading 
care must be taken not to read 
at the top of the hillock, but at 
the level of the lower portion of 
the meniscus formed at the con- 
tact of the urine with the stem. 

The specific gravity of urine 
should never be taken in a 
specimen freshly voided, as the 
latter is apt to be at or near the 
temperature of the body — i. e,, 98.6° F. (37.2° C.) — ^while 
the urinometer is made for about 60° F. (15.5° C). If an 
immediate examination is required, the specimen must be 
cooled rapidly to the proper temperature by immersing the 

Fig. 4. — Urinometer im- 
mersed, showing effect on the 
surface of the urine. 

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cylinder in cold water. A correction for temperature may 
^ be roughly made with sufficient accuracy for clinical pur- a 
I poses by adding o.ooi to the specific gravity read for every I 
\ 3° C. that the urine is below the point at which the urin- I 
It ometer is standardized, or subtracting the same amount I 
^ for every 3 degrees that the urine is above that point. 

Other and more accurate methods for estimating specific 
gravity are the Westphal-Mohr balance, the pyknometer, 
SprengePs tubes, etc. 

The Westphal balance is a beam scale, finely constructed, 
which has a small glass thermometer suspended by a fine 
wire from the balance end in the urine to be tested. The 
weight of this thermometer in urine, as compared to its 
weight in distilled water at standard temperature, gives the 
specific gravity of the urine. These balances are very 
accurate, but their price is somewhat high and the urin- 
ometer is sufficiently accurate for the practising physician. 

The methods for determining the specific gravity by 
means of the pyknometer, SprengePs tubes, etc., may be 
found in text-books on physics. They require an accurate 
analytic scale, and depend upon the principle of comparing 
the weight of a very accurately measured volume of dis- 
tilled water with exactly the same volume of urine of the 
same temperature, the specific gravity being deduced from 
the ratio of these two weights. They constitute the most 
accurate methods for taking specific gravity, but are useful 
only for strictly scientific work. 

In taking the specific gravity of small amounts of urine — 
i. e.j amounts less than the 30 cc. which are required to 
float a Squibb's urinometer — we are compelled to resort 
to some expedient other than the ordinary method. The 
use of test-tubes instead of cylinders is not to be counte- 

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nanced, inasmuch as the readings cannot be accurate, the 
instrument constantly adhering to the wall of the tube by 
capillary attraction. The method of diluting the urine with 
water a certain number of times and multiplying the specific 
gravity of the diluted urine by that number is, if anything, 
still less accurate, for the error is multiplied in propor- 
tion to the dilution, and no urinometer is made accurate 
enough to read such exceedingly low gravities as are shown 
by diluted specimens. The use of the Westphal balance 
enables us to read the specific gravity of 15 or 20 cc, and 
the pyknometers and SprengePs tubes may be used with 
still smaller quantities, but all these are inaccessible to 
the physician on account of the high price of the apparatus 
they require. 

The Author^ s Method for Small Amounts of Urine, — 
A special method devised by the author for the estimation 
of specific gravity in the smallest amounts of urine without 
recourse to expensive appliances or complicated manipula- 
tion consists in the use of a urinopyknometer, which is a new 
form of hydrometer that determines with clinical accuracy 
the specific gravity of about 3 cc. of urine. 

In this instrument the urine is placed in the hydrometer 
instead of the hydrometer being floated in the urine. The 
urinopyknometer is a little smaller than the ordinary urin- 
ometer, and consists of a small flask with a well-fitting glass 
stopper, the head of which bears a tiny bead of mercury 
(Fig. 5, D-E) . This flask is attached to a small spheric bulb 
(Fig. 5, c), over which is the stem (a-b) of the instrument, 
graduated in reverse order as compared to the ordinary 
urinometer — that is, the mark 1060 is at the top of the 
stem and the mark 1000 at the bottom. When the flask is 
filled with distilled water up to the mark m, and when the 

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instrument is closed and immersed in distilled water, it 
reads looo at the level of the distilled water. When urine 
is poured into the flask to the same mark, the instrument 
sinks in distilled water in proportion to the specific gravity 
of that urine, which is then read on the 


scale. The same precautions in read- 
ing are taken in using this instrument 
as with the urinometer, and, in addi- 
tion, the flask must be dry and per- 
fectly clean (washed with alcohol or 
ether). The urine must be poured in 
accurately with a small dropper until 
it reaches the mark, so that the lower 
meniscus touches it as the flask is 
held at the level of the eye. The 
urinopyknometer is of special value in 
cases in which very small amounts are 
furnished for analysis, as in infants, in 
catheterizing the ureters, and in emer- 
gency work,^ when but small quantities 
are voided by the patient. 

Pathologic urines often show an 
increase or a diminution in specific 
gravity, but inasmuch as the latter 
varies normally to a considerable ex- 
tent with the quality of meals, the 
amount of exercise, etc., an abnormal 
specific gravity is of value only when obtained from a 
twenty-four-hour specimen the volume of which is known. 

The specific gravity is increased in t hfr bfg^'^^^'^g of 
acut e fever, after prolonged surgical operations, esp ecially 
* New York Med. Journal, Oct. 1 7, 1903. 



-— M 

Fig. 5. — The author's 

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with ether anesthesia, on account of the hemorrhage and 
the perspiration, in acute Bright's disease in its early stages, 
and in other conditions accompanied by blood in the urine. 
In the pre sence of lar ge amounts of sugar in diabetes t he 
specific gravity may be very high and sometimes reaches 
1050^! When a large amount of urine is passed of a high 
specific gravity we suspect diabetes, but absence of sugar 
must not be inferred from a low specific gravity. 

A dimini shed specific gravity occurs in diabetes insipid us, 
in hysteria, and in chronic interstitial n ephritis. In all 
forms of Bright's disease, except in the acute in its first 
stage, and in stasis in the kidneys of heart disease, there is 
a tendency toward a lower specific gravity as well as a les- 
sened percentage of urea. If no albumin and no sugar be 
present, the rule is that a lower specific gravity usually 
means less urea. A marked decrease in specific gravity 
is a serious symptom in chronic Bright's disease. 

Total Solids. — T he determination of the total solid s 
eliminated in the urine durin g the twenty f on r V|mir<; i<; 
useful cl micaliy, masm uch as it g ivef=^ «n irmjgV>t mtn thp 
re lations ot quantity and specific gravi ty. The general 
rule is that the quantity of urine is small when the specific 
gravity is high; in other words, that the specific gravity 
varies in proportion to the concentration — i. e., in propor- 
tion to the amount of solids dissolved in the fluid. In 
certain diseases there is a noteworthy diminution of the 
total solids excreted, reflected in a lower specific gravity, , 
and it is useful to know whether a lower specific gravity 
in a given case depends largely or materially upon an 
increased amount of the watery element of urine or upon a 
markedly decreased amount of total solids. 

For clinical purp oses, the a mount of total solids in_t he 

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twenty-four-hour urine is d pt^rmineH approYi matelv hv 
multiplying the two last figures of the specific grav ity 
by Haesefs coefficient, which is 2,;^:^, and thus obtain ing 
roughly the number of p^rams of solids in 1000 c c. (i liter) 
of urine (ss-S oz.). T his number, multiplied by the num - 
ber of cubic centimeters passed in twentv-four hours and 
divided by 1000, will give the a mount of solid constituents 
el iminated in twenty-four h ours. 

Example: The specific gravity of urine is 1020. Multi- 
ply the last two figures by 2.33: 20 X 2.33 = 46.6 grams 
in 1000 cc. of urine; therefore, ^^'\^^°° = 69.9 grams of 
solids in twenty-four hours. 

This method is sufficiently accurate for clinical purposes, 
but for scientific work a given amount of urine is evaporated 
in a previously weighed porcelain dish, the residue dried, 
allowed to cool, and weighed repeatedly until there is no 
further loss of weight from drying. The variations be- 
tween the solids found by weighing and those found by 
multiplying by 2.33 are, on the average, very slight. The 
a verage excr etion of solids is 61.14 grams {q^<, ^r.) in twenj y- 
f our hours tor k pfel^son weighing i4t; pounds avoirdup ois 
(66 kilos). The excretion of solids varies according to 
age, weight, and height. 

Parkes lays down the rule, which he worked out by means of the 
combined observations of a number of authors, that 10 per cent, must be 
deducted from the average solids in persons between forty and fifty years 
of age; 20 per cent, between fifty and sixty; 30 per cent, between sixty and 
seventy; and 50 per cent, above seventy. The normal standard applies to 
an ordinary diet of mixed foods and to the ordinary exercise of a healthy 
man in daily work. In persons who have fasted for two days or longer, as 
in fevers, etc., one-third should be deducted from the average solids; one- 
eighth, if the diet be spare; one-tenth, if somewhat below that of health. 
For perfect rest one-tenth should be deducted; for comparative rest, one- 

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It should be noted that no deductions can be drawn as to the amount 
of any particular solid from the weight of the total solids, and especially 
that although urea normally constitutes about one-half of the solids ex- 
creted, an estimation of the urea present by dividing the amount of total 
solids by two is of no value, as the proportions of the various constituents 
vary markedly. 


Amount. — What is the normal amount of urine passed by an adult? 
What is the average? How does it vary according to the sex and size 
of the person ? According to the amount of liquid drunk and the amount 
of exercise? According to the time of day in health? According to 
season ? • 

Define oliguria; anuria; polyuria; poUakuria. 

When is diminution in quantity noted? 

When is an increase noted ? What is noted in Bright's disease, as a 
rule, as regards the quantity of urine? 

Color. — What is the normal color of urine ? On what does it depend 
in health? In disease? In what diseases do very pale urines occur? 
Highly colored urines ? To what is a reddish urine due ? A dark-brown 
urine? A ** smoky" urine? A black urine? A yellowish-green foam ? 
A blue urine? A greenish-blue urine? 

Odor. — What is the odor of normal urine ? What is it due to ? What 
does an ammoniacal odor in a freshly passed urine indicate? An odor 
of sulphuretted hydrogen ? A fecal odor ? An odor of violets ? A drug 
odor? A fruity odor? 

Consistence. — When does urine become thick and stringy ? When does 
it tend to froth ? What is the consistence of chylous urine ? 

Transparency. — Describe normal urine as regards transparency. 
What is the nubecula? How is the nubecula noteworthy in women? 
When is it increased and how does the cloud behave then? How is 
this cloud distinguished from other causes of turbidity ? What are these 
other causes ? How does a cloud due to bacteria behave ? A cloud due 
to phosphates? To urates? How are these clouds distinguished from 
one another? What is the behavior of cloudiness due to pus? What is 
Donne's reaction for pus ? How is chylous urine distinguished ? Give in 
tabular form the tests distinguishing all these causes of cloudiness. 

Reaction. — What is the normal reaction of urine ? What is it due to ? 
When is urine neutral or amphoteric ? How does its acidity vary nor- 

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mally ? When is freshly passed urine alkaline ? How do you test reac- 
tion in urine? 

What is the best way to obtain an idea as to the total acidity of the 
urine? What do we mean by acidity " in terms of oxalic acid"? In 
terms of HCl? In terms of decinormal NaOH solution? Under what 
condition is acidity increased ? Decreased ? 

What is the normal specific gravity of urine ? How does it vary and 
why ? What is needed for accurate determinations ? Describe the urin- 
ometer and its mode of application. What other methods may be used ? 
What is the Westphal balance ? Describe the urinopyknometer and its 
uses. What precautions should be taken in reading the specific gravity 
with any urinometer? When is the specific gravity of urine increased? 
When is it diminished ? In what disease is a marked diminution of the 
specific gravity a grave symptom? 

What is the clinical value of a knowledge of the amount of total solids ? 
How is this amount calculated approximately? What is the average 
amount of solids excreted in twenty-four hours ? What changes must be 
made in this figure to allow for age ? For exercise and diet ? 

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The most common proteid in the urine in disease is 
serum-albumin, although pathologic conditions of the kid- 
neys, of the blood, or of other organs may also result in 
the excretion of other proteids, such as serum-globulin, 
fibrin, hemoglobin, albumose, peptone, nucleo-albumin, 
etc. By albuminuria we nmiallv mean the pre sencg of 
serum-a lbumin and serum-globulin, with due regard to the 
possib ility and probability of the presence of other pro teid 
co nstituents of minor Irnportanr e. 

It has been shown (Leube, Flirbringer, Senator, and Pos- 
ner) that a healthy kidney may excrete a certain amount 
of albumin, although very careful experiments have proved 
that not every urine contains albumin (Leube and Winter- 
nitz). Ac cording to Grainp[pr Stewart, the minute quan ti- 
t ies of albumin m normal urines are due to epit helial and 

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Other debr is. At any rate, there is no doubt that occasion- 
ally serum-albumin and serum-globulin in small quantities 
occur in the urine without any changes in the kidney, 
probably owing to a sudden disturbance of the circulation 
(von Jaksch). R ecent studies by Ott and others have_ 
showp that so-called nucleo-albumin is preiy Tif in all 
healthy urines , and that, consequently, it is very important 
to distinguish this proteid from serum-albumin. (See 
Mucin, Mucoid, Nucleo-albumin, p. 87.) 

Albumin, like other proteids, is a colloid which does not 
crystallize and does not penetrate through animal mem- 
branes. So long as the animal membrane — in this case 
tubular epithelium — remains intact; so long as the proteid 
itself remains unchanged; so long as the pressure in the 
blood-current and in the excretory channel remains normal, 
no albumin is excreted by the kidney (see Secretion of 
Urine, p. 389). Albuminuria mav b^ due^ the^ f fm-r, ^^ ^^^ 
^fjjjjxuiactors, namely: (i) Changes in the kidney which 
affect the excretory epithelium; (2) changes in the blood 
which render its serum-albumin more diffusible; (3) 
changes in the blood-pressure. Serum-albumin in notice- 
able amounts is never found in healthy urine, and its pres- 
ence is always an important clinical symptom. 

Albuminuria, — By albuminuria, in the clinica l sense, 
w e have come to understand the presence of amounts of 
alb umin which are detected bjy the ordmary tests , and not 
the presence of minute traces discernible onlv with very 
delicate m ethods. Hofmeister lays down a good rule when 
he says tkat whenever Heller's ring test is positive within 
three minutes after contact, albuminuria is present. 

Albuminuria may be subdivided into false and true al- 
^^/V buminuria. False albuminuria (accidental albuminuria, 

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spurious albuminuria, pseudo-albuminuria) jsjlfipendent 
ii]wi an afJTTnYtnrpof Rlhnmin^nq s^ubstances /mucus^ pus, 
b lood, semen, pros tatir fluid) witVi thp nnnp fji iring iff; 
transit from the kidney downward . This condition occurs 
in pyelitis, ureteritis, cystitis, prostatovesiculitis, sperma- 
torrhea, etc., and in the presence of fistulous, openings 
into the urinary or genito-urinary tract, through which 
proteid exudates, etc., may enter the urine. The se 
albuminurias are distinguished by microscopic examina - 
tion of the sediment, by catheterizing the ureters and 
examinmg the urine direct from the kidneys, and by th e 
fact that oth er proteids than serum-albumin ar e, as a rule, 
relatively increase d. Fifty thousand pus-cells can give 
one part in a thousand of albumin. The false or extra- 
renal albuminurias are especially noteworthy in connec- 
tion with life insurance examinations. 
• True or renal albuminuria is dependent upon the e x- 
cretion of serum-albumin (and usually of serum-globulin, 
q, V.) by the renal tubules . This form of albumin uria^ 
however, may occur without any anatomic lesions of th e 
kidney^ The following classification of true albuminuria 
is intended to show the various clinical types which are 
distinguished with reference to their origin or to some 
special features, such as periodicity, etc. 

I. Fiinr.Hn||pl ^Ihnm inurjas . — Physiolog ic Albuminuri a. — Properly 
speaking, this term should be applied only io the excretion of the minute 
quantities of albumin occurring normally in the urine. According to 
Senator, any amount over 0.4-0.5 gm. in twenty-four hours cannot be 
physiologic. Hofmeister considers any quantity as pathologic which 
gives a ring with Heller's test within three minutes. Traces shown by 
such delicate tests as Spiegler's are not considered pathologic. 

A group of conditions at times accompanied by albuminuria are 
sometimes classed as " physiologic." They are, more properly speaking, 
functional albuminurias occurring under special conditions: 

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1. A fter Severe Muscular Exertion. — A comparatively slight, tem- 

porary albuminuria, sometimes with casts, occurs in young men 
who indulge in unaccustomed physical exertion. This is seen 
in soldiers, football players, bicycle riders, mountain climbers, 
etc. The tendency to albuminuria diminishes as these persons 
become accustomed to the exercise. 

2. After Eating an Excess of Proteid Foo d. — * 'Alimentary albumin- 

uria," also slight and transient, may occur in young robust 
subjects (soldiers, etc.) after a heavy proteid meal. 

3. Followinff Nervous Shocks and Other Vasomotor Chan ges, — 

' Prolonged cold baths have given rise to transient albuminuria. 
The same is true of mental shock, mental strain or fatigue, and 
after faradization. The amount of albumin in these cases does 
not exceed 0.5 per cent. 

4. T)urifLt r Jjih nr. — ^Women in childbirth frequently have albumin- 

urias which disappear during the first forty-eight hours of the 
lying-in period. This albuminuria is independent of renal 
lesions and is probably due to muscular fatigue, to changes in 
the circulation, or possibly to the excretion of toxins after labor. 

5. Newborn Childre n. — During the first week or ten days of life 

a slight albuminuria (at times with casts) may occur, without 
any special significance. 
II. Essential Albuminuria s. — The word " essential" is here used for 
want of a better name to designate a group of comparatively rare albumin- 
urias the cause of which is unknown, but which are not ph)rsiologic nor 
apparently purely functional, yet which are not accompanied by any renal 

I. Cyclic albuminuria (Pavy) or orthostatic {posturaT) albuminuria; 
albuminuria of adolescence (Leube). 

(a) By cyclic albuminuria is meant one which recurs periodically at 

certain hours in the twenty-four (usually between 12 and i p. m. 
and again from 7 to 11 p. m. — double cycle). ^ 

(b) Orthostatic (orthoti( [) r>r ^n^^uml albuminuria occurs only when 

the patient is standing, and disappears when he goes to bed. 
(These albuminurias are, of course, also cyclic if they come on 
regularly in the daytime and disappear at night.) 
These albuminurias occur for the most part in young anemic and 
neurasthenic subjects (male and female), amount to about 
one part per 1000, and are probably the result of abnormal 
conditions of the * circulatory apparatus (Serkowski). As 

* The term " intermittent " is discarded as confusing. 

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these cases occur chiefly during the years of growth (puberty, 
adolescence) it has been surmised that the kidney does not 
seem to be able to keep pace with the patient's bodily develop- 
3. Albu minuria Minima (Lecorch^ and Talamon). — This occurs 
in adults, and is a very slight albuminuria, which persists after 
infectious and debilitating diseases. The amount never ex- 
ceeds 0.5 per 1000. These cases may go on with a mere trace 
of albumin for years or may develop into chronic nephritis. 
According to Albarrant a persistent minimal albuminuria 
may be the precursor of renal tuberculosis. Some French 
authors regard it as a premonitory sign of gout. It may be 
due to a healed acute nephritis which has left some small 
part of the kidney badly functionating. These cases are on 
the borderline, close to the nephritic group. 
III. Traumatic Albuminurias^— These may be transient^ due to 
slight injuries to the kidney and pelvis (massage of the kidney will pro- 
duce it — Menge), to movable kidney, and to injuries to the brain, apo- 
plexy, etc. When the kidneys are seriously injured healing carries with it 
a chronic (interstitial) nephritis with albumin and casts. 

IV. Hematogenous Albuminurias . — A number of changes in the 
blood can cause albuminuria without renal lesions. Among them are 
severe anemia; purpura, scurvy, cholemia, diabetes, leukemia, severe 
wasting diseases, and after the use of anesthetics (ether, chloroform). 

V. Nervous Albuminuri as. — Insanity, conditions of mental depres- 
sion, psychoses, paralyses of certain parts of the brain, epilepsy, delirium 
tremens, etc., may be accompanied by an albuminuria (up to 0.6 per cent. 
— Serkowski). 

VI. Albuminuria of Renal Stas is. — In conditions of passive con- 
gestion— ^T^TmcardialTpu^^ hepatic diseases in the presence 
of mechanical pressure (stones, tumors) — albuminuria may occur (not 
over 0.1-0.2 per cent), with casts and usually a few red blood-cells. 

VII. Toxic A lbuminuriag. — Among the toxic causes of albuminuria 
may be mentioned Irritants (cantharides, turpentine), poisoning with 
arsenic, mercury, phosphorus, lead, antimony, alcohol, and mineral acids. 
Phosphorus, turpentine, and cantharides may, however, produce true 
renal lesions. In syphilis there may be albuminuria in the early second- 
a ries (later there may be a nephritis due to syphilitic lesions in the kid- 
neys). Albumin and casts may also occur during the administration 
of balsamic drugs (sandalwood oil, etc.). 

The febrile^ diseases^ especially those of infectious character, are fre- 

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quently accompanied by transient albuminuria during the height and the 
decline of the fever. These albuminurias may or may not be followed 
by nephritis and are known as febrile albuminurias. 

VIII. Nephritic Albuminurias. — This class is characteried by actual 
more or less permanent lesions in the kidneys. It must be remembered 
that in some forms of nephritis (chronic interstitial) the urine is often free 
from albumin. The albuminuria of nephritis may also be intermittent, 
disappearing for a time with rest, diet, etc., reappearing under the prov- 
ocation of indiscretions in diet, etc. 

The following table shows the amount of albumin which 
may be expected in various conditions of the kidney : 


Renal congestion. 
Acute parenchymat- 
ous nephritis. 

Subacute parenchy- 
matous nephritis. 

Chronic parenchy- 
matous nephritis. 

Chronic interstitial 

Amyloid kidney. 


Usual Amount. 

Highest Amount. 


I to 5 per looo (glob- 
ulin high). 

0.5 per 1000. 

Usually not over 10; 
rarely 15 per 1000 
(enormous amount, 85 

4 to 8 per looo. 

per 1000 in early neph- 
ritis of syphilitics). 
Rarely 10 per 1000. 


i.o per 1000 

Faint traces or none. 

Traces seldom over 0.5 

Small amount usu- 

per 1000. 
Large quantity, especi- 
ally globulin, in some 


Trace, or disappears 
before attack. 

Often increases during 

It will be seen, therefore, that the mere fact that the urine 
contains albumin does not mean that the patient has neph- 
ritis, although this was the general view formerly, and many 
of the older practitioners still cling to it to-day. No diag- 
nosis of Bright's disease can be made from the presence of 
albumin alone. Another point to be remembered is that 
the quantity of albumin present is not a measure of the ex- 
tent or advancement of a renal lesion. Indeed, in the worst 

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cases of chronic Bright's disease — interstitial nephritis — 
albumin is frequently present in very small quantities and 
often temporarily or permanently absent. In the presence 
of an acute inflammatory process in the kidney or of a 
chronic parenchymatous nephritis the variations in the 
daily amount of albumin, taken together with the amount of 
urea, the number of casts, etc., may assist in determining 
the prognosis of a case. 

The physician must be on his guard against the false 
alarms of accidental albuminurias and the comparatively 
less important types of albuminuria grouped under the 
heading of circulatory, febrile, hematogenous, and inter- 
mittent. A careful study of all the clinical features in the 
case, especially as to the periodicity of the symptom, the 
quality of the proteid substance found, the condition of the 
circulation, and the presence of microscopic features 
indicating renal disease, is the basis of accurate diagnosis 
in such cases. 

Precaution s. — In testing for albumin, it is most im- 
portant to have a fresh specimen of urine and to have a 
perfectly clear urin e. Decomposition gives rise to an 
abundant bacterial growth, which in itself may give a faint 
albumin reaction in some cases. The urine should be 
filtered through several thicknesses of the better quality 
of white filter-paper, such as is used for chemical analysis. 
Loosely textured filter-paper of the cheaper grades is 
useless. Even with the best of care, filtration may not 
remove bacteria. An asbestos filter may also be used or 
the urine may be shaken with a small amount of heavy 
calcined magnesia. If the latter is used, the urine should 

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be rendered acid by the addition of a few drops of nitric 
acid before it is tested. Fine sand may also be used for 
filtering, but care should be taken to have it perfectly free 
from organic matter. 

If the urine is concentrated, it should be diluted be fore 
testin g, as dilution eliminates the action of certain bodies, 
such as urea, phosphates, etc., which interfere with al- 
bimiin tests. 

The best time to detect small amounts of ^-Ihnmin^ k^- 
in the eve ning, especia lly in walking patients. Inthemorn- 
ing, after a night's rest, the urine of such patients is fre- 
quently free from albumin. 

Heat Test, — With Nitric Acid.— A test-tube is filled 
with clear urine ^ and the upper portion of the fluid is 
heated to boiling. If the heated portion becomes cloudy, 
even in the slightest degree, as we can see by holding the 
tube against a black surface, the turbidity is due either to 
albumin or to earthy phosphates. If the cloudiness is due 
to the latter, it disappears on adding a few drops of nitric 
acid; if it is due to albumin, it remains. If no precipitate 
appears or if the precipitate redissolves on shaking upon 
the addition of the acid, two or three more drops of the acid 
are added, and if a flocculent precipitate results, albumin 
is present. 

TTnHpr favnrahj e conditions heat will detect i part of 
albumin in loo.oo ^ parh ^f ^i^^'^^, but there ar^ ma ny 
sources of error in the test by heat. The effects of t he 
p resence of earthy phosphates have already been spok en of. 
A nother so urce of error is th e fact that jf th ere is v ery little 
albumin, the amount of acid will be in ex ces s an d the al- 

^ When the urine is not clear, it should be filtered before applying any 
of the§e tests. 

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bjLimm will dissolv e: on the other hand, if both phosphates 
and albumin are present and too littl e acid be used, the 
acid is taken up by part of the phosphates, wh ile the re- 
mainder of these salts un ite with the albumin to form sol- 
uble al kaline albuminates, the urine r emaining clear. 

Very hi ^y^ly nri^ nrmf> from natural causes may fail to 
precipitate albumin by heat on the addition of acid, owing 
to the fact that a soluble acid albumin is formed under 
these conditions. The latter may be precipitated on the 
further addition of nitric acid or on neutralizing with potas- 
sium hydrate. There is a danger, however, of converting 
the albumin into soluble alkali albumin with the least ex- 
cess of alkali, and so redissolving the precipitate. Highly 
al kaline urine conv erts the albumin into a soluble alkali 
albimiin which is non-coagulable by heat, like the acid al- 
bumin. In this case the addition of a few drops of dilute 
acid will convert the alkali albumin into serum-albumin, 
which will be precipitated by heat. 

If the tes t-tllbf ^'^ P^^ ^i^ar> and happens to contain a 
drop of nitric acid, boiling may fail to cause a cloud on 
account of the conversion of serum-albumin into non- 
coagulable acid albumin. A flocculent precipitate formed 
before the addition of acid in the heat test may be calcium 
phosphate, which is soluble in an excess of acid. Such 
a precipitate occurring after the addition of acid is albumin. 
The urine should not be heated after the addition of the 
acid, as the coagulated albumin is soluble in the heated 
acid, and this is the reason why this test is not good for 
very small amounts of albumin, as the latter may be dis- 
solved upon the addition of the acid if the fluid is hot 

Another source of error is the pres ence of uric acid or 

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urate s, which may give ris ^ ^^ pr^ripitatpg th^|; arp rryt;- 

tallin e (not flocculent) and which do not appe ar if the urin e 
be diluted with three parts of water before the J est. The 
precipitate of uric acid is dark brown in color and does not 
fall until the specimen begins to cool. The presence of 
resinous acids in cases in which copaiba, cubebs, turpen- 
tine, benzoin, sandalwood oil, or Peru or tolu balsams have 
been taken gives a precipitate which dissolves in alcohol, 
while albumin is precipitated by this substance. Urines 
full of bile-pigments at times give a precipitate of bili- 
verdin, but this is soluble in alcohol. 

With Acetic Acid and Sal t. — The heat test may be 
performed in the same manner as has been already de- 
scribed, with acetic instead of nitric acid. Formerly, the 
urine was rendered slightly acid with a few drops of 2 
per cent, acetic acid, and the upper portion of the test-tube 
was boiled. The precipitate which results may be either 
serum-albumin or it may be partly composed of nucleo- 
albumin and partly of serum-albumin. As we shall see 
later, nucleo-albumin (or a substance thus designated) 
occurs very frequently in normal urine, and it is exceed- 
ingly important to eliminate the possibility of a mistake 
resulting from the appearance of a precipitate of nucleo- 

The elimination of nucleo-albumin in the test with acetic 
acid is best secured by the use of a sufficient amount of jt 
saturated solution of sodium chlorid, which when added 
to the urine prevents the precipitation of nucleo-albumin. 

The principle underlying the use of salt solution is the 
fact that nucleo-albumin is coagulated by heat in urine 
only when the urine is poor in neutral salts. This fact 
has been known for some time, but it was due to Cohn- 

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heim* that it has been so systematically applied to the 
dififerentiation of proteids. If saturated sodium chlorid 
solution is added to the urine any lack of neutral salts that 
may have been present in the urine as voided is balanced 
by this addition. The salt solution, therefore, is used 
simply to make sure that there are enough neutral salts 
in the urine to keep the nucleo-albumin from coagulating 
when the acetic acid and heat test is applied. 

Method of Performinf; the Tes t, — Purdy ^ gives the fol- 
lowing method of performing this test: A test-tube is 
filled about two-thirds full of the previously filtere d 
urine and about one-si xth of this volume of a satur ated 

s o3mift Chlorid so lution i s added. Next, from 5 to_io 

drops of acetic acid (50 per cent.) are_ _a<^^^^7-^"'^ 
the upper p ortion of the conten ts__of..tb£.j£St-tube is 
boiled for one-half minute, giving a precipitate if albumin 
be present. * ———————— 

Hastings performs the test as follows: To the urine 
one-fifth volume of a saturated sodium chlorid solution 
(30 per cent.) is added. The upper third of the tube is 
heated. If a cloud appears it may be due to phosphates. 
From 2 to 5 drops of acetic acid (50 per cent.) are now 
added, and the upper portion of the tube is again heated. 
If the cloud was due to phosphates, it will disappear on the 
addition of the acid, and the upper portion of the tube will 
clear up, while the phosphates in the lower portion, which 
by this time have become heated, will cloud the tube until 
the acid permeates the entire liquid, when the contents 
will be cleared. If the cloud persists at the top of the fluid, 
after the addition of acetic acid and after heating again, 

^ Chemie der Eiweisskorper, Braunschweig, 1900. 

^ Practical Urinalysis, Philadelphia, 1900, fifth edition, p. 72. 

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serum-albumin is present (sometimes associated with 

This test, while somewhat less delicate than the heat 
and nitric acid test, is very satisfactory for routine use. In 
the author's hands it has given very accurate results in 
upward of 3000 urines tested by the modification of Hast- 
ings just mentioned. When very faint traces are present, 
however, the test should be confirmed by some of the other 
methods, notably the nitric acid ring test and the ferro- 
cyanid test. 

Great care should be taken in the use of the acid and 
heat tests to have the urine perfectly clear (as has already 
been mentioned). A test for albumin with any of these 
methods is absolutely worthless with cloudy urines unless 
tnere be a large amount of proteids present . The practice 
of testing the urine without filtering, as is done in labora- 
tories which employ the "quick lunch" methods of exam- 
ination and which handle a very large number of urines 
in a short time, is to be especially deprecated. No reliance 
can be placed upon findings under these conditions, for 
nearly every urine will be found to contain faint traces of 
albumin unless the tests are performed with all due pre- 
cautions against error. 

The Nitric Acid Test {Heller's Tg^/).— This test is 
exceedingly sensitive, and for all practical purposes is 
probably the best. The urine should be filtered, even 
t hough it appears perfecdy cle ar. A small amount of pur e, 
colorless nitric acid — HN Oo (c. p.) — is poured into a sma ll 
te st-tube; the latter is held obliquely in the left hand, wh ile 
th e urine is allowed tn trickle down the sif ^ of thp tnhp from 
a pipet consisting of a glass tube 6 or 8 inches long and 
drawn to a point. The urine will overlie the ac id if it 

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has been poured in gently enough. If albumin is presen t, 
a distinct, sharp, white zone will appear at the juncti on 
ot the two nuias , varying in thickness — not according to the 
amount of albumin, but according to the rapidity with 
which the urine is poured and also according to the effer- 
vescence that follows the addition of the urine (Ogden). 
The band may vary from ^^2" ^^ i ^^^^ in width, and in 
the presence of large quantities it is narrow, but very 
dense. If minute traces are present, it takes the shape 
of a hazy ring or cloud, which becomes more distinct after 
a few minutes. 

Another way of performing this test is to pour the urine 
into the tube first and to allow the acid to pass down the 
side and under the urine. This manner of using nitric 
acid is not so convenient as the first. 

Still another method involves the use of a small wineglass. 
This is filled one-half full of the filtered urine, the glass is 
inclined so that the urine reaches nearly to its edge, and 
the nitric acid is poured under the urine, as slowly as pos- 
sible, from a small bottle, until the acid reaches about one- 
third the volume of the urine. The objections to this 
method are that it requires more acid and is not so con- 
venient as the test-tube method. 

Precautions in Using Heller's Tes t. — ^When nitric 
acid is placed in contact with normal urine, a brown ring 
appears which increases on standing and is due to the 
action of the acid on the coloring-matters, ^ n^urine with 
much colo r ing-matter the albumin, if present, will also be 
colored brown, or if there is much indican, the albumi n 
r ing[ will assume a red dish or violet tinge; if muc h bloo d- 
coloring matter, a browni sh-red; li biliary pign ients, a 
green color. 

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The overlying of nitric acid with urine precipitates the 
albumin as acid albumin, since the latter is not soluble in the 
excess of acid at the point of contact. Mucin is also pre- 
cipitated, but is dissolved by the excess of nitric acid at the 
point of contact, and, therefore, does not form part of the 
ring. Peptones are not precipitated in this test, but albu- 
moses and resins are. The differentiation from resins is 
best made by using some other test which does not pre- 
cipitate the latter (sulphosalicylic acid) . Nucleo-albumin ^ 
gives a ring which is fainter and is about i cm. above 
that due to albumin. A white zone is also formed by the 
action of nitic acid on the mixed urates if these are in excess. 
This zone of acid urates is found over the zone of contact 
between the acid and the urine; it tends to diffuse rapidly 
into the urine above and is' dissipated on the cautious ap- 
plication of heat. If uric acid is present in large amounts 
urea nitrate precipitates in crystals, but this can occur 
only in very concentrated urines. 

If there is a large amount of carbonic acid and ammo- 
nium carbonate, as after alkaline fermentation, a vegeta- 
ble diet, etc., the contact of urine with nitric acid produces 
so much effervescence that the test cannot be used. In 
this condition the following method (Hoffmann and Ultz- 
mann) may be used: Add to the urine about one-quarter 
part of potassium hydrate solution, warm the mixture, 
and filter; if the fluid is still cloudy and cannot be 
cleared by ordinary filtration, add i or 2 drops of the 
magnesium solution (see p. 218), warm again, and filter. 
The urine thus cleared will show albumin with Heller's 

In the presence of resins, coloring-matters, etc., rings 

^ Or (as we shall see later), more accurately, euglobuliit, etc. 

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of precipitate which are soluble in alcohol will occur (com- 
pare under Heat Test with Nitric Acid, p. 57). 

Other Tests for Albumin. — The heat tests and Hell er's 
test are the most important modes of detecting album in. 
They are usually sufficient, but in case of doubt and when 
we desire extreme delicacy, the tests which follow may be 
used. In practice it is a much better plan to use one or 
two tests as a matter of routine, to know these tests with 
all their possibilities and fallacies, and not to burden one's 
self with too many tests and reagents. Many of these less 
important tests are very sensitive, but clinically extreme 
delicacy is not desirable, as it leads to confusion when we 
remember that normal urine contains very faint traces of 
albumin. In the following enumeration of tests the order 
of preference is shown, the first four described being the 
most important and most satisfactory to use for general 
work. These four tests are in constant use in the author's 
laboratory as confirmatory tests for albumin. 

Potassium Ferrocyanid Test . — To 10 cc. of urine ad d 
l_^''tiP'^ ^^ cf,.^r.g ^fef']r flrid. If a precipitate appears, it is . 
due to nucleo-albumin and should be filt ered off. T hen a 
few drops of a «; per cenL s^UlULlUli Of botassium terrocyanid 
a re added, and the turbidity, varying; from slight- opal es- 
cence to a denser cloud, shows the presence of albumin . 
An excess 01 me reagent will dissolve the precipitate, which 
is best observed by holding the test-tube in front of a black 
surface and by comparing it with a test-tube of normal 
urine. Albumose and nucleo-albumin give precipi tates, 
t he former dissolving with heat, the latter, on the addition 
of a few drops of lead acetate solutio n. An excess of this 
solution will also dissolve the albumin. 

Nitric-magn esiiun Test (Robe rts), — T he s olution is 

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c omposed of i part of strong nitric acid and q parts 
o f saturated solution of magnesium sulphate, making 
a mixture safe to handle. It is applied by the usual 
contact method. It is more sensitive than Heller's test. 
In the author's experience with this reagent, which has 
been extensive, its delicacy has been found rather con- 
fusing clinically. It shows a double or triple ring, the low est 
and densest of which is due to albumin, the upper to nucle o- 
qjbumin or urates, or both . Urine which does not show a 
ring with Heller's test occasionally shows a faint reaction, 
especially on standing, with 
Roberts' test. Unless the 
lower ring is sharply de- 
fined, dense, and appears 
almost instantiy, clinical al- 
buminuria cannot safely be 
diagnosticated with Roberts' 
test. It is most conveniently 
employed in the simple glass 
instrument known as the 
horismascope or albumo- 
scope (Fig. 6). The urine is 
poured into the large end 
of the tube, and Roberts' 
solution is then poured 
down the small funnel 
imtil the level of the solu- 
tion reaches about the center 

of the black background in the larger tube. The rings 
are seen very distinctly against this background. The 
instrument can also be used with Heller's and with many 
other tests. 

Fig. 6. — The horismascope. 

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Mercuric Chlorid Test (Spiegler), — The reagent con- 
sists of 8 gm. of mercuric chlorid, 4 gm. of tartaric acid, and 
20 gm. of glycerin in 200 cc. of distilled water. It is used 
by the contact method, like Heller's test. This test reacts 
with globulin and albumoses, but not with peptone. Spieg- 
ler's test has recently been modified by Jolles, with the 
result of rendering it much more delicate. Jolles recom- 
mends HgClj, 10 grams; succinic acid, 20 grams; sodium 
chlorid, 10 grams; water, 500 cc. A very sharp white ring 
is produced by albumin. The urine must first be filtered 
and acidified with acetic acid and filtered again to remove 

Salicylsulphonic Acid Test {Sulphosalicylic Acid Test, 
Roch and MacWilliams), — Add i or 2 drops of a sat- 
urated solution of the reagent, or more if the urine is 
alkaline, to dbout 20 drops of the urine in a small test- 
tube. On shaking, opalescence or turbidity immediately 
appearing, shows albumin. Turbidity occurring slowly 
implies minute traces. On boiling, the precipitate is due 
to albumin or globulin. 

Picric Acid Test {Johnson). — Into a test-tube 6 
inches long pour 4 inches of filtered urine. Hold the 
test-tube obliquely and gently pour an inch of a saturated 
solution of picric acid over the surface of the urine. To 
make the reagent add 6 or 7 grains of picric acid to 
I ounce of boiling distilled water. In the portion of the 
tube where the reagent mixes with the urine a yellow tur- 
bidity of coagulated albumin will appear. If the amount 
of albumin is small, the upper part of the tube may be 
heated to increase the turbidity. Picric acid precipitates, 
besides albumin, urates, peptone, albumose, the vegetable 
alkaloids and mucin, all of which, except mucin, are dis- 

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solved with moderate heat. There must be an actual mix- 
ture of the urine with the reagent, not a mere surface 

Potassio-mercuric lodid Test (Tanret), — This is 
very sensitive and is prepared as follows: Mercuric 
chlorid, 1.35 gm.; potassium iodid, 3.32 gm.; acetic acid, 
20 cc; distilled water, enough to make 100 cc. The two 
salts should be separately dissolved in portions of the water 
and the solutions mixed. The reagent is heavy, and is 
used by the contact method without previously acidulating 
the urine. It precipitates the same substances as picric 
acid, and the precipitates are also dissipated by heat or 
alcohol; they reappear on cooling. According to Oliver, 
the precipitate of nucleo-albumin is not dissolved by heat 
if a large excess of the reagent is used. Albumin gives a 
white, sharply defined zone. 

Trichloracetic Acid Test (Raabe, GrossterUy and Fuda- 
kovsky), — A saturated solution of the crystals of tri- 
chloracetic acid (§ ounce of the crystals to 2 drams of 
water) is made and used by the contact method. It is 
claimed by some not to precipitate peptone or nucleo- 
albumin, and is esteemed very highly as a delicate test. 
The trouble with it is that it is too delicate, as it precipitates 
mucin and, therefore, cannot be regarded as trustworthy. 
It also precipitates albumoses, alkaloids, and sometimes 
uric acid, all these disappearing on the addition of 

Potassium Sulphocyanid Test {Zouchlos), — A few 
drops of a mixture of 100 cc. of potassium sulphocyanid 
solution (10 per cent.) and 20 cc. of acetic acid are added 
to urine. A cloud or precipitate occurs if albumin is 
present, and the test is said to detect 0.007 per cent, of the 

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proteid (Schick), but Huppert classes it among the less 
delicate tests. 

Phenic-acetic Acid Test (M6hu and Millard). — ^The 
formula for this is: Glacial phenicacid, 2 dr.; acetic acid 
(c. p.), 6 dr.; potassium hydrate solution, from 6 dr. to 
2 oz. Apply by the usual contact method. It reacts with 
peptone, nucleo-albumin, albumoses, and alkaloids, all of 
which precipitates are said to disappear with heat. It is 
supposed to detect i part of albumin in 200,000 parts of 

Mercuric Chlorid and Citric Acid Test (Stiitz and 
Fiirbringer). — A mixture of the double salt of mercuric 
chlorid and sodium chlorid with citric acid is put up in 
gelatin capsules. A solution of this reagent is not so sen- 
sitive as Tanret's, does not precipitate alkaloids, but some- 
times gives opacity in urines that do not contain albumin. 
Concentrated urines which contain much uric acid must 
be diluted before using this reagent. 

Resorcin Test (Carrez). — One gm. of resorcin is 
dissolved in 2 cc. of distilled water in a test-tube, and the 
urine is poured upon the surface. A white ring shows 
albumin. Peptone also gives a white ring, but it disap- 
pears on immersing the tube in boiling water. 

Betanaphthol-sulphonic Acid Test (Riegler) .—Ten 
gm. of the crystalline reagent are dissolved in 200 cc. 
of distilled water and filtered. Five cc. of urine are 
treated with 20 or 30 drops of the solution. Turbidity in- 
dicates the presence of albumin. Boiling will not make 
the precipitate disappear if it was due to albumin. If it 
was due to albumose or urates, boiling will redissolve the 

Other Tests. — A great variety of substances besides 

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those named have been employed to precipitate albumin. 
It would be useless to enter into a description of all these 
tests. Examples are: Tannin (Alm^n); sodium sul- 
pho-antimoniate (Schlippe) ; potassium antimoniate 
(Palm); phosphomolybdic acid (Sonnenschein) ; chromic 
acid (Kirk); iodin and potassium iodid (Cohen); cal- 
cium chlorid and hydrochloric acid (JoUes); formalin 
(latrona); formalin and mercuric chlorid (Polacci). 

Comparative Delicacy of Albumin Tests. — The order of delicacy 
of the tests described above is a matter still under discussion, the 
opinions of various authorities differing somewhat on the subject. In 
the following table the author has endeavored to give the order which 
has the largest number of indorsers and which corresponds to his own 
results. It is essentially the order given by Huppert, who bases his 
list on the researches of Lecorch^ and Talamon, Vass and Ott: 

Reagent and Author. Detects Albumin in — 

* I. Mercuric chlorid (Spiegler; JoUes' modifica- 

tion) 1 : 350,000 parts urine. 

* 2. Trichloracetic acid (Raabe, etc.) i: 75,000 " " 

* 3. Salicylsulphonic acid (Roch and MacWil- 

liams) 1 : 60,000 " " 

4. Phenol acetic acid (Millard). 

5. Potassiomercuric iodid (Tanret). 

* 6. Heat and nitric acid i : 50,000 " " 

* 7. Heat and acetic acid (with NaCl). 

* 8. Potassium ferrocyanid i : 40,000 " " 

* 9. Nitric acid (Heller) i : 40,000 " " 

10. Betanaphthol sulphonic acid (Riegler) i: 40,000 " " 

11. Resorcin i : 30,000 " " 

*i2. Magnesium and nitric acid (Roberts) i: 15,000 " " 

13. Potassium sulphocyanid (Zouchlos). 

14. Metaphosphoric acid i : 1000 " " 

15. Picric acid (Johnson). 

16. Mercuric chlorid citric acid. 

The most delicate test is not necessarily the most desirable in prac- 
tice. The tests marked with an asterisk in the table are most impor- 
tant, and are practically the only ones a physician need use. 

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Gravimetric Method.— This is the only accurate method 
of determining the amount of albumin, but is entirely too 
elaborate for clinical work. It consists of boiling a certain 
volume of urine, to which enough acid has been added to 
render it distinctly acid in reaction. The coagulum is col- 
lected upon a dry, weighed filter; washed, dried, and 
weighed again. The increase in weight in the filter corre- 
sponds to the amount of albumin by weight in the given 
volume of urine. 

Another method is to remove the albumin by coagula- 
tion, to determine the diminution in specific gravity in the 
supernatant fluid, and to multiply this difference in specific 
gravity by 400 (Zahor's coefficient). 

A third method is to determine the total nitrogen in a 
urine containing albumin (by KjeldahPs method) , and to 
find the difference in nitrogen in the same volume of the 
urine, deprived of albumin by coagulation, multiplying 
the difference by 6.3 (Van Nuyes and Lyons). A fourth 
method is to determine the difference in refraction between 
the urine containing albumin and the same urine after 
coagulation. The error is said to be very small (Ehlenger) . 

The simplest and least accurate mode of estimating the 
percentage of albumin consists in boiling the urine with 
acid, allowing the coagulum to settle, and then measuring 
the comparative bulk of the precipitate as compared with 
the total volume of urine. It is this method that gave rise 
to the confusing expressions of 25, 50, 75, or even 100 per 
cent, of albumin, and its use has been encouraged by the 
introduction of graduated tubes devised for the purpose of 

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indicating the relative bulk of the coagulum. Such quan- 
tities as 75 per cent, are obviously impossible when we 
remember that urine cannot possibly contain more than 5 
per cent, of albumin by weight, the usual amounts meas- 
ured being less than i per cent. This 
method of estimating the bulk of the 
coagulum is, therefore, very misleading 
and should never be used. 

Esbach's Method.— This is the most 
convenient method of quantitative esti- 
mation of albumin, and if carefully per- 
formed is sufficiently accurate for clinical 
purposes. A graduated glass tube, or 
albuminometer (Fig. 7), with walls rather 
thicker than the ordinary test-tube and 
provided with a rubber stopper, is the 
apparatus used. This tube is filled 
with urine to the letter u; then Es- 
bach's reagent is added up to the mark 
R. This reagent consists of 10 parts of 
picric ac'd and 20 parts of citric acid in 
1000 parts of distilled water. The tube 
is closed with the stopper, and the urine and reagent are 
mixed by inverting the tube several times. It is then al- 
lowed to stand for twenty-four hours in a vertical position. 
The number at the level of the precipitate shows the num- 
ber of grams of albumin contained in i liter of urine — 
that is, the number of parts per thousand. Each part per 
thousand represents yV of ^ P^'' cent, by weight, so that 5 
gm. per liter means 0.5 per cent, of albumin. It is best to 
use the latest form of Esbach's tube (Fig. 7), which has a 
foot and graduations in small fractions of i gram at the 

Fig. 7. — Esbach's 

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lower part, so that minute quantities of albumin can be 
estimated. For urines with large quantities of albumin, 
exceeding 0.7 per cent., which is the highest mark on the 
tube, we must use dilutions with equal parts of distilled 
water. The same procedure may be used when very small 
quantities of urine are available, the reading being, of 
course, multiplied by the number of times the urine has 
been diluted. 

Precautions in Using Eshach^s Method. — Esbach's method has a limit 
of accuracy, but in most cases it is accurate within approximately o. i per 
cent. The error is greater in very large and in very small quantities. 
In fact, very small amounts will not even settle, but will remain as a diffuse 
cloud in the tube. This is especially the case in concentrated febrile 
urine. If the urine is not strongly acid, it must be made so with acetic 
acid before the test is used. The tube should be inverted and not shaken 
while mixing the urine and reagent. The divisions are calculated for 
room temperature, and the tube should be allowed to remain at about that 
temperature. If the room is too warm the sediment will settle much more 
rapidly. If the patient has been taking balsamics or resins, such as 
sandal-wood oil, Esbach's method cannot be used, because the resinous 
acids are precipitated by picric acid. 

Tsuchiya's Method. — ^Tsuchiya^ has worked out a 
method which is said to be more accurate than Esbach's.^ 
The reagent consists of a solution of 1.5 gm. of crystal- 
line phosphotungstic acid in 100 gm. of 96 per cent, alco- 
hol and 5 gm. of concentrated hydrochloric acid. 

The urine must be diluted to a specific gravity of 1006 
to 1008, and still further if it contains more than 5 or 
6 parts per 1000 of albumin. The diluted urine is placed 

^ Centralblatt fiir Innere Medizin, 1908, No. 5. 

^ Attention is called to the fact that phosphotungstic acid precipitates 
in acid solutions a large variety of other bodies besides albumin, includ- 
ing uric acid, xanthin, etc. These, however, are present in very small 
amounts in the dilution used in this method. 

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in an Esbach tube up to the mark u and the reagent 
is filled to the mark r. The closed tube should be in- 
verted cautiously at least ten or fifteen times and should be 
allowed to stand for twenty-four hours, whereupon the 
amount of albumin may be read on the scale. This 
method gives no precipitate with normal urine, as is some- 
times the case with Esbach's reagent. The precipitate of 
albumin settles more regularly and uniformly than with 
Esbach's solution. The method is more accurate and is 
applicable to urines with small amounts of albumin, espe- 
cially in febrile urine, in which Esbach's reagent gives 
merely a cloud. 

Goodman and Stern^s Modification. — Goodman and Stem ^ make use 
of Tsuchiya's solution as a basis for a titration method. They deter- 
mined the amount of albumin necessary to cause the first sign of cloudi- 
ness. They found that the solution precipitated exactly 0.000 1 gm. 
albumin, and worked out the following method: First the Heller test 
is made, and if much albumin is present, the urine is diluted ten times 
(i: 10). If not, undiluted urine is used. Five cc. of the phosphotungstic 
acid solution (see p. 72) are put in a test-tube, and then, with a 2-cc. 
pipet, graduated in tenths of a cubic centimeter, the filtered urine is 
added to this, and shaken after the addition of each tenth, and urine 
added again until a whitish cloud appears. The numbet* of tenths of 
a cubic centimeter is then read off. The calculation is then as follows: 
If it takes i cc. of diluted urine (i : 10) there is 0.000 1 gm. of albumin 
in o.i cc. of undiluted urine, or in 100 cc. there is o.i gm. albumin, 
and in 1000 cc. there is i gm. of albumin. If 0.7 cc. diluted urine 
(i : 10) is used, then 0.07 cc. undiluted urine contains o.oooi gm. albu- 
min, 7 cc. diluted urine contain 0.0 1 gm. albumin, and 700 cc. contain 
I gm. albumin. The following equation gives the percentages: 

700 : i.o : : 100 : x or 0.142 per cent, or 1.42 gm. per thousand. 

Centrifugal Method (Purdy). — For t;his purpose a 
centrifuge revolving at a uniform speed of 1500 revolu- 
tions a minute and a special percentage- tube, holding 15 
* Jour. Amer. Med. Assoc., December 12^ 1908, 

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cc, are employed. To lo cc. of the urine add 3 cc. of a 
10 per cent, solution of potassium ferrocyanid and 2 cc. 
of 50 per cent, acetic acid. Allow to stand for ten minutes 
to insure the entire precipitation of the albumin. Place the 
percentage-tube in a centrifuge with a radius, with tubes 
extended, of exactly 6f inches; revolve at 1500 revolutions 
a minute for three successive periods of five minutes each, 
and read off the bulk-percentage. This method is simple, 
fairly accurate, and convenient, provided it be performed 
exactly as prescribed. According to Purdy, each yV cc. of 
precipitate represents i per cent, bulk measure of albumin. 
Ogden found that in order to find the percentage of albu- 
min by weight from this bulk measure we must divide the 
latter, expressed in j\ cc, by 6. The great source of 
error in this method is an excess of urates, which adds to 
the bulk of the precipitate. When this is known, it is better 
to centrifuge the precipitate, decant the supernatant fluid; 
to add hot water, which dissolves the urates, and to cen- 
trifuge again. The most important part of this method 
is to allow the precipitate to settle thoroughly before cen- 
trifuging and to employ a centrifuge of the proper arm- 
length and proper uniform speed. 

The table on page 75 from Purdy will serve to convert 
bulk-percentage into weight-percentage. 

Vassilieff's Method of Titration.— This consists 
in titrating the urine with a solution of sulphosalicylic acid 
until all the albumin is precipitated, and then obtaining 
an end-reaction for the excess. The urine, which is ren- 
dered slightly acid with acetic acid, is measured off in a 10- 
cc. pipet and diluted with water to 50 cc. Two drops of a 
watery i per cent, solution of a yellow dye, known as 
"Echtgelb," are added, and the whole is titrated with a 

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Table showing the relation between the volumetric and gravimetric percentage of albumin 
obtained by means of the centrifuge with radius of six and three-quarter inches; rate 
of speed, 1500 revolutions per minute; time, three minutes. 


>* ^ 







e« u S 



e^ M 2 





M ^ a 

K u 

M a 


H h3 





w < & 






J w 5 











0.0 1 












































































































































































































































































1. 1 





































Test. — Three cc. of 10 per cent, solution of ferrocyanid of potassium and 2 cc. of 
50 per cent, acetic acid are added to 10 cc. of the urine in the percentage-tube and stood 
aside for ten minutes, then placed in the centrifuge and revolved at rate of speed and time 
as stated at head of table. If albumin is excessive, dilute the urine with water until 
volume of albumin falls below 10 per cent. Multiply result by the number of dilutions 
employed before using the table. 

25 per cent, solution of sulphosalicylic acid until the mix- 
ture takes on a permanent brick-red color. The amount 

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of albumin can be computed by multiplying the number of 
cubic centimeters of sulphosalicylic acid used by 0.01006. 
This is a convenient and accurate method. 

To Remove Albumin from Urine.— Hofmeister's 
method may be used when other tests are to be made with 
which albumin would interfere. About 10 cc. of a 40 
per cent, sodium acetate solution are added to the urine, 
and then some concentrated ferric chlorid until a red 
color is produced throughout the fluid. The urine is 
rendered neutral or faintly acid and is boiled. The pre- 
cipitate of basic ferric acetate throws down all albumin and 
the filtrate is clear and free from proteids. This method 
cannot be used if sugar is present. When this is the case 
the urine is simply boiled and acetic acid is added until the 
precipitate is flocculent and the filtrate no longer clouds. 
For quantitative work the urine should be restored to the 
original volume before further tests are made. 

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The tests that have thus far been described for albumin 

^ _i -^ 

m ake no distinction between serum-albumin an d serum- 
g lobulin; for, when we speak clinically of ^^ albumin ^^ in the. 
u rine, we mean the precipitate of albumin and globulin 
which results on testing for proteids in. the urine . As these 
two substances almost always appear together, a differenti- 
ation of globulin from albumin and a knowledge of their 
comparative amounts do not seem of great clinical value. 
There are some cases, however, in which the presence of 
globulin has a special significance. Serum-globulin con - 
stitutes a variable proportion of t |]f ff^^^^ prr^foMc ;n 
albuminurias (from 8 to 60 per cent.). It is noted in 
unusual quantities in the urine of catarrhal cystitis , in 
acute nephrit is, and particularly in amyloid degenerat ion 
of the kidney and other conditions accompanied by con - 
siderable destruction of the renal epithelium . In chronic 
Bright's disease globulin is present in comparatively small 
amounts or is even absent. The distinction between 
serum-globulin and serum-albumin chemically is, there- 
fore, a refinement of urinalysis which may sometimes be 
of value to the clinician. 

* Under this heading it is intended to consider the entire globulin group 
of proteids occurring in urines. The differentiation of globulins into 
euglobulin, pseudoglobulin, and fibrinoglobuUn (Hofmeister) has not 
t>een attempted, 


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Qualitativ e X^^^^- — i- A layer of faintly alkaline urine 
is floated over a saturated solution of M^SO^, and the 
precipitate which results is globulin wit hout the serum - 
albujjiui. -*^^^ 

jf2. The urine is exactly neutralized, filtered, and satu- | 
^ated completely with magnesium sulphate at ordinary 
temperature, or with a saturated solution of ammonium 
sulphate. A white precipitate immediately forming is 
globulin. A precipitate appearing later, with the use of 
ammonium sulphate, may be ammonium urate. 

3. If the globulin precipitate be filtered off, the same 

V urine may be tested for serum-albumin by heating with a • 
few drops of acetic acid, j^ ^-^ 

"^. A very simple method is that of Roberts. It depends 
upon the fact that the globulins are insoluble in water and 
are held in solution in the urine by the salts therein. A_ 
wineglass is filled w ith water and a few drop?^ of allj^umi n- 
ous urine are allowed to fall into it. If globulin is prese nt 
in any quan tity, e ach drop is followed by a milky str eak, 
until the wat er assumes an opalescence, which disapp ears 
on addmg acetic acid. 

(quantitative I est.— The amount of globulin may be 
determined separately from the albumin by carefully 
neutralizing the urine with ammonia and by precipitating 
the globulin with an equal volume of saturated neutral 
solution of ammonium sulphate. The mixture is well 
shaken and allowed to stand for some hours. The pre- 
cipitate is thoroughly washed with saturated magnesium 
sulphate solution, dried at 100° C, boiled with water, 
extracted with alcohol and ether, then dried, weighed, in- 
cinerated, and, finally, weighed again, the last weight being 
the amount of globulin. 

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Fibrin is a product of coagulation of blood, l)maph, 
transudates, or exudates. It is an elastic, white, stringy 
substance, insoluble in water, ether, and alcohol; soluble 
with difficulty in solutions of sodium chlorid (5 to 15 per 
cent.), of potassium nitrate (6 per cent.), and of magnesium 
sulphate (5 to 10 per cent.). When fibrin is dissolved in 
saline solutions, a globulin is found in the solution. Fibrin 
is coagulated by heat from its solutions, precipitated by 
saturating them in magnesium sulphate, and dialyzing 
the salts from these solutions. The addition of weak hy- 
drochloric acid causes fibrin to swell up into a transparent 
jelly, while the addition of strong acids dissolves it, with the 
formation of acid albumin or syntonin and albumoses. 
Pepsin and hydrochloric acid digest it, as does the pan- 
creatic juice, the results being albumoses and peptone. 
Fibrinogen, which is the predecessor of fibrin in circulating 
blood, has been found to possess properties resembling 
those of globulin. 

Clinical Significance.— Fihnn in thp. nrinp nmially 
means the presence of blood, the nuantitv depending upon 
the extent of the hemorrhage. Sometimes fibrin is present 
when there are no blood-corpuscles, and the urine may 
coagulate spontaneously on standing, or throw down a 
sticky sediment. 

Detection. — Tt i^ important to distinguish betwe en 
f ibrin and larprp. amounts of pus forming a gelatin ous, 
s ticky mas s. In the latter case, the addition of water thins 
the urine and the addition of an alkali forms a white pre- 
cipitate of alkaline albuminate. To test a fibrin coagulum 
it should be separated by filtration and washed with water. 
The residue should show the chemic characteristics al- 

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ready detailed. A part of-4h£jnass may be treated with 
a dilute' solution of sodium hydroxid. If it is insoluble 
on standing for a long while, it is probably fibrin, since 
albuminous bodies dissolve in this solution. A fibrin clot, 
however, dissolves completely if warmed gently for several 
hours on a water-bath with a i per cent, solution of sodium 
carbonate, This solution is filtered and treated with 
Millon's reagent, which gives a deep-red color. 

Millon^s Reaction, — One part of metallic mercury is 
dissolved in 2 parts of nitric acid, evaporated to ^ volume, 
and li parts of water are added. Allow to stand for twenty- 
four hours and decant. A drop of this reagent produces 
a precipitate which turns red on heating, or a red color 
on heating if the proteid is present in small amount. 


RvJ^^alhij^^ are mea nt suhstAnces derived from th e 
native albumin s (serum-albumin, globulin), which cons ti- 
tute the first sta^e in the transformation of native proteid 
substances in the process of digestion with ferment s (pep- 
sin, trypsin). Albumoses may, however, also be derived 
from albumins or globulins under the influence of acids or 
alkalis, or in virtue of metabolic changes in tissue proteids 

The albumoses, as a class, possess certain definite char- 
acteristics which distinguish them from the proteids' thus 
far discussed. While they give the general reactions of the 
proteids, they are uncoagulable by hea t and behave diflfer- 
ently toward precipitating reagents than do albumin and 
globulin. T hey are precipitated with nitric acid and with 
p otassium ferrocyanid and acetic acid, but the pr ecipi- 
tates again di ssolve on heating and reappear on cooling . 

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They are precipitated with phosphotungstic and tannic 
acids and respond to the biuret test. 

A great deal of confusion existed formerly between al- 
bumoses and the so-called "peptones." Modem bio- 
logic chemistry accepts Kiihne's definition of a peptone 
as a proteid body which cannot be precipitated by " salting 
out," i. e.y by complete saturation of the solution with 
anmionium sulphate. The peptones are the last stage 
of evolution of native proteids (albumin, globulin, etc.) 
in the process of digestion. When peptones are split up 
their products of decomposition no longer give any of the 
characteristic proteid reactions, but are substances of totally 
different compositions, e. g,y the amino-acids, etc. Judg ed 
by this definition of these bodies, peptones are not prese nt 
as such in the urine, and the term "peptonuria," formerl y 
used so freauentlv^ has been changed to "albumosuria." ^ 

The definition of albumoses, therefore, places them 
between serum-albumin and serum-globulin on the one 
hand and peptone on the other, in the sequence of proteol- 
ysis. Albumoses are soluble products of native albumins 
that do not coagulate with heat, and that are still precipi- 
tated by saturating with certain salts (ammonium sulphate, 
zinc sulphate in acid solutions) . Peptones are not coagu- 
lated by heat, but no longer are precipitated by saturation 
with the salts mentioned. 

Presence of Albumoses in the Body-fluids. — It was formerly 
thought that albumoses (and peptones) exist normally in the different 

^ True peptone, however, occurs occasionally in the urine, e. g.y in lobar 
pneumonia, pulmonary tuberculosis, gastric ulcer, and during the puer- 
peral period (Neumeister, Ito, Emerson). Furthermore, the pepsin which 
is always present in the urine digests albumoses into peptones (Neumeis- 
ter), and these have been erroneously assumed to have been directly ex- 


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tissues and fluids of the body. Neumeister, in 1888, however, showed 
that this is not true, and that albumoses and peptones had been formed 
artificially in the process of chemic analysis. He found that fiormallv 
no albumoses nor peptones exist (in any appreciable amounts) anywhere 
m tne body save m the digestive tra ct. The albumoses and peptones 
of the food are retransformed into albumins and globulins in the intestinal 
wall (Hofmeister). Pathologically albumoses are formed in the body in 
the course of pus formation and in the absorption of exudates^ Buchner 
accounts for this formation of albumose by the action of peptic or tryptic 
ferments secreted by leukocytes or other body cells. In fevers albumose 
has been found in increasing amounts in the blood (Krehl), and an albu- 
mose is probably the cause of the febrile reaction of Koch's tuberculin. 
Alb ^pinses occur pathologically in the urine in similar conditions as those 
just mentioned (Cohnheim). 
X Classification of Albumoses. — This is quite complex, but for our 
purposes the following explanation, containing the essential facts to be 
remembered in this connection, will suffice. 

The scheme of classification for the purposes of urine analysis may 
be thus arranged: 

Acid albumin 


Primary albumoses 



Secondary albumoses (Deutero-albumoses) 

Reading from above downward we note the successive stages in the 
transformation of acid albumin into peptone, and thus perceive the 
relative position of the albumoses. 

The first step in the formation of albumoses from acid albumin is 
represented by the primary albumoses. These are precipitated by com- 
plete saturation of their solution with NaCl. 

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The primary albumoses are subdivided (Kuhne) into: (o) The protal- 
bumoses, which are precipitated by saturation with NaCl only from 
neutral solutions, and are soluble in water; and {b) the hetero-albumoses, ' 
which are completely precipitated by saturation with NaCl only ixomoAd 
solutions, and are insoluble in water, but soluble in weaker salt solutions. 

The secondary albumoses or deutero-alhumoses are derived from the 
primary albumoses by further digestion (also artificially by boiling with 
acids or with superheated steam). These are precipitated by NaCl with 
acetic acid or by ammonium sulphate, most of them being thus af- 
fected in neutral, a few in acid or alkaline, solutions. 

V».^5econdary Albumoses (Deutero-albumoses). — These 
will be considered iSrst, as they are by far the most fre- 
quent form of albumoses found in the urine (Hof^neister). 
In fact, if primary albumoses occur more frequently than 
is now supposed, they are changed rapidly to secondary 
albumoses by the pepsin always present in the urine. 

Clinical Meanim . — S econdary albumoses occur in a 
preat variytv of conditions, but almost always associate d 
w ith feyer or with breaking down of tissue elements^ th e 
absorptiov nf f>^^j/lyif^c r^r r>f frtvi'nc Secondary albumose 
is present i n about 90 per cent, o f all febrile disease s, par- 
ticularly in cases with an exudatiye inflammation (pneu- 
monia, pleurisy), in suppuratiye conditions , such as abscess, 
appendicitis, empyema, osteomyelitis. It is also noted in 
infections (rheumatism, septicemia, typhoid, tuberculosis, 
[cayities, feyer], erysipelas, measles, scarlet feyer, small- 
pox), particularly when the toxins ;^ r ^. being elimina ted 
rapidly and the te mperature falls (Emerson). Gangrene, 
cancer, and other concl itjong nf rliVprt \\ ^s>ue brea kdown 
cause it. I n pregnp ^^^y nr^ in thr pnnrprriwm nlh^un^ 
suria may indicat e al^orption of tox ins. 

ine a estructi on ofmany red blood-cells may giye rise to 
albumosuria, as in the absoption of large hemorrha ges, 
in purpura, scuryy, leukemia, etg, In ulcers of the in- 

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testine (tuberculosis, typhoid) or of the stomach albumo- 
suria may be present as the result of direct absorption of 
albumose from food into blood. Albumosuria also occur s 
in diseases of the liver (acute yellow atrophy, cirrhosis, 
catarrhal jaundice, etc.). 

An important form of albumosuria is associated wit h 
nephritis , where it may occur with albuminuria. Albu- 
mosuria may be the first sign of an impending nephritis, 
or may remain as a vestige of a nephritis which has healed. 
It is especially marked in syphilitic nephritis. 

Diagnostic Value. — T he detection of albumose — an d 
b y album ose in the urine we mean secondary album ose 
(deutero-albumose), unless otherwise stated — j^ not nf v ery 
great practical value. This body occurs in so many con- 
ditions that its presence cannot be regarded as especially 
characteristic of any disease. It does not usually occur in 
large amounts; on the contrary, usually in small quantities, 
and bef ore we conclude anything as to its meaning we mu st 
eli minate three sources of error (Emerson): 

1. The admixture of albumose to the urine from the 
genital or genito-urinary tract (spermatorrhea, prostatitis, 
postcoital urine). 

2. The formation of albumose from albumin in the j 
process of testing the urine. 

3. The possibility of direct excretion of albumose fromj 
the food (milk) in nephritis. 

These sources of error being excluded, a marked albu- 
mosuria may be of value in the diagnosis of abscesses 
(appendicitis) in inaccessible parts of the body; in the 
differentiation of cerebrospinal meningitis from tubercu- 
lous meningitis; and of gastric or intestinal ulcer from other 
conditions (excluding cancer) which may simulate these. 

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Detection of Secondary Albumoses. — i. Hofmeister's Test. — One- 
fifth volume of concentrated acetic acid is added to the urine. To the 
mixture phosphotungstic acid is added, and the whole is allowed to stand 
for half an hour. If no cloudiness appears, secondary albumoses are 
absent. If they are present, a milky opacity appears within a few minutes. 

2. Biuret Test. — This test is universally used, but has the disadvantage 
of being obscured by the color of the urine if used directly upon urine. 
It consists in rendering the urine alkaline with an excess of NaOH and 
adding dilute copper sulphate (5 cc. saturated solution to 1000 cc. water) 
or by pouring the dilute copper solution upon the surface of the urine. In 
the former case the urine will turn reddish brown, in the latter a ring of 
the same color will appear. 

The biuret test should be performed with the precipitated (or isolated) 
albumose. For this purpose the albumose may be precipitated with 
phosphotungstic acid (see Hofmeister's test), the sediment centrifuged 
and dissolved in a small amount of water. The biuret test will then give 
a characteristic violet color. 

3. Hammarsten-Bang Method. — This is the best and most accurate 
method for the isolation and testing of albumose. Its object is to remove 
the urobilin which interferes with the final biuret reaction: Ten parts 
of urine are thoroughly mixed with 8 parts of saturated solution of 
ammonium sulphate. The mixture is heated to the boiling-point and 
kept there for a few seconds. While hot it is then centrifuged, until 
fairly solid sediment is formed, and the supernatant fluid decanted or 
pipeted off. The precipitate is shaken with alcohol (to remove urobilin), 
the residue is mixed with water, and the mixture heated to the boiling- 
point and filtered to remove albumin. The filtrate is shaken with 
chloroform (to remove any possible traces of urobilin) and the watery 
portion is tested with the biuret reaction, which should give a charac- 
teristic violet color. 

Primary Albumoses ( Bence^ Jones* Bod^) >— Pii=> 
mary albumoses in the urine are exceedingly rare . Prac - 
ti cally t he only form to be considered is a type of prote id 
e xcretion kn ow n by its discoverer^s ndimitr -B ence-Jon es^ 
a lbumosu ria. 

Bence-Jones^ Body. — This was classified as a primary 
albumose (a hetero-albumose) , but recent researches have 
thrown considerable doubt as to the real character of the 

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so-called Bence- Jones' body. Some authors (Dechaume) 
consider it to be a mixture of several albumoses. For the 
present, for want of a better place, we continue to classify it 
under the primary albumoses, chiefly to distinguish it 
sharply from the secondary albumoses that are ordinarily 
found in the urine. 

Clinical Significance. — Bence- Jones' body occurs very 
rarely in urine. It seems to be derived from the bone- 
marrow. There are at present not over 35 cases on record 
(Boston). It has been found in cases with multiple my- 
eloma, with severe involvement of the bone-marrow, and 
in one case of lymphatic leukemia. The cases in which 
Bence- Jones' body was found were usually fatal in from 
one to two and a half years and ran a rather acute course. 
Males were found affected in 80 per cent, of cases. In 15 
per cent, there was a history of severe traumatism to th e 
bones or join ts. UJIfJ^t4/v /$ ^ g-^XjL^^ ^MjJc^l CaJL 

The amount of this body in the urine in these cases ran as 
high as 7 per cent., but usually it was below i per cent. In 
some cases (Boston) the excretion was intermittent. 

Detection. — i. Acetic Acid Test. — The urine is rendered acid with 
acetic acid. From 10 to 40 cc. are placed in a beaker and heated gently 
on a water-bath, noting the temperature. A slight cloud appears at 
52° C; a marked turbidity at 54° to 56° C; a dense cloud at 56° to 60° C. 
As the urine approaches 90° C. a tough sticky coagulum forms, but 
when the urine is boiled for five minutes the coagulum dissolves and 
reappears on cooling (Boston). 

A simpler way to perform this test is with a test-tube and a small 
flame. V^arminp causes th ^ ^'^yIi^ opa^'fY, })f^atinffl-np:| rlv to boilinpr, the 
precipitate ^ which redisso ^y***^ "H prolonging the b^ jlinp^ i^pH rpj^pp^ars 
on cooling. 

2. Nitric Acid Test. — To the urine nitric acid is added, drop by drop, 
shaking after each addition. A pinkish tint appears in the heated por- 

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3. Boston* s Method. — From 15 to 20 cc. of urine in a test-tube are 
mixed with an equal amount of saturated NaCl and well shaken. To 
this are added 3 cc. of 30 per cent. NaOH and the mixture shaken 
thoroughly. The upper portion of the urine is heated to boiling and 
10 per cent, lead acetate solution is added, drop by drop, heating after 
each drop. A brown color, turning black, is obtained within one minute, 
and is due to lead sulphid, the sulphur being derived from that loosely 
bound in the albumose. 

TViP mnn'riQ prp prnfpiH hoHjY<; whirh nrmr in tVif RPrrp- 

tion of mucous glan ds, e. g,, in the saliva, the bronchial 
secretion, the i ntestines, the bile, and t he secretions of the 
genito-unnary t ract. Mucins are soluble in water, and 
their solutions when concentrated are syrupy, slimy, and 
viscous, and by addition of acetic acid are converted into 
thick, tenacious, gelatinous masses. 

On adding acetic acid t o dilute solutions of mucin a 
t hickTsTriii^y dup0!3ll is lormed, not a flocculent prec ipitate. 
An excess of acetic acid does not redissolve mucin precipi- 
tates, or does so only with difficulty (Cohnheim). Mucins 
are not pre ripitntpH hy hoi]jngr. and the aHHition of neutral 
salts rsod ^^im r^^^''^'^) ^*"*^p° rv.ii^in \^ qnlntinn pvpn after 

a cetic acid i?; add^ d. (This addition of neutral salts 
serves to keep mucin in solution when heat and acetic acid 
are used in testing for albumin, in order to avoid confusion 
between mucin and albumin.) 

Chemically, mucin belongs to that class of proteids known 
as the "glycoproteids" because it is a compound of a 
proteid molecule with a molecule resembling a carbohy- 
drate (a glucosamin) and capable of reducing Fehling's 

Mucoid. — ^K. Moemer^ found that the normal urine 

* Skand. Arch. f. Physiol., 1895. 

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c ontains small quantities of a substance similar to mucin, 
which he classed as a "m ucoid /^ The latter term was 
applied by Hammarsten to substances sharing some of the 
properties of mucins, but differing from them in other par- 
ticulars.* Moerner's mucoid differs from true mucin in 
that it dissolves fairly readily in an excess of acetic aci d. 
On boiling with acids or alkalis it is easily changed to an 
acid or alkali albumin, and, like mucin, contains a carbo- 
hydrate molecule. 

Moerner's researches showed that the "nubecula" of 
normal urine, and also to a lesser degree the fluid itself, 
contained small amounts of "mucoid." In 260 liters of 
urine he was able to isolate but 4.3 gm. of this mucoid. 
This substance cannot be precipitated from urine with 
acetic acid under ordinary conditions, because it is held in 
solution by the urinary neutral salts. Moerner was able to 
obtain his mucoid only after treating the urine with acetic 
acid and extracting with chloroform. 

Clinical Significance of Mucin or Mucoid. — For the 
present the terms "mucin" and "mucoid" may be used 
without distinction, preference being given to "mucoid," be- 
cause in all probability all mucin in the urine is in the form 
described by Moerner, although this remains to be shown 
definitely. In norma l urines small traces of iTmroid orr ur 
which are not discernible clinically except by such methods 
as Moerner used. Ordinary tests do not reveal normal 
mucoid. In pathol o p;ic conditi ons (catarrhal inflamma- 
tion) involving a hyp ersecretion of mucus anywhere alon^ 

*The line of demarcation between mucin and mucoid is, for the 
present, somewhat vague, but the term mucin is preferably applied to 
the proteid in the secretion of mucous glands, while the term mucoid 
is applied to substances resembling mucin which may occur in other 
parts of the body. 

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the urinary or genito-urinary tract an increase of mucin in 
t he urine is to be expected . I n marke d cases the mucus 
appears as an increased form of the normal cloud or nubec - 
ula, floating in the urine or slowly sinking as a strin gy 
mass. In less marked cases the mucus may be in solution 
and chemical tests will show its presence. 

Detection. — The urine should be diluted with water to 
diminish the solvent action of its salts on mucin or mucoid, 
and acetic acid should be added in the cold, care being 
taken not to add an excess. The precipitate may be treated 
with a dilute mineral acid and the product tested with 
Fehling's solution, whereupon a reduction of copper 
will show that the precipitate was mucin or mucoid, while 
the absence of a reduction will exclude the precipitate from 
this class of proteids, and will point to their probable mem- 
bership in the class to be spoken of next. 


So"Called Nucleo-albumin (Moerner's Body, Eu« 
globulin). — ^For many years it was believed that "nucleo- 
albumin" occurs normally in urine and is found very fre- 
quently also in disease. The fainter ring which appears at 
some distance above thetrue albumin ring in Heller's nitric 
acid test was regarded as due to "nucleo-albumin, " as was 
also the precipitate obtained with diluted urine in the cold 
upon addition of acetic acid. The ring above the contact 
surface in Heller's test can be obtained in a very large 
proportion of urines, especially if these be diluted. The 
opalescence or precipitate with acetic acid in the cold due 
to the same body is not easily soluble in an excess of acetic 
acid (contrast with "mucoid"). 

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The controversy as to the true nature of the proteid sub- 
stance which gives rise to these phenomena in so many 
urines has been a long one, and various investigators have 
given different names to the substance thus detected. For 
example, Reissner called it "soluble mucin"; Hofmeister 
regarded it as a "mucin-like body"; F. Mueller, as a 
"globulin"; Huppert, as a " nucleo-albumin or a mucin- 
like body"; Obermeyer, as a "nucleo-albumin." Ober- 
meyer's work had an important bearing on the question, as 
he found this body in 32 cases of jaundice, increasing with 
the intensity of this symptom, and called it a nucleo-albu- 
min; henceforth precipitates with acetic acid in the cold 
were regarded as nucleo-albumin. The researches of 
Moerner and those of Matsumoto, however, have placed 
the whole matter in a different light: 

(a) Moerner^ s Work. — K. Moerner,* in the memoir (already quoted 
on p. 87) in which he described urinary mucoid, also presented the 
results of very careful experiments with normal urines which were in- 
tended to solve the question as to the nature of the substance which 
had hitherto been called " neucleo-albumin, " and which had so fre- 
quently responded to the tests mentioned in the preceding paragraph. 

Moerner found that the so-called " nucleo-albumin" was in reality a 
compound of serum-albumin and of one or more of three organic acids 
which occur in the urine — chondroitin-sulphuric acid, nucleinic acid, 
and taurocholic acid. The first is always present in the urine, the two 
last mentioned, occasionally. The addition of acetic acid gives rise to 
a combination of the serum-albumin with the organic acids mentioned 
and a precipitate results. The precipitating acids are present in the 
urine in excess, but in variable amounts. The greater the amount of 
these precipitating bodies, the closer the resulting precipitate resembles 
nucleo-albumin, and this accounts for the fact that it had been so long 
taken for nucleo-albumin. 

Moerner found his compound in a large number of normal urines, 
but as he worked with very large amounts of urine and found only small 
quantities, some of the workers who followed him failed to obtain his 

* Skand. Arch. f. Phys., 6, 1895, p. 332. 

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results. Therefore, while Moerner's work is of great importance, there 
is some doubt as to the acceptance of his explanation of the precipitate 
obtained with acetic acid in the manner mentioned. 

(b) Mahumoio's and Oswald's Work (1903-04). — These observers 
regard the body precipitated by acetic acid and giving the superimposed 
ring with Heller's test as a compound of euglobulin and fibrinogen 
(fibrinoglobulin). As such it is probably present in all normal urines 
in traces, and is increased in such conditions as cyclic and orthostatic 
albuminuria and in nephritis. 

Clinical Significance. — W hether the proteid substan ce 
which reacts to these tests and is so often found nor- 
mally is Moerner '^^ ]}^Y ^^ wVipthpr it k a ^ngir^KiJm 
therefore, is not yet settled. The important facts to 
remember are that (i) Small traces of a proteid the true 
nature of which is not yet known definitely may occur nor- 
mally in the urine; (2) that the term ^^ nucleo-albumin^' 
should not be carelessly applied to this proteid; (3) that this 
proteid is increased in non-nephritic albuminurias (cyclic, 
orthostatic), and may occur in increased amounts as a 
premonitory sign of impending nephritis. It is also in- 
creased in leukemia (Mueller), in jaundice (Obermeyer), 
in acute infections and fevers (typhoid, pneumonia, men- 
ingitis, erysipelas). 

Detection of ''Moerner's Body" or Euglobulin. — 
Heller^s test is the most satisfactory clinical method for 
detecting this proteid. The ring appears about half a 
centimeter above surface of contact, but it may diffuse 
and merge with the acid on standing. Dilute urines give 
better results with this test. The urate ring should be 
excluded by gently heating or by still further diluting the 

Citric Acid Method. — L. Grimbert and A. Dufau^ ap- 

^ Journ. de Pharm. et de Chimie, vol. xxiv, 1906, p. 193. 

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plied the method of Lecorch^ and Talamon* to the detec- 
tion of Moerner's body. A solution of loogm. citric acid 
is made in 75 cc. of distilled water. The fluid is cooled. 
A small quantity of the solution is poured into a test-tube 
and the filtered urine layered over it. Moerner's body 
gives a white, nebulous ring at the zone of contact, and 
sometimes the cloudiness permeates the superimposed 
urine. Pathologic albuminuria (serum-albumin and glob- 
ulin) give no ring or cloud with citric acid. This test is 
useful when Heller's test gives a ring which is doubtful 
as regards its origin from true albumin or from Moerner's 


I n the preceding section we dealt with a proteid body, 
hitherto rallpH "nnrleo-fllhnmin^^ We must now , 
for the sake of completeness, ronf^idpr hripfly f\)^ nrrnrrpnrp 

of triie nucleoproteid in the urin e. We use J:he term nucleo- 
proteid as the more accurate term, in place of nucleo- 
albumin, for the two are not synonymous. 

Definitions. — A nucleoproteid is a compound of nucle in 
with so me prot eid matt er. A nuclein, in turn, is a com- 
bination of some form of proteid matter with nucleic acid 
(Chittenden). The following schema from Cohnheim 
shows this: 


/ \ 

Proteid >.Nuclein>. 

Proteid Nucleic acid 

Nucleoproteids when digested with pepsin yield nuclein, 

^ Traits de 1' Albuminurie et du Mai de Bright, Paris, O. Doin, 1888, 
p. 82. 

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and when boiled with dilute mineral acids yield purin 
bases (see below). 

Niicleo-albumins yield, not nuclein, but pseudonuclein 
on digestion, and do not yield purin bases on cleavage with 
dilute acids (Hammarsten). 

Clinical Significance. — Nucleoproteids do not occur 
normally in the urin e. (The substances formerly taken 
for them have been considered on p. 89.) In certain p atho- 
logic COD fjjf jf>rt^ a<;<;nriatpH pre.s^ima.hly with destruction o f 
cell-nuclei in the kidnev or elsewhere nucleoproteid s have 
been found in th e urine. 

'i'he presence ot nucleoproteid in the urine may be re- 
garded, for the present, an evidence of cell breakdown, 
either in the kidneys (acute nephritis, renal degeneration 
due to poisons, renal stasis) or along the urinary tract 
(inflammatory or suppurative desquamation or degenera- 
tion of epithelia and leukocytes, e, ^., in pyelitis). Un- 
fortunately, however, we are still in the dark as to the exact 
relation of nucleoproteid to serum-albumin and globulin, 
and in the few cases in which thorough investigations were 
made an increase of nucleoproteid has not always been 
found when it should have been expected theoretically, 
e. g.y in the presence of certain suppurative conditions. 

Detection. — The difficulty lies in the detection and 
identification of nucleoproteids. The acetic acid precipi- 
tate of nucleoproteid is insoluble in an excess of this acid. 
Magnesium sulphate added to urine to saturation also 
throws down the nucleoproteids. On boiling the precipi- 
tate, after treating it with dilute acids, no reducing substance 
is obtained which affects Fehling's solution (distinction 
from mucin). Nucleoproteids contain phosphorus, and in 
order to prove the precipitate to be such we must demon- 
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strate the presence of phosphorus. Furthermore, these 
products when digested with pepsin must yield nuclein. 
These tests are not only impossible of execution in a clinical 
laboratory but also are extremely difficult to perform in 
the urine, even for an expert 'chemist (Emerson). 


Albumin. — ^What is usually meant by albuminuria? Can normal 
urine contain albumin? What proteids are present in normal urine 
constantly? What are the physical conditions for the excretion of 
albumin? What three factors determine albuminuria? What is meant 
clinically by "albuminuria" ? What do we mean by " false albuminuria" ? 
By true or renal albuminuria? How may renal albuminuria be sub- 
divided? Define: Functional albuminuria; physiologic albuminuria; 
essential albuminuria; cyclic, orthostatic; albuminuria minima. Trau- 
matic, hematogenous, nervous, circulatory, toxic nephritic albuminuria. 

What amounts of albumin are usually excreted in (a) acute congestion; 
(b) acute, subacute, and chronic parenchymatous; (c) chronic interstitial 
nephritis; (d) amyloid kidney? 

Describe the heat test with nitric acid. How is the cloudiness 
differentiated from that due to phosphates? What are the sources 
of error in this test? Describe the heat test with acetic acid. How 
do you distinguish nucleo-albumin in this test? 

Describe Heller's test. What are the different methods of per- 
forming it? What precaution should be taken in testing with this 
method? What is the value of the other tests for albumin in practical 

What does picric acid precipitate besides albumin? Describe the 
tests with potassium ferrocyanid and nitric magnesium. What is the 
comparative delicacy of these tests? 

What is the most accurate method of determining the amount of 
albumin in the urine? What other methods may be used for this purpose? 
What is the value of the method by "bulk percentage"? Describe 
Esbach's method; Tsuchiya's method; Purdy's centrifugal method; 
Vassilieff's method of titration. 

What chemic substances do we mean by " albumin" in the urine? 
In what conditions is it useful to differentiate globulin? Describe 
Roberts' simple method of testing for globulin. 

Describe fbrin and its chemic characters. What does its presence 
in the urine indicate? How is it distinguished from pus precipitate? 

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What are alhumosesf In what conditions have albumoses been 
found in the urine? Secondary albumoses? What are the chief chemic 
features of these two classes of bodies? What is Bence-Jones' body and 
how is it detected? 

Define mucin. What is mucoid? What is the clinical significance 
of this body? How is it detected? 

What substances were formerly called nucleo-albumins? How do 
they show in Heller's test? What is nudeoproteid? When does it 
occur in urine? How is it detected? 

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The question as to whether glucose is present in normal 
urine has not been finally settled, although the latest 
researches of Wedenski apparently affirm this statement. 
For clinical purposes this question is not of import- 
ance, as the quantities of sugar that may be present in 
normal urine are so exceedingly small that they cannot be 
recognized by the ordinary tests such as are employed in 
routine examinations. Glucose is present in small quanti- 
ties in normal blood, and this amount becomes greatly 
increased in some diseases, reaching its highest point — 
about O.I per cent. — in advanced diabetes. 

Clinical Significance. — ^The presence of glucose in the 
urine is no more synon)nnous with diabetes than the pres- 
ence of albumin is with Bright's disease, but diabetes is t he 
condition which most commonly causes glycosuria. Dia- 
betes is now assumed to be a dise ase of metabolism whic h 
prevents the conver sion of the carbohydrates into th eir 
simpler elemen ts. The glucose in the urine of diabetics 
is derived either from the food or, in severe cases, from the 

* A number of carbohydrates are met with in the urine, including 
glucose, levulose, lactose, etc. The general properties of carbohy- 
drates should be known to the student or may be studied in books on 
general chemistry. As in the case of proteids, there is one carbohy- 
drate which is of great importance clinically, namely, glucose. 

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tissues. I t does not originate only from the carbohydrat es 
i ngested, for some proteids may b ecome split up, liberating 
a carbohydrate,^ e, ^., nucleins and mucin, which contain 
30 per cent, each of a carbohydrate group. Glucose may 
als o be formed synthetically from the decompos ition 
p roduct of pro teids. Von Noorden and Rumpf found that 
sugar (glycogen) could be formed by the decomposit ion 
qfJatS^ It is probable, therefore, that in advanced cases 
of diabetes with wasting, glucose is derived from several 
classes of tissue products, chiefly, however, from the pro- 
teids. The amount of glucose in the urine in diabetes 
mellitus varies from 0.5 to 12 per cent, (see p. 380). 

Besides diabetes, a series of other causes may produce 
glycosuria: Thus, alimentary glycosuri a is due to an excess 
of carbohydrates in the food; medicinal fjlycosuria is due to 
drugs, such as chloroform, amyl nitrite, phloridzin, the 
inhalation of illuminating gas, etc.; secondary glycosuri a 
accompanies cirrhosis of the liver, severe injuries of the 
brain, apoplexy, paresis, and other nervous diseases; 
exophthalmic goiter, the removal of the thyroid, or the use 
of large doses of thyroid extract; a new growth in the pan- 
creas or the occlusion of the pancreatic duct by a stone, 
followed by atrophy of the gland. Glycosuria may also 
occur during pregnancy, in the course of acute infectious 
diseases, such as diphtheria, and just before death in cases 
of chronic nephritis, possibly as the result of edema of the 


The Copper Tests . — These tests are most commonly 
useJ for the detection of glucose in the urine. They all 
depend upon the power of glucose to reduce copper oxid 
in an alkaline solution. 

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Trftnin^#>r>B Tftgf — This IS the oldest of this group of 
tests, and while there are better methods for clinical use, 
the student should practice with Trommer's in order to 
familiarize himself thoroughly with the process of copper 
reduction in the urine. Emerson has lately emphasized 
the great importance of this test: 

A tes t-tube is filled half full of u rine, and a bout o ne-th ird 
volume of 10 per cent. DOta^ xi^jiiTT ^y^^^^^ g^l^^inn ii nddrd 
T o this mixture a 10 per cent, solution of copper sulpha te 
is added, drop by drop, shaking after each addition u ntil 
th e copper hydrate which forms as the solution is adde d no 
lon ger dissolv es. The upper portion of the mixture is now 
heated, and if suprar is present, f^ vpIIqw pf j-pd pr^^ip'^''^'^ 
wil l at once appear (copper suboxid). The heating 
should immediately be stopped and the tube allowed to 
stand, when the precipitate will spread downward. 

The urine should be examined while fresh, and if thprp i<; 
much albumin, it should be previously remove d (see p. 76). 
If the reaction is at all doubtful, it is better to perform the 
test without heating, and to allow the tube to stand for a 
day, when the precipitate of cuprous oxid will be found 
present. According to Neubauer, most of the other or- 
ganic substances which reduce the salts of copper do so 
only when heated. 

The explanation of the reaction is as follows (Emerson) : 

" If to pure water be added KOH and then the CuSO^, the first drop 
of the latter will cause a precipitate of Cu(OHj) (CUSO4 + 2NaOH = 
NajSO^ + Cu(OH)2). These flakes of CuCOHj), on heating, will 
blacken, since Cu(OH)a2CuO is formed. If the glycerin or the tartrates 
be added to the water, all of the Cu(OH)j is dissolved to a blue solution, 
which will not blacken on heating, as it does if undissolved. If, instead 
of these, glucose be added to the water, the same blue solution of the 
Cu(OH), is obtained. This, however, on warming is reduced, and a 

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yellow or red precipitate falls. In the case of glucose the body giving 
the bright blue solution is CBHiaOesCuCOH)^. 

" In performing the test it is particularly important that an excess of 
copper should not be added, since the black oxid will cover the precipi- 
tate of the cuprous salts. Normally, 3 to 5 drops of the CUSO4 are suffi- 
cient to give a blue precipitate. In case sugar is present, however, the 
addition must continue until the first flakes of Cu(OH)j remain. The test 
is positive only when a yellow or red precipitate falls, yellow (Cua(OH)2) in 
a relatively weak alkaline, red (CujO) in a strongly alkaline, solution. In 
case under 0.2 per cent, sugar is present there will be no precipitate, and 
yet even then the test may be very suggestive, since the yellow solution 
will be of such a clear brilliant color. Again, the precipitate should occur 
under the boiling-point or when the urine is just brought to that point to 
exclude the reduction by those bodies normally present." 

Precautions to Be Taken in All Copper Tests, — Certain 
precautions must be taken in all copper tests. These may 
be summarized as follows; 

Albumin in terferes with the reduction of the copper oxid and mus t 
always be remove d if present in more than a faint trace. Concentrated 
unnes. with high specific gravity, and especially urines with an excess of 
coloring-matters, urea, uric acid, and other nitrogenous bodies, must be 
diluted before testing with copper solution. An excess of copper sulphate 
or too strong solutions should never be u sed, and all copper tests are pref- 
erably to be performed with dilute reagents. The rules given in this 
respect under the different tests should be carefully observed. 

Prolonged boiling should be avoided, t hirty seconds being ample in the 
great majority of cases, for prolonged boiling reduces copper when other 
organic substances than sugar are present. A positive reaction is con- 
stituted by the precipitation of a yellow orange or red, heavy, dense pre- 
cipitate, which spreads through the test-tube on standing, and eventually 
falls to the bottom. An amorphous, flocculent precipitate, pale grayish 
in color, is due to earthy phosphates. A flocculent precipitate may also 
be due to albumin or other proteids. 

A change of color does not constitute a reaction, although in the presence 
of very faint traces of sugar, less than o.i per cent., the contents of the 
tube changes to a yellowish or greenish color. In these cases confirmatory 
tests are necessary if there is any doubt as to the cause of the change of 
color. In the majority of cases a change of color due to other substances 
thap sugar can be avoided by using sufficiently dilute urine and by avoiding 

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excess of copper sulphate and prolonged heating. When these factors are 
disregarded, a change of color is produced with any of the copper tests, 
from blue to various tints of green, brown, and yellow, and in these cases 
is due to other organic compounds in urine. 

It is well to remember that the compounds which may reduce copper 
besides carbohydrates in the urine are as follows: Uric acid, creatinin, 
hippuric acid, urate, hypoxanthin, mucus, indican, and the series of drugs 
which increase glycuronic acid. The latter are principally chloral 
hydrate, chloroform, camphor, menthol, morphin, phenol, resorcin, and 
thymol. Drugs which give rise to the elimination of pyrocatechin, hydro- 
quinon (these urines are light colored when passed, but become dark on 
standing, or on the addition of KOH). Furthermore, a positive reaction 
may occur in some cases after the use of salol, salicylic acid, benzoic acid, 
phenacetin, sulphonal, rhubarb, santonin, crysophanic acid, oxalic acid, 
glycerin, copaiba, and other resinous drugs. It is to be noted, further- 
more, that the use of saccharin in considerable amounts may interfere 
with the reduction of copper, a point of value in considering minimal 
glycosurias in patients who are on a sugar-free diet, but who use saccharin 
for sweetening their food. 

The invariable rule to follow in testing for sugar by any of the cop- 
per methods is that a confirmatory test, preferably the bismuth test 
(Nylander's), or in case of further doubt, the phenylhydrazin test, or, 
finally, the fermentation test, should be employed in all cases in which 
there is any doubt as to the positiveness of the copper reaction. Pa- 
tients under observation for glycosuria should, moreover, be kept free 
from any drugs which may influence the reaction for several days 
before the test is applied. 

Fehling's Te st. — This is by far the most popular test 
for sugar in the urine. It has the advantage of being easily 
applied and of being sufficiently delicate for clinical pur- 
poses. I ts principle is that of copper reduction, but in 
order that the solution may hold dissolved as much copp er 
as possible there is added to it sodium potassium tart rate 
(Rochelle salt). The addition of a tartrate, or of glycerm, 
or ammonia is, indeed, employed in several other copper 
tests (Purdy, Haines, Pavy) for the same purpose. 

Fehling's solution is composed of two reagents which 

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must be kept separate in a dark place, in glass-stoppered 
bottles, the stoppers of which should be greased with a 
mixture of vaselin and paraffin to prevent adhesion to the 
neck of the bottle. The formulas for these solutions, ac- 
cording to the researches of Marshall, are as follows: 

1. Copper solution: 

Copper sulphate 34.652 gm. 

Distilled water, enough to make 500 cc. 

2. Alkaline solution: 

Sodium-potassium tartrate (Rochelle salt) 173 gm. 

Sodium hydrate solution (specific gravity 1.140)^. .500 cc. 

Ten cc. of the combined reagent (5 cc. of each reagent) 
require 0.05 gm. (50 mg.) of glucose to complete the 
reduction in this amount of solution. In other words, 
each cubic centimeter of the combined reagent corre- 
sponds to 0.005 (S ^gO of glucose. 

The calculations of Marshall, upon which the formula 
given above is based, showed that 5 molecules of crystal- 
lized cupric sulphate are reduced to cuprous oxid by i 
molecule of glucose, thus: 

CgHjjOg : 5CUSO4+5H2O : : glucose : cupric sulphate 
180 : 1247.5 : : 5 g"^- ' 34-652 gm. 

In other words, 34.652 gm. of cupric sulphate will be 
reduced by 5 gm. of glucose. 

Method of Testing with Fehling^s Solutio n, — Equal par ts 
of each of the solutions should be diluted with about fo ur 
ti mes the amount of water, and the mixture should be boiled 
for a few seconds. The mixed reagent keeps for a day only. 
The separate reagents keep longer, but the preliminary 

* The sodium hydrate solution, specific gravity 1.140, contains 77.0 gm. 
of caustic soda and enough distilled water to make 500 cc. 

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boiling of the diluted mixture should never be neglected 
as a test for the stability of the solution. If the solution 
remains clear on boiling, the reagents are to be regarded 
as fit for use. If cloudiness or a precipitate occurs, the 
reagents should be rejected and fresh solutions procured. 

To the diluted mixed reap;ents add the suspected urin e, 

^/ drop by drop, boiling the mixture at the top of the tube only 

I Xo^ for a second or two after the addition of each drop . If 

f • I -'Sugar is present in considerable amounts, the first two drops 

v*' ^ will cause a heavy precipitate at the upper part of the fluid. 

If no precipitate occurs, urine may be added, drop by drop, 

boiling for a second after each drop, until we are satisfied 

that no reaction takes place. 

A jpositive reaction is rViarartpriVpH Ky hf^^YY) finHy 
powdere d, yellow, orange or red precipitate of copper syi b- 
oxid. If the precipitate does not appear until five minutes 
or longer after the addition of the urine, the quantity of 
sugar is very small, less than 0.5 per cent. If no pre- 
cipitate occurs within thirty minutes on standing, allow 
the test-tube to stand for a day, as traces of sugar may show 
after a few hours. 

It cannot be emphasized too strongly that th e use o f 
insufficie ntly dilute Fehling^s solution , thf ^^*^^ ^^ rnnr^p- 
trated u rine without previous dilutions, and prolon ged 
boilmg atter the addition of t> |f ^irinp mnQt hp avniHpH in 
order to get accurate results with this test. All the pre- 
cautions already spoken of above as applying to the copper 
tests in general must be observed in working with Fehling's 
test. In doubtful cases confirmatory tests, which will be 
considered further on, are necessary. The value of Fehl- 
ing's test as a routine method is universally acknowledged, 
but it is trustworthy only if properly performed. 

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Pavy's Test. — The solution used in this test consists of: 

Cupric sulphate. . , .• 320 grains 

Neutral potassic tartrate 640 " 

Caustic potash 1280 " 

Distilled water 20 fluidounces 

This solution is made and used in the same way as 
Fehling's, but the proportions of copper in it are calculated 
on the assumption that the formula for grape-sugar is 
CeHj^Oe instead of CgHjjOg, as Fehling had it. There- 
fore, in Pavy's solution 100 minims correspond to 0.5 grain 
of glucose. 

Haines' Test. — This is a modification of Fehling's. 
It is claimed that the solution prepared according to Haines' 
formula is stable and keeps indefinitely, while the ordinary 
Fehling's solution does not. In the author's experience, 
Haines' solution keeps well for several weeks if kept care- 
fully stoppered in a dark place, but there is a tendency to 
deposit a film of copper upon the walls of the reagent bottle, 
as shown by a reddish color visible when the bottle full of 
reagent is looked at by reflected light. Later, a deposit 
of copper may appear at the bottom of the bottle. Haines' 
solution keeps far better than Fehling's when the latter is 
mixed, yet the former is not indefinitely stable. For 
qualitative tests Haines' solution is available even when 
there is a slight film of copper upon the walls of the bottle, 
but the solution should not be kept longer than needful. 

The formula for Haines' solution is as follows: 

Copper sulphate 30 grains 

Distilled water J ounce 

Pure glycerin J " 

Potassium hydrate solution 5 ounces 

The copper is dissolved in the water, the glycerin is mixed 

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thoroughly, and the potash solution is added. One part of 
this solution is diluted with 3 parts of water in a test-tube 
and the reagent is boiled. Six or 8 drops (not more) of 
the suspected urine are added and the mixture is boiled for a 
few seconds. If sugar is present, a yellow or yellowish-red 
precipitate appears. 

The author's experience with this test has been very 
satisfactory and it may be recommended as an excellent 
routine test for practitioners. Its advantages are that it is 
effective with small amounts of urine and that it does not 
quite so readily cause confusion in the presence of other 
copper-reducing substances as does Fehling's solution. 
A worker of experience, however, will prefer Fehling's 

The Bismuth Tests , — These depend upon thf pp^'^"'''^^ 
glucose to reduce the salts of bismuth, giving a black pre- 
c ipitate of the met allic base. 

I. Nylander's Tes t. — This is one of the most valuable 
tests for glucose, especially as a confirmatory method in 
cases of doubtful reactions with the copper methods. The 
Nylander te st, when negative, is conclusive proof of the 
absence ot sugar. When positiv e, however, itshould be 
coniirmfid By fiittner tests. 

1 he reagent consists ot^ gm. of Rochell^ salt , dissolved 
in 100 cc. of a 10 per cent, solution of sodium hydratp . 
The solution is warmed and 2 gm. of bismuth subnitrate a re 
added. One part of this fluid ^^^^'^^'^ *^ TO pp^^'^ ^^ nrjpp> 
and the mixture is heated. _ In from t hr ee to five minute s 
it turns blac k if supar is present. The reaction demon- 
strates the presence of o.i per cent, of sugar. 

Precautions. — The reagent should be perfectly clear (filtered when 
necessary) and should be kept in a dark bottle. The fluid in the test- 

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tube may be boiled vigorously, and if more than o. i per cent, of sugar is 
present the fluid will turn black cU once or soon after boiling (formation 
of bismuth suboxid). When traces of sugar are present, the fluid will 
turn brown. 

Reduction of bismuth ajter the fluid has cooled is not due to sugar. 
When no sugar is present there may be a white precipitate due to phos- 
phates. Albumin may cause a red precipitate, and if present in excess 
may give rise to a black deposit which may be mistaken for that due to 
sugar. A positive reaction, which is usually partial, however, may occur 
in the presence of an excess of urinary coloring-matters, indican, glycuronic 
acid, hydrogen sulphid, and ammonium carbonate. Dark-colored urine 
should, therefore, be diluted, while decomposing urines (ammoniacal 
cystitis, pyelitis) should not be tested with this method. Practically the 
same drugs as interfere with Fehling's and other copper tests cause a re- 
duction with Nylander's solution. In case of doubt, therefore, confirm- 
atory tests are necessary (phenylhydrazin, fermentation, polariscope). 

The other bismuth tests are not as satisfactory nor as 
delicate as Nylander's. They are mentioned here for the 
sake of completeness: 

2. Boettger's Test. — Equal volumes of potassium hy- 
drate solution (U. S. P.) and urine are mixed in a test-tube, 
and a pinch of bismuth subnitrate is added. The mixture 
is shaken and boiled. A black or gray precipitate appears 
in the presence of sugar. This test is used but rarely, as it 
is deceptive in the presence of traces of sulphur, which pre- 
cipitates bismuth sulphid. Briicke modified it as follows: 

3. Briicke's Modification. — To remove the sulphur 
compounds Frohn's reagent is used. It consists of 1.5 gm. 
of freshly precipitated bismuth subnitrate mixed with 20 gm. 
of water and heated to boiling, whereupon 7 gm. of potas- 
sium iodid and 20 drops of concentrated hydrochloric acid 
are added. Ten cc. of water are poured into a test-tube 
and the same bulk of the suspected urine is poured into 
another tube. To the water add a drop of Frohn's reagent, 
which will cause a precipitate. Then add, drop by drop, 

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concentrated hydrochloric acid until the precipitate is 
redissolved. In this way we ascertain approximately the 
amount of reagent to be added to the suspected urine. 
Add the same quantity of hydrochloric acid to the urine 
in the other test-tube, then add the bismuth solution until 
precipitation is complete, and filter. Further addition of 
hydrochloric acid or of the reagent should not render the 
filtrate turbid. The filtrate is then boiled with an excess 
of alkali, as in Boettger's test. If sugar is present, a gray 
or black precipitate appears. According to Briicke, this 
test will detect 0.4 per cent, of glucose in water. 

Pseudoreactions for Glucose. — ^The following table 
shows briefly the conditions in which deceptive reactions 
resembling those for glucose occur with the copper and 
the bismuth tests: 


I. Normal urinary constituents when present in sufficiently large 
quantities may give rise to deceptive reactions with: 

Copper Tests. Bismuth Tests, 

Traces of carbohydrates, as dex- Uro-erythrin. 

trose, isomaltose, pentoses, ani- Urinary pigments (urobilin in par- 
mal gum, glycuronic acid com- ticular) when present in greatly 

pounds. increased amounts cause a 

Pyrocatechin. brownish discoloration of the 

Bile-pigment. phosphatic deposit. 

Urinary pigment. Indican. 

Uric acid. 





^ After Sahli, Diagnostic Methods of Examination, Philadelphia, W 
B. Saunders Company, 1905, p. 486, 

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Concentrated urines are particularly apt to effect reduction, and the 
same is true of urines containing a moderate or large quantity of formed 
elements (leukocytes, erythrocytes, epithelial cells). 

II. Products of abnormal metabolism which effect reduction: 

Copper Tests. 
Homogentisic acid. 
Uroleucinic acid. 

Bismuth Tests. 
Hexoses (dextrose, levulose, iso- 
maltose, lactose [in puerperal 
women]), pentoses, glycogen, in- 
creased quantities of glycuronic 
acid compounds. 
Increased quantities of hemato- 

Uroleucinic acid (weak). 
Homogentisic acid (weak). 
III. Reducing substances added to the urine as preservatives, which 
consequently make the reduction tests for sugar impossible: 

Copper Tests. Bismuth Tests. 


IV. Drugs or the derivatives 
bolic change: 

Copper Tests. 
Benzoic acid. 
Copaiba balsam. 
Glycuronic acid compounds 

drugs (see p. 127). 
Salicylic acid. 

obtained from them as the result of meta- 

Bismuth Tests. 
Benzoic acid. 

Quinin (large doses). 
of Glycuronic acid compounds of 
drugs (see p. 127). 
Rheum (also frangula and cascara 


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Other Tests for Glucose. — ^The first two of these are 
important confirmatory tests, but are somewhat too elab- 
orate for every-day use. 

Rubner's Test. — " Ten cc. of a concentrated solution of 
neutral lead acetate (i part of lead acetate to lo parts of 
distilled water) are added to lo cc. of urine. The mixture 
is filtered and ammonia carefully added to the filtrate, 
drop by drop, until a cheesy precipitate remains. The 
mixture is then heated over a water-bath to 80° C. During 
the heating, if dextrose is present the precipitate will be- 
come a beautiful rose or salmon red. The chemistry of 
this reaction is not positively known. The test is reliable, 
very delicate, and, therefore, particularly appropriate when 
Fehling's test seems doubtful. If the precipitate is heated 
too much the color becomes brown, like cafe au lait, and is 
no longer characteristic. Milk-sugar gives a yellow-red to 
brown color " (Sahli). This test is too intricate for routine 
work. Glycuronic acid compounds may give a similar 
reaction, but with this exception Rubner's test is one of the 
most reliable we have. 

Pbenylhydrazin Test. — This test should be employed 
whenever there is doubt whether the reduction of copper 
or bismuth is due to the presence of glucose (or some other 
carbohydrate) or to the presence of creatinin, uric acid, 
hippuric acid, etc., in excess. It is based upon the principle 
that with glucose present in o.oi per cent, or even smaller 
amounts, phenyl glucosazon (C18H22N4O4) is formed by 
this method, a compound which crystallizes in character- 
istic yellow needles recognizable under the microscope, 
and usually arranged in sunburst fashion (Plate 3). 
These crystals (glucosazon) are almost insoluble in water, 
but soluble in boiling alcohol and melt at 204° C. Similar 

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Plate 3 

Crystals of Phenylglucosazone {after von Jahch), 

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compounds are formed with this method in the presence of 
lactose (galacosazon) , levulose (levosazon), the pentoses 
(pentosazon), and glycuronic acid, but these differ in their 
melting-points or in other respects as shown in the fol- 
lowing table (Zunz, quoted by Emerson) : 



I. Gives crys- 
tals of phe- 
in urine it- 

A. Melting-point 
of crystals about ' 
200° C. 

(a) Fermenta- f i. Dextrorotatory=GLUCosE. 
tion positive. ( 2. Levorotatory =Levulose. 

(b) Fermenta- 
tion negative Lactose. 

B. Melting-point f (<»> ^run reac- 

of crystak about > ^^^ posiUve Pentoses. 

150° C. I (6) Ordn reac- 

l tion negative Isomaltose. 

II. Gives crystals with phenylhydrazin only after urine has been J \.J[S*'^°!i!£, 
treated by lieating with dilute H2SO4. \ ^^^^ 

Method of Testing with Phenylhydrazin,— -Into a beak er 
0.% gm. of the colorless crystals of phenvlhvdrazin hyd ro- 
chlorate and 1.5 gm. of s odium acetate are place d. Enough 
water is added to dissolve this mixture, when the beaker i s 
placed ove r a water-bath an d gently heated. Five cc. of 
urine are now added and the mixture is kept boiling for 
nve minutes. It is then slowly cooled. In the pres ence 
of sugar the crystals will settle at the botto m. TheHuid 
Tiidy lllimi Uy U^litriiuged (especially it the crystals are 
scanty), and if desired the crystals may be separated by 
decanting, dissolving them in hot 60 per cent, alcohol, 
adding water, and boiling the alcohol away. Under the 
microscope the crystals appear as small, bright yellow 
needles, arranged in sunbursts, sheaves, fans, etc., or 
sometimes distributed singly. Lactosazon (with lactose) 
gives shorter, heavier crystals, often pointed at both ends. 

The Melting-point of Crystals. — This may be necessary in differenti- 
ating pentoses, which of late have been more thoroughly studied and are 
assuming greater clinical importance. For this purpose the following 
simplified method is recomimended by Emerson and has given satisfac- 

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tion in the writer's laboratory: Into a small flask filled three-quarters 
full of concentrated HaSO^, a test-tube, half full of the same acid, is fitted 

by means of a perforated stopper. 





Fig. 8. — Melting-point of crys- 
tals: A, Flask; 5, test-tube of 
sulphuric acid; C, thermometer; 
Z>, fine-bore tube for crystals. 
(From Emerson's "Clinical Di- 
agnosis" by permission.) 

The whole is held by a clamp to an 
upright support. Into the test- 
tube a thermometer (Centigrade) 
is carefully dipped, submerging the 
mercury bulb in the acid. To the 
lower part of the thermometer and 
parallel to it is fastened a pointed 
glass tube of small caliber, closed 
at the tip, containing the crystals 
(Fig. 8). This tube is attached 
to the thermometer by means of 
a rubber band (above the acid). 
The flask is warmed slowly with a 
Bunsen burner and the point noted 
at which the crystals melt. A tem- 
perature of about 2oo°-2o5** C. is 
characteristic for glucose, levulose, 
or lactose (see table), while pen- 
toses give lower melting-points 
( 1 59^ to 1 6o° C. ). The crystals for 
the purposes of this test should be 
dissolved in hot (6o® C.) alcohol, 
the solution poured into water, and 
the crystals redeposited by evapo- 
rating the alcohol. When impure 
the crystals obtained with the 
phenylhydrazin test show a lower 
melting-point than when pure. 


For quantitative analysis 
with any method the entire 
amount of twenty-four hours 
should be collected, meas- 
ured, and a sample of the 
thoroughly mixed urine should be examined. The amount 

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of sugar eliminated varies a great deal according to the 
time of day and the length of time after the meal. The 
urine should be kept 
as has been described 
in the introductory 
chapter, to prevent 
fermentation. Quan- 
tities of sugar are ex- 
pressed usually in 
percentage, but the 
total number of grams 
of sugar eliminated 
must be calculated, 
as this is the final 
criterion. The prog- 
ress of the disease and 
the result of treatment 
may be judged partly 
by comparative study 
of the quantity of 
glucose eliminated 
daily. The albumin 
should be removed 
before making quanti- 
tative tests for sugar: 
Place 50 cc. of the 
urine in a porcelain 
evaporating dish, add 
2 or 3 drops of dilute 
acetic acid, and boil 
thoroughly. If albumin does not appear, add acetic acid, 
drop by drop, stirring constantly, and heating until the co- 

Fig. 9. — Apparatus for the quantita- 
tive estimation of sugar: w, Meniscus 

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agulum forms. Filter and wash the precipitate once or 
twice with water. Collect the filtrate; wash with water 
into a graduate, and add enough water to make the ori- 
ginal 50 cc. Mix the contents of the graduate thoroughly 
and use for quantitative tests. 

Fehling's Method.— The principle of Fehling's method 
has already been explained above (p. 100). The quantita- 
tive application of it consists in titrating a known quan- 
tity of Fehling's solution in a flask with the (diluted) urine 
and heating the mixture till no more copper precipitates, 
and until the supernatant fluid is perfectly free from blue 

The apparatus required is shown in Fig. 9. The 
burner should be one which can be carefully regulated; 
the flask should have a capacity of 100 cc, and the buret 
should be graduated in xV cc. The tripod should be about 
20 cm. high and be covered with wire gauze or asbestos. 

Diluting the Urine. — This is extremely important, as the best results 
are obtained with urines containing from J to i per cent, of glucose. 
The specific gravity of the urine should be taken. The quantity of urine 
voided in twenty-four hours being known, the specific gravity of the urine 
is compared with that which would normally correspond to the quantity 
eliminated, i. e.y 2 liters of normal urine daily would have a specific 
gravity of 1015; 3 liters of the same urine, a specific gravity of loio; 6 
liters, a specific gravity of 1005. If a diabetic urine measures 3 liters and 
has specific gravity of 1030, it contains enough sugar to raise the specific 
gravity from normal (10 10) to 1030. The difference is a specific gravity 
of 1020. The last two figures of this " corrected specific gravity" multi- 
plied by 0.23 (in this example 4.6 per cent.) will give very roughly the 
percentage of sugar in the urine. The urine should, therefore, be so 
diluted that it contains 0.5 per cent., i. e., ten times for a urine containing 
5 per cent, glucose. The dilution should be accurately done by means of 
pipets and with distilled water. The dilution must be well shaken. 

Five cc. of each of the two solutions are measured accurately and 
placed in the flask. To this 30 cc. of distilled water is added, and the 
mixture is heated to the boiling-point. The diluted urine (see above) is 

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poured into the buret accurately to the zero mark, allowing all the urine 
above zero adhering to the walls of the buret to settle on the surface 
of the liquid in the buret. (Waiting for two minutes is usually sufficient 
for this purpose.) The stopcock is opened and the urine is allowed to 
settle down to zero if needful. The buret is placed in position over the 
flask, and when the fluid in the latter has just come to a boil the diluted 
urine is added from the buret, the contents of the flask being kept gently 
boiling ut^Jil the faintest trace of blue color disappears. 

The chief difficulty with Fehling^s method lies in determining this 
end-reaction. It is best, according to some authorities (Emerson), to 
add the urine from the buret and to heat the mixture, but to remove it 
from the flame as soon as it has begun to boil. An abundant red 
precipitate forms, which if allowed to stand in the air becomes reox- 
idized. For this reason we must allow this precipitate to settle only 
for a few moments, and then watch the color of the meniscus or clear 
uppermost layer in the flask. If there is still blue color in this men- 
iscus, more urine must be added and the boiling repeated until all 
traces of blue disappear. 

Calculatio?!. — Inasmuch as 10 cc. of the combined solutions are reduced 
by exactly 50 milligrams (0.005) ^^ glucose, the amount of urine required 
to reduce the solution in the flask will contain just 0.005 of glucose. From 
this the percentage of glucose in the urine can be easily calculated as 

If 15 cc. of diluted urine, 1:10, were needed to reduce the copper in the 
flask, then 15 cc. of the diluted urine contained 1.5 cc. of undiluted urine. 
Hence, 1.5 cc. of urine contained 50 mgm. of glucose. The percentage 
is then calculated according to the following equation: 

1.5 : 0.050 : : 100 : x, therefore, x = 3.33 per cent. 

If the total amount of urine voided was 2000 cc. in twenty-four hours, 
then 3.33 per cent, multiplied by 2000 and divided by 100 equals 66.6 gm., 
the amount of sugar in twenty-four hours. 

Although Fehling's quantitative method has been con- 
sidered a standard for years, it has never been satisfac- 
tory, even in the hands of experts, owing to the great 
difficulty of determining the exact point of end reaction, 
i. e., that point when all the copper had been reduced 
and the solution was perfectly colorless. For this reason 


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the writer has during the past few years ceased using and 
teaching this method, which, in his opinion, is most un- 
satisfactory for the practitioner and most trying for the 
laboratory worker. 

Purdy's Method. — The most convenient and satis- 
factory modification of Fehling's method is that of Purdy. 
This method has the advantage of giving a sharper end 
reaction than does Fehling's, and for this reason gives 
more accurate results than the latter. 

The solutions required are as follows: 

I. Copper sulphate, pure, crystals 4.158 gm. 

Distilled water, enough to make 500.0 cc. 

II. Rochelle salt 20.4 gm. 

Potassium hydroxid, pure 20.4 " 

Ammonia (sp. gr. 0.88) 300.0 cc. 

Distilled water, enough to make 500.0 " 

Five cc. of each solution (lo cc. in all) are used in the test 
and correspond to 0.005 S^- ^^ glucose. The method of 
using it and the method of calculating the percentage of 
sugar in the diluted urine are the same as described with 
Fehling's solution. The urine is very slowly added from 
the buret until no trace of blue color remains, the fluid in 
the flask being kept gently boiling. 

Fermentation Test. — This test is very convenient for 
clinical use, but is not so accurate as the other quantitative 
methods. A very convenient method of performing it is 
with the aid of Einhorn^s saccharometer (Figs. 10 and 11). 

Two sets of the apparatus are used, one with the sus- 
pected urine, the other with normal urine as a control 
test. A small piece of yeast, which should be fresh, is 
mixed thoroughly with a definite quantity of the suspected 

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urine, measured in a marked test-tube furnished with the 
apparatus. The mixture is then poured carefully into 
the graduated tube, which resembles the Doremus urea 
apparatus, care being taken to expel all the air by slanting 
the tube so that the bubbles escape. The tubes are allowed 
to stand at a temperature of about 86° F. until fermenta- 
tion has ceased — i, e,y for about twenty-four hours. The 
carbon dioxid resulting from 
the fermentation collects at 
the top of the tube and the 
percentage of sugar is read off 

Fig. lo. — Einhorn's saccharometer. 

Fig. II. — Einhorn's saccharometer 
with stop-cock. 

at the level of the fluid. If the second tube also shows 
a small amount of gas, this is deducted from the reading of 
the first tube. The results are only approximate. 

Lohnstein^s Method. — A valuable fermentation sacchar- 
ometer has been described by Lohnstein, which directly 
indicates the percentage of sugar from o to lo per cent, 
without requiring dilution. According to a number of 
observers, this instrument is very accurate, although Riva- 

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rono, of Turin, found that comparative tests with polar- 
imetry, Fehling's method, and Lohnstein's apparatus 
showed marked errors, which increased especially with 
the amount of albumin in the urine and the degree of 
dilution of the specimen.^ 

Lohnstein's saccharometer is intended to rectify the 
errors which are apt to enter in an estimation with Ein- 
horn's apparatus, because in the 
latter no allowance is made for tem- 
perature, pressure, etc., as should 
be done in all volumetric gas anal- 
yses. Lohnstein's instrument con- 
sists of a U-shaped tube with a long 
arm, and another ending in a bulb. 
Mercury is poured into this bulb up 
to the zero mark on the scale of the 
long arm. A definite quantity of 
urine is poured over the mercury, a 
little yeast is added, and the appa- 
ratus is closed with a glass stopper 
greased in vaselin. The stopper is 
weighted with lead so as to prevent 
the escape of any gas. The appa- 
ratus is set aside at a fixed tem- 
perature (20° or 35° C), and the 
mercury rises as the gas of fermen- 
Its level is read directly on the scale of 
The temperature and 

Fig. 12. — Lohn stein's sac- 

tation develops. 

the tube in percentage of glucose 

tension in this method remain always the same. 

The disadvantages of all the fermentation methods are 
their inaccuracy and the fact that they require twenty- 

^ Riforma Medica, March 30, 1904, p. 343. 

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four hours for their completion. According to Ogden, the 
fermentation tests yield results that are about 0.5 per 
cent, lower than those obtained with Fehling's method. 

Roberts^ comparative density method is also approximate, 
but is preferred by some, as it requires no apparatus to 
speak of. Four ounces of the urine are placed in a 12- 
ounce bottle and a piece of compressed yeast is added.* 
The bottle is then stoppered with a nicked cork, to allow 
the escape of CO2, and set aside in a warm place. A tightly 
corked 4-ounce bottle filled with the same urine without 
any yeast is placed next to it. Fermentation goes on for 
eighteen to twenty-four hours. The fermented urine 
is then decanted into a cylinder and its specific gravity is 
taken. At the same time the specific gravity of the un- 
fermented urine is also taken and the loss of density is 
noted. According to Roberts, the loss of each degree of 
specific gravity corresponds approximately to i grain of 
sugar to the fluidounce. Thus, if the specific gravity of 
the urine was 1040, and after fermentation 1020, it con- 
tained 20 grains of sugar to the fluidounce. The two 
specimens of urine should be kept at exactly the same 

Roberts' comparative density method may also be em- 
ployed in an apparatus devised by Heinrich Stern, of New 
York, styled a urinoglucosometer (Fig. 13). This consists 
of a small and a large glass tube, united at their bases to 
form a U. The small tube is marked at 50 cc, the large 
one at 100 cc. Both are closed by means of perforated 
metal caps. The smaller tube is filled with urine to the 
mark, and is tightly closed with a rubber stopper. A 
small piece of compressed yeast is placed in the larger tube 

* One-sixteenth of a cake of Fleischman's compressed yeast. 

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and urine is added up to the mark. A urinometer is then 
inserted into each tube, the metal caps are put over the 

tubes, and the apparatus 
is set aside at a tem- 
perature of 80° F. for 
from twelve to fifteen 
hours. The larger tube 
is opened and the con- 
tents stirred to liberate 
the CO2. The floccu- 
lent mass is allowed to 
settle and the cap is 
replaced. Then the spe- 
cific gravity of the urine 
in both tubes is read 
from the flat tops of the 
metal caps. Each degree 
of specific gravity lost 
equals 0.2196 gm. of glu- 

Fig. 13.— Stern's urinoglucosometer. COSe per ICO CC. of Urine. 

The difference in specific 
gravity between the urines in the two tubes, multiplied by 
0.2196, is the percentage of sugar present. The method 
is convenient and, though open to the objections of in- 
accuracy which obtain in all fermentation tests, is suflS- 
ciently exact for clinical purposes. 

Schiitz^s Method, — An instrument devised by J. Schiitz 
is styled an areosaccharomeiery and its construction is 
based upon the difference in the density, of urine before 
and after fermentation. The instrument consists of a ves- 
sel which is filled with urine and immersed in water, the 
long neck of the instrument being so graduated that the 


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divisions indicate the percentage of sugar corresponding 
to the difference in density before and after fermentation. 
The vessel is filled with urine to the proper mark and i 
gm. of compressed yeast is added. Enough shot is put in 
to allow the vessel to sink to o. The contents are shaken well 
and are allowed to ferment at room-temperature for from 
twenty-four to thirty-six hours. The instrument is then 
immersed in water and the specific gravity and the per- 
centage of sugar read. This method is said to be more 
accurate than Einhorn's, but the latter is more convenient 
for every-day work. 

Polarization. — ^The polariscope offers the most accurate 
and quickest method of determining the amount of glucose 
when the quantity exceeds i per cent. The best instru- 
ments in the hands of experts can detect smaller amounts 
(o.oi per cent.), but, unfortunately, the apparatus is so 
costly that it is out of the range of the practitioner. The 
method depends upon the fact that glucose rotates polarized 
light toward the right, and that the degree of rotation 
varies in proportion to the percentage of sugar in the urine. 

Although theoretically accurate for grape-sugar solu- 
tions, polarimetry is open to the objection, when used with 
urine, that the latter contains sometimes levulose, oxybu- 
tyric acid, etc., which rotate polarized light to the left. 

A polariscope especially devised for clinical work by 
Ultzmann is made by Reichert of Vienna. It is very con- 
venient and sufficiently accurate for all purposes, 
reading from o.i up to 25.0 per cent. 

By means of this saccharimeter the percentage of sugar in urine may 
be read directly upon the Vernier scale of the instrument. The polari- 
scopic tube is set upon a stand. A concave mirror illuminates the visual 
field. Fig. 14 shows the Ultzmann polariscope in section. In this figure 
a and b are a system of magnifying ocular lenses focusing the image at the 

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point p. The upper prism is marked c, the lower, /. The upper prism 
is connected with the movable part of the sliding scale; /> is a transparent 
plate of quartz, polarizing to the right and left respectively. The scale is 
so arranged that each division corresponds to i.o per cent, glucose in the 
urine at 20° C. Tenths of i per cent, can be read with the aid of the 

Ultzmann's polariscope. 

sliding Vernier. To read the tenths of a degree it is necessary to see at 
which mark of the Vernier there is a perfect alignment with one of the 
marks of the percentage scale. In Fig. 15, the zero mark on the Vernier 
is between the fourth and fifth percentage degree on the right half of the 
scale. To determine how many tenths per cent, besides the 4 per cent, 
of sugar are present, we count the divisions on the small scale from o, and 

Fig. 15. — Vernier scale of Ultzmann's polariscope. 

find that the sixth division is the first to be directly opposite one of the 
marks of the large scale. The reading then is 4.6 per cent, glucose in 
the scale as shown in the figure. 

The urine to be examined is placed in a glass tube with metal screw 
ends, into which are fitted optically inactive glass disks. The lower end of 
the tube is closed, the fluid poured in, and, avoiding air bubbles, the upper 
glass disk is placed in position and screwed down. If the urine is very light 
colored and perfectly clear, it may be examined as such. If not, it must 
previously be decolorized and cleared by mixing it with a sufficient amount 
of powdered basic lead acetate, and filtering through several thicknesses 
of filter-paper till the fluid is perfectly clear. The addition of the lead 
acetate in bulk does not alter the volume of the fluid, and for this reason 
this method of clearing is preferable. In some cases, however, it is very 

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difi&cult to clear the mixture by filtration, and then it may be necessary 
to mix the urine with a solution of basic lead acetate before filtering. If 
this is done, the volume of the urine should be known and one-fourth 
of this volume of lead acetate solution (lo per cent.) should be added to 
the urine. Instantly a fine white precipitate of lead chlorid, sulphate, and 
phosphate will be thrown down, and the mixture should then be filtered 
through a dry filter. One-fourth of the amount of sugar read on the scale 
should then be added to get the true amount in the urine thus prepared. 

When the glass tube is filled with water, dr when it is filled with normal 
urine, the two halves of the disk p seen through the ocular appear of the 
same color. If a solution of glucose be placed in the tube, however, 
there will be a difference in the colors of the two sides when the zero mark 
of the Vernier is at zero of the scale, and only by moving the Vernier to 
the right can the two halves of the disk be made to appear of the same 
color. When this point is reached, the amount of glucose may be read 
upon the scale. 

Albumin, if present, must be previously removed, the original volume 
being noted and allowances made for any changes due to the removal of 
the albumin. The reason for removing albumin is that it polarizes light 
to the left, thus neutralizing the action of sugar. The Ultzman polari- 
scope is simple enough to be used by practitioners and is not a very ex- 
pensive instrument. 


Glucose. — What does its presence in the urine indicate? What is 
diabetes? What other causes may produce glycosuria? What class of 
tests are most commonly used for searching for glucose in the urine? 
On what principle do they depend ? Describe Trommer's test. What 
precautions should be taken when using any of the copper tests ? Name 
the principal substances other than sugar which reduce copper sulphate. 
Describe Fehling's qualitative test. What method is used with a more 
stable solution? Describe the phenylhydrazin test. On what principle 
are the bismuth tests based ? Describe Boettger's test; Brucke's modifi- 
cation; Nylander's test; picric acid and potash test; Rubner's test. 

How should a sample be collected for quantitative analysis of sugar, 
and why ? What are the disadvantages of Fehling's method for quantitative 
analysis of sugar ? Describe the technic of Fehling's quantitative method. 

Describe Purdy's method. What are its advantages? Describe 
the fermentation test. Describe the comparative density method for 
sugar. What is the polarization test for glucose and what is its value ? 
Describe the Ultzmann polariscope. 

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Lactose (mil k-sugar) is found som^ timfS ^'" ^^^ nor- 
^al uri ne of nur sing women, b ut usually it is present in 
such cases m very small quantities, although Ralfe reports 
a case in which as much as 3 per cent, occurred. It is 
more apt to occur near the end of gestation, and especially 
in cases of mastitis. In women who have weaned their 
children early it is also frequently seen for a few days or a 
week. Lactose has no pathologic significance in urine, 
and is important only because it is apt to be mistaken for 
gl ucose. 

Lactose (C12H22OH + HjO) is characterized by crystal- 
lization in white or colorless four-sided prisms, with 
acuminated ends, bounded by four triangles, and by turning 
polarized light to the right with a rotating power of + 59.3 
degrees, while the rotation of grape-sugar is +53.1 de- 
grees. It reduces salts of copper, but does not undergo 
alcoholic fermentation with yeast. Certain cleft fungi, 
however, convert milk-sugar into alcohol, and ferments 
induce lactic acid and butyric acid fermentation readily 
with lactose. It is quite soluble in cold and freely solu- 
ble in hot water; insoluble in alcohol and ether, and 
precipitated by acetate of lead and ammonia. 

Lactose can be recognized with certainty only by isolating 
it, and the methods for doing this will be found in works 

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on physiologic chemistry. If the urine reduces Fehling's 
solution feebly, but does not ferment with yeast, and if it 
rotates polarized light strongly to the right, especially if 
the urine is that of a pregnant or nursing woman, lactose is 
probably present. 

The phenylhydrazin test with lactose forms a crystalline 
body called phenyl-lactosazone, which occurs in yellow 
needles grouped in clusters, melting at 200° C. 

T^vn^^cip (frnit-gngar) k rarply fo und in the urinc a nd, 
w hen present, is usually associated with glucose. It 
rotates polarized light to the left, thus partly neutralizing 
the action of glucose, so that when present with glucose 
more sugar is found by chemic tests than by polarization. 
(It must be noted that other bodies, such as glycuronic acid, 
cystin, and beta-oxybutyric acid, etc., diminish the optic 
activity of urine.) 

Levulose (CgHiaOg) is non-crystallizable when impure, 
but when pure forms long wavy needles. It reduces salts 
of copper much more feebly than does grape-sugar. It is 
detected by the polariscope in the following manner 
(see also Phenylhydrazin Test, p. 108): To distinguish 
left-handed rotation of light caused by substances other 
than levulose, the urine is subjected to alcoholic fermenta- 
tion. If the rotation is due to the levulose, it disappears; 
if due to the other substances, it persists after fermentation. 


Laiose (Leo's sugar) was found by Leo, in 1887, in 
some severe cases of diabetes. Laiose (CgHiaOg) is left- 
rotating, reduces copper salts, and forms a compound with 

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phenylhydrazin. It does not ferment and is not sweet in 
taste. Its isolation is troublesome and of no consequence 
clinically, except that samples of urine that contain it 
show more sugar by titration than by polarization. 


Pentoses are sugars containing five atoms of carbo n 
(CgHjLjjOs) , and are products of hydrolysis of the other j: ar- 
bohydrates in the body. Pentoses form the carbohydrate 
molecule in the glycoproteids contained in the nuclei 
(see Nucleoproteids, p. 92) of such organs as the liver, 
spleen, pancreas, thyroid, thymus, and brain. Examples 
of pentoses are arabinose, rhamnose, and xylose. The 
last is of greatest importance. 

[Xylose rotates polarized light to the right, and its osazone (see Phenyl- 
hydrazin Test) crystals melt at 150*^ to 160° C. Xylose reduces copper 
as well as bismuth solutions, and reacts with Rubner's test, but in con- 
. trast to glucose it does not ferment with yeast. Arabinose gives similar 
reactions, but reduces copper more readily than xylose.] 

Clinical Significance. — There are three varieties of 
pentosuria (Janeway): (i) Alimentary pe niosuriay which 
is of no clinical significance, but should be noted to avoid 
confusion with the other forms. Pentoses are excreted 
after the ingestion of beverages and foods containing large 
amounts of soluble and assimilable carbohydrates — e. g., 
fruit syrups, malt liquors, etc. 

(2) Diabetic Pentosuria^ — Kultz and Vogel found pen- 
toses in a number of diabetics. Diabetic pentosuria is rare 
and is confined to very severe forms of diabetes. 

(3) Idiopathic Pentosuria , — This has assumed import- 
ance of late by the report of a collection of 24 cases by 
Janeway in 1906. Small amounts of pentose (0.05 to 0.6 

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per cent.) occur in these cases without clinical symptoms. 
The cause of this pentosuria is not known, but it is sup- 
posed that for some reason excessive quantities of pen- 
toses are formed in the organism. 

Detection. — Pentoses may be suspected when the ordi- 
nary sugar tests show the following peculiarities: (a) 
Fehling's or the other copper tests do not show a reduction 
while hot, but do so suddenly on cooling; (6) Nylander's 
test shows not a brown or black, but a gray precipitate; 
(c) the fermentation test is negative. 

Orcin Test {BiaVs Method). — The pentoses give a characteristic reac- 
tion with orcin. The following method was devised by Bial ^ as a modi- 
fication of a test described by Salkowski and Blumenthal. It is the 
easiest of this group of methods and is said to be sufficiently accurate to 
differentiate glycosuria from pentosuria. If glucose is present also, it 
should be removed first by fermentation and the residue tested for 

" Bial's reagent consists of 500 cc. of 30 per cent, hydrochloric acid, 
I gm. of orcin, and 25 drops of the official liquor ferri sesquichlorati 
(German Pharmacopeia). Four to 5 cc. of this reagent are boiled in a 
test-tube, and, after removal from the flame, several drops or, at most, i cc. 
of urine are added. A green color should appear at once or almost imme- 
diately. If the test is carried out in this manner^, Bial states that the small 
amount of heat employed is not sufficient to cause any reaction between 
the reagent and the most unstable glycuronates " (Sahli). 

There are a number of substances closely allied to glucose 
which are comparatively less important in urine analysis. 
Inosite {muscle-sugar) (CgHijO^ + 2H2O) is occasionally 
found in conjunction with grape-sugar and also in the last 
stages of chronic nephritis, in tuberculosis, syphilis, and 
typhus fever, as well as after drinking large quantities 
of water. Properly speaking, inosite is not a sugar, but 

^ Deutsche med. Woch., 1903, No. 27, 

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should be placed among the aromatic compounds. It does 
not reduce the copper salts; does not ferment with yeast; 
is optically inactive, and does not combine with phenyl- 

Its isolation and detection are cumbersome and not of 
sufficient clinical value to warrant further description here. 

Saccharose (cane-sugar) (C12H22O11) is veryrarely 
found in urine and is of no clinical importa nce. It 
has been found after eating large amounts of cane-sugar 
and in urines contained in a bottle that had not been prop- 
erly cleaned (s)n:up). It is at times added to the urine 
by persons who wish to deceive the physician. When 
traces are present, they are usually overlooked. When 
larger amounts are present, the urine may be boiled with 
dilute hydrochloric and sulphuric acid, and the cane-sugar 
is converted into dextrose and levulose, the solution rotating 
light to the left, while sugar alone rotates strongly to the 
right. Puire saccharose does not reduce Fehling's solu- 

Maltose. — Maltose is found occasionally in the urine 
in health and in disease. Von Jaksch found it in cases of 
malignant tumors. 

Dextrin. — Reichard has found dextrin in the urine of 
diabetes instead of grape-sugar. In such cases the urine 
behaves with Trommer's test just like a solution of dextrin, 
the fluid becoming first green, then yellow, and sometimes 
dark brown. 

Qum. — A gum-like substance has been found in the 
urine by Landwehr, who calls it "animal gum" and con- 
siders it a normal constituent. 

Qlycuronic acid (QHioO, or CHO . (CH . OH),. 
COOH) does not occur as such, but as a glucosid-like 

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combination with a variety of aromatic substances of the 
urine, especially indoxyl, phenol, etc. Its chief clinical 
importance is that it is apt to be mistaken for glucose. 
Glycuronic acid is dextrorotatory, but its paired combina- 
tions, which exist in normal urine, are levorotatory, so that 
Haas, Johannovsky, and others found that normal urine 
turns polarized light slightly to the left. It reacts to the 
reduction tests with copper and forms a crystalline com- 
pound with phenylhydrazin, but does not ferment with 
yeast. According to Zunz (see p. 109) glycuronic acid 
compounds form an osazone with the phenylhydrazin test 
only after the urine is heated with dilute HjSO^. In other 
respects glycuronic acid seems to act like the pentoses and 
is difficult to differentiate from these. 

Glycuronic acid apparently has nothing to do with 
diabetes. It is increased after the administration of those 
compounds with which it forms combinations in the urine — 
i. e., phenol (Kiiltz), benzol, naphthol (Nencki), menthol, 
camphor, turpentine, resorcin, hydroquinon, thymol, 
chloral, acetanilid, curare, morphin, chloroform, etc. 
With these it forms fixed compounds, as naphthol-glycu- 
ronic acid, etc. 

Glycuronic acid, when pure, is a s)n:up soluble in water 
and alcohol, which, on boiling with water, forms an anhy- 
drid (lactone), glycuron (CgHgOJ, which crystallizes in 
colorless plates. By the action of bromin it is converted 
into saccharic acid (CeHioOg), and is regarded as in- 
termediate between this acid and gluconic acid (CeHijO^), 
obtained by the oxidation of glucose with bromin (Ham- 

Alkaptonuria. — A r are condition known as "alkap toiL 
nuria" is characterized by a dark urine which grows darker 

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(redd ish-brown) on stand ing. The change is more rapid 
when an alkali is added, hence the name "alkapton." 
When a piece of cloth is dipped into such a urine it is dyed 
black. When voided the urine is highly acid. It reduce s 
Fehling's solution, but fails to give Nylander's test. It 
doe s not polarize light, does not ferment, and g ives no 
crystals with phenylhydraz in. 

formerly these urines were supposed to contain pyro- 
catechin, but alkaptonuria is now known to depend upon 
the presence of a number of other compounds, two of 
which have been isolated — ^homogentisic acid (hydro- 
quinon-acetic acid) and uroleucinic acid. The former 
appears to be derived from tyrosin {q, v). 

Clinical Significance. — Alka ptonuria, i?; due to an 
o bscure disturbance of proteid met abolism and seems to be 
congenital. It occ urs without symptoms and is discov ered 
usu ally by acc ident"! It is said to occur in members of the 
same family and especially in children of consanguineous 
marriages. Only 40-odd cases are on record. 


Before closing the consideration of carbohydrate bodies 
we must give a brief account of Cammidge's method for 
t he detection of a glycerin-like com pound which is ex - 
cret ed in th e urine in some diseases of t he pancrea s. 

"Cammidge's reaction was introduced in 1904, but has not 
as yet gained universal acceptance. Further studies are 
needed to confirm its clinical value as set forth by its 
author. The reaction depends upon the fact that in pan- 
creatitis and pancreatic necrosis glycerose is set free from 
the fat and enters the blood, whence it appears in the 
urine. It is converted into glycerose by boiling with min- 

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cammidge's reaction 129 

eral acids. The latest technic described by Cammidge is 
as follows: 

The urine examined must be from a twenty-four-hour specimen or 
from the mixed morning and evening excretion. If albumin is present, 
the specimen must be faintly acidified, boiled, filtered, and made up to the 
original bulk with distilled water. If sugar is present, it must be removed 
by fermentation with yeast, and if the urine is alkaline, it must be made 
just acid before proceeding. 

1. To 40 cc. of urine add 2 cc. of strong HCl, place in a small flask 
with a funnel in the mouth (to act as a condenser), boil for ten minutes, 
then cool the flask thoroughly in a stream of water, and make up the result 
to 40 cc. with distilled water. 

2. Add slowly 8 gm. of powdered lead carbonate, allow the mixture 
to stand for a few minutes, and when the reaction is complete, cool and 
filter through a close-grained filter-paper until the fluid is perfectly clear. 
Ten cc. of this clear filtrate are diluted to 20 cc. with distilled water. 

3. Shake this clear filtrate with 2 gm. of powdered tribasic lead ace- 
tate;^ filter several times, getting as clear a filtrate as possible. 

4. Add 2 gm. powdered sodium sulphate and bring mixture to a boil. 
Cool the flask in a stream of water and filter (to remove the lead as lead 
sulphate) to make 20 cc. 

5. To 20 cc. of the filtrate add 0.8 gm. of phenylhydrazin hydrochlo- 
rid, 2 gm. of sodium acetate, and i cc. of 50 per cent, acetic acid. Boil the 
mixture on a sand-bath for ten minutes and filter while hot through a 
small funnel moistened with hot distilled water. If the result is less in 
volume than 15 cc, make up to that bulk with hot distilled water, thor- 
oughly mixing the whole. 

In case of pancreatic disease, a light yellow flocculent precipitate 
forms. This must be examined microscopically, and will be found to 
consist of thread-like crystals arranged in sheaves and bundles. They 
dissolve in ten to fifteen seconds on being irrigated with 33 per cent, 
sulphuric acid. Any precipitate other than the crystalline deposit men- 
tioned is not to be regarded as evidence of a positive reaction. 

6. A control test is carried out in exactly the same way, except that the 
preliminary boiling with HCl is omitted; this, of course, gives crystals 
if sugar is present, and, in that case, the test has to be repeated after fer- 
mentation with yeast. 

^ Tribasic lead acetate (Pb(C2H302)22PbO) must be used. Mislead- 
ing results occur with the use of the solution of lead subacetate, U. S. P. 

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Clinical Significance. — Cammidge claims that his 
reaction is positive in all cases of pancreatitis. It is said 
to be negative in healthy subjects, in 75 per cent, of cases 
of cancer, and "with very few exceptions" in non-pan- 
creatic diseases. 

The solubility of the crystals obtained by this method is 
claimed to be of diagnostic import. If the crystals dis- 
solve (under the microscope) within one-half to one minute 
in 33 per cent. H2SO4, acute pancreatitis is present; if they 
take longer (two minutes), chronic pancreatitis; if five 
minutes, pancreatic cancer is probably present. These 
points are not generally conceded. 

As yet Cammidge's reaction can be looked upon only in 
the light of a confirmatory sign. It has no negative value 
so far as the writer's experience with it is concerned, and 
its positive value must be checked by the clinical features 
of each case. 


What is the clinical significance of lactose in the urine? What are 
its characteristic properties ? How is it detected ? 

What are the properties of levulose and how is it detected ? 

What is meant by laiose? 

Name a few of the other substances allied to sugar that may occur in 
the urine. 

Define the pentoses. What is their clinical significance? How are 
they detected ? What is the significance of glycuronic acid ? How is it 
detected? What is meant by alkaptonuria? What are the characters 
of the urine in this condition and to what acids is it due ? 

What is Cammidge's reaction, and in what diseases is it supposed to 
aid in diagnosis ? 

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The most accurate measure for the metabolism of the 

proteids is the output of nnnary nitrngpn. This OUtput 

de pends upon two factors: (i) The amount of nitrogen - 
ous foodstuffs (chiefly proteids) taken in, and (2) the burn - 
ing up and wasting of the tissues of the body (the prot eid 
constituents of cells, etc.). Formerly, the determination 
of the urea contained in the urine was regarded as all that 
was necessary to determine clinically the condition of 
nitrogenous excretion. Urea, however, forms from 85 to 
90 per cent, of the total nitrogen excreted in the urine. The 
remainder is present in the form of ammonia (2 to 5 per 
cent.), as uric acid (from i to 3 per cent.), and as extrac- 
tives (7 to 12 per cent. — Hammarsten) or ** undetermined 
nitrogen." At least 10 or 15 per cent, of the total 
nitrogen, therefore, is due to substances other than urea. 
Of the total nitrogen eliminated by man, 95 per cent, is 
excreted in the urine and about 5 per cent, in the feces 

Unfortunately, the determination of the total nitrogen 

'and the differential determination (so-called partition) of 

the several quantities of ammonia, uric acid, creatinin, etc., 

which contribute to the total nitrogen output necessitate 


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time, training, and apparatus quite beyond the limits of 
ordinary clinical work. For this reason, the technic of the 
elaborate methods of analysis which are required in this 
work has been omitted from these pages. The practitioner 
should be acquainted, however, with the value of nitrogen 
determination as well as with the importance of separate 
determinations of the quantities of urea, uric acid, am- 
monia, etc., entering into the total nitrogen output. 

By the t erm nitrogen balanre we mean the proportion between the 
i ntake a na the out put of nitrogen . When these are equal, a s is the case 
when a pati ent is fed on a constant. siItttCtgntiY luii aiet. we sav that he 
is in a state of nitrogenous equilibrium. Normally, the total amount 
ol nitrogen in tne urine on a mixed diet is from 10 to 15 gm. daily. The 
healthy body has a tendency of compensating or accommodating the 
nitrogen output during one period of twenty-four hours to the nitrogen 
intake during the preceding day. Even if the amount of nitrogen taken 
in varies from day to day, the average urinary nitrogen excreted during 
a period of days will equal the average of the nitrogen taken in during 
these days. For this reason, determinations of nitrogen must be made 
over a period of several days. The character of the food, the amount of 
water drunk, and the amount of exercise should also be carefully watched. 
The amount of nitrogen intake may be calculated with the aid of tables, 
showing the N. contents of various foods. 

Normally^ the total nitrogen is increased by anything that will increase 
the assimilation of proteids. The amount is greater upon a meat diet, 
after meals and after exercise, as well as after hot baths. By drinking 
considerable amounts of water the nitrogen excretion may also be in- 

In disease^ the nitrogen output is increased in febrile conditions, in 
diseases accompanied by a rapid waste of tissues, in diabetes, arsenic, 
antimony, phosphorus, and other metallic poisoning. A nitrogen in- 
crease also takes place whenever there is a diminished absorption of oxy- 
gen, as in severe hemorrhages, suffocation, dyspnea, etc., and when exu- 
dates or transudates are absorbed. 

The total nitrogen is diminished in convalescence from wasting diseases 
in myxedema and during pregnancy. After labor, the nitrogen again 
increases. Anything that interferes with the absorption or assimilation 
of proteids will diminish the nitrogen output. This is the case in very 

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tJREA 133 

Severe depression of bodily vitality. When ascites or other exudates or 
transudates are forming and when water is retained in the body, nitrogen 
is also diminished. In nephritis the kidneys may cease to excrete urea, 
thus announcing the probable onset of uremia, and in such cases, of 
course, the nitrogen is very markedly decreased. 

The relative proportion of nitrogen due to urea, to am- 
monia, and to amino-acids (the latter, the so-called "un- 
determined nitrogen") is disturbed markedly in toxemias 
of pregnancy and other toxic conditions. As this subject 
has assumed great importance of late years, a separate 
chapter has been devoted to it in another part of this book 
(see p. 386). 



Urea is the principal nitrogenous organic constitu ent 
of urine, and is derived chiefly from the metabolism of th e 
proteids . As has been said above, urea is but a partial 
index of the amount of nitrogen excreted, though, clin- 
ically, the test for the percentage of urea is the simplest 
method of determining the state of nitrogenous excretion. 
Urea, however, represents only abou t 85 per cent, of th e 
total nitrop;en of the urine, while 1 1^ per cent, is represented 
by uric acid, the p urin bodies, hippuric acid, ammonia, and 
by creaimm. 

Furthermore, the quantity of urea excreted is very 
variable in health, according to the amount of nitrogen 
intake. The quantity of urea, as determined clinically, is 
to be regarded, therefore, not as an absolute criterion, but 
only as a factor, valuable in diagnosis only when the nitro- 
gen intake is duly accounted for. 

The quantity of ur e a changes not onlv with the amoiint 
md composition oj the food but also with the rapidity of 

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tiss ue- waste in health and in disea se. The amount of urea 
excreted fluctuates at times from day to day, even in health. 
It is c onsiderably increased in feve r, on account of the in- 
creased breaking down of the proteids of the body, and also 
in diabetes. Urea is diminished in diseases of the live r, 
such as acute yellow atrophy, its place being taken by leucin 
and tyrosin (see p. 201), and also in cirrhosis of the liver. 
It is also diminished in chronic diseases accompanied by 
wasting and in renal diseases characterized by interstitial 
changes. The use of thyroid extract is often followed by an 
increase, the use of alcohol in children by a decrease, of 
urea, and a diminution has been observed in chronic al- 
coholism in adults (see table on p. 135). 

The amount of urea normally excreted with an averag e 
diet is^from 20 t o 40 gm. (308.6 to 617.2 grains) in twen ty- 
iour hours in adult s, or from i.< to 2.< per cent. With a 
milk diet or with a diet containing little nitrogen, 15 gm . 
a day may be excreted, while in fever 50 gm ^xf nftpn fminH 

The usual standard amount of urea in the urine of a 
healthy adult on a mixed diet is taken as 2 per cent., or 
20 gm. per liter, or 10 grains to the ounce. 

Tests for Urea.— Urea (CH4N2O) is an isomere of 
ammonium cyanate, and may be prepared artificially by 
the action of ammonia on carbonyl chlorid, by the hydra- 
tion of cyanamid, and from ammonium carbonate. 

It is soluble in alcohol and water; insoluble in ether; 
odorless, with a salty taste and a neutral reaction in solution. 
It crystallizes in colorless four- or six-sided prisms with 
oblique angles, or in delicate, white, silky needles. On the 
addition of nitric acid it forms urea nitrate, which crystal- 
lizes in plates of an octahedral, hexagonal, or lozenge shape 
(Fig. 16). With oxalic acid it forms urea oxalate, in the 

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form of flat or prismatic crystals. If a drop of fluid is 
suspected to be urine, it is placed on a glass slide, and the 
latter is carefully warmed over the flame and set aside to 
crystallize after a drop of nitric acid has been added. 
Crystals of nitrate of urea will form and will be recog- 
nized under the microscope. This test is facilitated by the 
evaporation of the urine to a more concentrated form, 

EXCRETED. (After Ogden.) 

I. The Amount of Urea is Increased: 

1. A plentiful diet of mixed character. 

2. Increased exercise. 

3. During the day as compared to the night, 
(a) Normally: 4. After the administration of ammonium compounds. 

5. After hot baths. 

6. When metabolism is temporarily increased by drinking large 
amounts of water or by any other means. 

1. In acute fevers, owing to increased metabolism, especially in 
the early stages. Exceptions: Cholera and acute inte&tinal 
diseases, acute nephritis, etc., with dropsy. 

2. In dropsies when the fluid is becoming reabsorbed (tempora- 
(6) Abnormally: \ rily). 

3. Before a chill in malaria (diminished afterward). 

4. In diabetes in^pidus, urea high, but specific gravity low. 

5. In diabetes mellitus, owing to increased metabolism. 

6. In chronic gout. 

II. The Amount of Urea is Diminished: 

1. With a diet poor in nitrogen (vegetarians) and in starvation. 

2. After very profuse perspiration. 

3. In normal pregnancy (often), the average being ao gm. per 
(a) Normally: •{ twenty-four hours. 

4. After taking small doses of quinin (slightly). 

5. Prolonged drinking of large amounts of water (for a short 
time, urea increased). 

In most diseases, especially in diminished metabolism and lowered nutrition, princi- 

1. In most renal diseases, especially in the chronic forms, inter- 
stitial and parenchymatous. Not so markedly in amyloid 
kidney. In acute nephritis, especially when dropsy is in- 

2. In functional disturbances of the kidneys; congestion. 

3. In acute fevers, after the acme and during convalescence, when 
(6) Abnormally: -j metabolism is low. 

4. In all dropsies while the fluid is increasing. 

5. Shortly before death; usually a marked diminution. 

6. After prolonged vomiting. 

7. With marked diarrhea, urea being partly eliminated in the 

8. In all degenerative changes of the liver. 

Quantitative Estimation of Urea.— Approximate 

Estimation. — As urea is the most important solid con- 


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stituent of the urine and is present in the largest amount, 
the specific gravity runs closely parallel to the amount 
of the urea, and this fact has been utilized for an approxi- 
mate estimation of the amount of urea present by means of 
the specific gravity. This can be done only when there is 
no sugar present, when the albumin is less than 0.2 per 
cent., and when the chlorids are normal. Such a urine 
with a specific gravity of 1020 to 1024 and a daily quantity 
of 1500 cc. (50 ounces) will contain from 2 to 2.5 per cent. 

Fig. 16. — Crystals of nitrate of urea (upper half) and oxalate of urea 
(lower half) (after Funke). 

of urea. A specific gravity of .1014 would indicate i per 
cent, of urea, and of 1028 to 1030, about 3 per cent. 

This method, however, is very inaccurate, inasmuch 
as the chlorids fluctuate markedly and materially influence 
the specific gravity. 

Hypobromite Method. — Clinically, this method, intro- 
duced by Knop, is the most readily available. It depends 
upon the principle that urea, when brought into contact with 

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sodium hypobromite, is decomposed into nitrogen, carbon 
dioxid, and water, according to the following formula: 

CH.NaO + 3NaOBr = 3NaBr + CO, + N, + 2H3O. 

The amount of nitrogen disengaged is the measure of 
the urea. The carbon dioxid set free at once combines 
with the excess of sodium hydrate in the hypobromite 
solution used, forming sodium carbonate, which re- 
mains in solution. All methods 
of quantitative analysis of urea 
which involve . the use of hypo- 
bromite solution depend upon the 
fact that I cc. of nitrogen at 
standard temperature and pressure 
equals 0.0027 g"^- of urea; or, 
conversely, that i gm. of urea at 
0° C. furnishes 370 cc. of nitrogen. 

Doremus^ Method. — ^Various ap- 
paratus have been devised for the 
application of these methods of 
urea estimation, but Doremus' 
(Fig. 17) is most frequently used in 
this country. It is, unfortunately, 
exceedingly inaccurate, and its re- 
sults should not be relied upon in Fig. ly.—Doremus' ure- 
cases in which the determination ometer. 

of urea is of vital importance. 

The apparatus consists of a bulb with an upright 
graduated tube, and a small nipple pipet holding i cc. 
of urine. Each of the small divisions on the tube repre- 
sents o.ooi gm. of urea in i gm. of urine, or -pQ of i per 
cent. Each of the large divisions represents o.oi gm. ^f 

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urea in i gm. of urine, or i per cent, of urea. The appa- 
ratus is supposed to read correctly at average room-tem- 
perature and average pressure. 

The bulb is filled with the hypobromite solution, the 
apparatus being inclined so as to remove the last air- 
bubble from the closed part of the tube. The pipet is then 
filled with urine accurately up to the i cc. mark. Care 
should be taken after filling the pipet with urine to wipe 
it dry, so as to remove all the adhering urine, and also to 
see that no drop escapes from the point before it is intro- 
duced into the bend of the tube. The point of the 
pipet is introduced into the bend of the tube just as 
far as it will go, and the nipple is slowly and gently com- 
pressed, so as to expel all the urine, but not to expel any air 
out of the nipple into the gas tube. The evolution of the 
nitrogen is allowed to proceed at the upper closed end of the 
tube, the apparatus being set aside until no more froth or 
bubbles are observed. The level of the fluid is then read 
upon the tube. Two forms of this apparatus are made — 
one graduated to read fractions of a gram per cubic 
centimeter of urine, the other to read the number of 
grains of urea per fluidounce of urine. In using the 
former, each of the large divisions corresponds to i per 
cent., each of the small divisions to -^-^ per cent, of urea. 

In using the Doremus apparatus the urine must be free 
from sugar and albumin, and the instrument should be 
allowed to stand a sufficient length of time after if has been 
filled until the level of gas remains stationary. The ap- 
paratus made with a base for support is the best. 

Knopfs solution of hypobromite is prepared by taking 70 cc. of a 30 per 
cent, solution of sodium hydrate, diluting it with 180 cc. of water, and 
then adding 5 cc. of bromin and stirring until all the bromin has been 

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dissolved. This solution keeps for about ten days if kept in a cool, dark 
place. The alkaline solution must be cold, and the bromin should be 
added out-of-doors or under a laboratory hood. Ammonia may be in- 
haled if necessary to neutralize the irritating fumes of bromin. Another 
way of preparing the hypobromite solution is by dissolving 100 gm. of 
caustic soda in 250 cc. of water and adding 25 cc. of bromin. 

Rice's solutions for the hypobromite method offer a convenient means 
of obtaining the same result without the disagreeable necessity of handling 
pure bromin. These solutions are put up in separate bottles, one con- 
taining the alkali, the other, the bromin. Five cc. of each of these solu- 
tions and 20 cc. of water make up the fluid to be poured into the Doremus 
apparatus. These solutions keep well and are very useful for clinical 

The formulas for Rice's solutions are: 

(i) Caustic soda 100 gm. 

Distilled water 250 " 

(2) Bromin 30 " 

Potassium bromid 30 " 

Water 240 " 

Hinds^ modification of Doremus^ 
apparatus (Fig. 18) is more accu- 
rate and convenient than the orig- 
inal form, as the urine is measured 
more exactly and no nitrogen is lost 
by escape from the bulb. 

A number of other methods have 
been devised for the determination 
of urea. Most of these methods 
are too elaborate for clinical work. 
Hufner's method, however, is com- 
paratively simple and far superior 
in accuracy to Doremus'. 

Hiifner's Method. — ^The prin- 
ciple of this method is similar to 
that of the Doremus — i. e., the decomposition of urea 
into nitrogen, carbon dioxid, and water by sodium hy- 

Fig. 18. — Hinds' modi- 
fication of the Doremus 

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Fig. 19. — Hufner's apparatus for esti- 
mation of urea. 

pobromite. This is much 
more accurate than the 
Doremus method and is 
practically sufficiently ex- 
act for all clinical pur- 
poses, provided it be per- 
formed correctly and due 
allowances be made for 
barometric pressure, etc. 
Hufner's apparatus 
(Fig. 19) consists of a cyl- 
indric vessel (C), sepa- 
rated from a smaller 
receptacle below {D) by 
a glass stop-cock. An 
open dish {B) fits upon 
the upper end of C in 
such a way that the upper 
end of C protrudes into 
By a rubber stopper mak- 
ing the joint water-tight. 
The eudiometer tube (^4), 
which is about 40 cm. long 
and 2 cm. in diameter, is 
graduated in tenths of a 
cubic centimeter. This 
tube is held in position 
bottom up over the pro- 
truding upper end of C 
by a clamp, the whole 
apparatus being attached 
to a stand. 

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UREA 141 

The solution required is the same as that used in the 
Doremus method (the first formula given on p. 139 should 
be used), or if desired, Rice's solutions may be employed 
with Hufner's method. 

Method of Estimation with Hilfner's Apparatus. — The urine is first 
diluted so that it roughly contains not more than i per cent, of urea. The 
dilution is carried out by estimating the urea probably present from the 
specific gravity (see p. 135). By means of a long pipet exactly 5 cc. of 
diluted urine are filled into the lower receptacle, carefully avoiding the 
entrance of any urine into the upper chamber. The pipet is carefully 
washed with distilled water and the washings are also allowed to flow 
into D until that receptacle is filled up to the stop-cock. The latter is 
now closed, and hypobromite solution is poured into the upper chamber 
C. The dish above it and the gas tube A are filled with saturated sodium 
chlorid solution and the tube inverted into the dish is placed in posi- 
tion exactly over the upper end of the hypobromite chamber with the aid 
of the clamp. The stop-cock is now opened, and as the hypobromite 
solution is heavier than the diluted urine, it flows into the lower receptacle, 
mixes with the urine, and develops COa and N. The carbon dioxid is 
absorbed by the sodium hydrate and the nitrogen rises into the gas tube 
A. The apparatus is allowed to stand for about twenty minutes. The 
eudiometer tube is tightly shut with the thumb immersed into the dish, 
and is removed from the apparatus and placed in a deep receptacle with 
distilled water at room temperature, in which it is allowed to remain for 
fifteen minutes. The level of the gas is then read by holding the tube in 
the distilled water so that the level of the contents of the tube and that of 
the water are equal. The temperature of the water and the barometric 
pressure are noted. The volume of gas thus read must be reduced to 
standard temperature (0° C), standard barometric pressure (760 mm.), 
and absolute dryness for exact determinations. For this purpose the 
tables on pages 142 and 143 (JoUes, quoted by Klopstock and Kow- 
arsky) may be used. 

While these tables were intended originally for use with Jolles' ap- 
paratus, they are equally useful with Hiifner's. They are the means 
of saving tedious and elaborate calculations, and render the readings 
of the apparatus more accurate than when corrections for temperature 
and pressure are neglected. The tables assume that 2.5 cc. of urine 
have been used in the test, and the volume N. read must be reduced 
first to correspond with this, as is shown on page 143. 

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Showing the grains of urea per liter represented by i cc. of nitrogen at 

Height of 







1. 000 
I. on 













1. 00 1 


. IS' 












1. 000 

To use the table, determine the temperature of the water in Centigrade 
and the barometric pressure at the time of observation. Find the figure 
in the proper column, giving the correction coefficient, and multiply this 
coefficient by number of cubic centimeters of nitrogen read upon the 
tube of the apparatus. If more or less than 2.5 cc. of urine has been 
used, make proper allowances. The result is the corrected amount of 
urea in grams per liter. 

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various temperatures (Centigrade) and at different barometric pressures. 
















0.9 1 1 






































0.9 1 1 






















♦ 0.910 















































0.942 . 










































































































































Volume, of N. = 9.3 cc. 

Dilution was i : 4 (1.25 cc. urine and 3.75 cc. water). 

Hence 9.3X2 = 18.6 cc. N. in 2.5 cc. urine. 

0.998 X 18.6 = 18.56 grains urea per liter. 

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Absolute Analytic Methods. — For physiologic studies 
and for accurate scientific work urea is determined by 
more elaborate methods, which will be found described in 
the larger works. Of these, the Moerner-Sjoqvist method 
is probably the best. By the use of this method all the 
nitrogenous constituents of the urine except the urea and 
ammonia are precipitated by means of alcohol and ether 
after the addition of a solution of barium chlorid and 
barium hydrate, and finally the urea is determined in 
the concentrated filtrate by Kjeldahl's nitrogen method 
after driving off the ammonia. KjeldahPs method consists 
in converting all the nitrogen of organic compounds into 
ammonia by the use of sulphuric acid and heat. The 
ammonia is distilled over and collected in standard sul- 
phuric acid. These methods are not employed in ordi- 
nary clinical work. 


Nitrogen. — ^What does the total nitrogen output indicate? What do 
we mean by the " nitrogen balance " ? What factors influence the nitrogen 
output ? 

Urea. — ^What is urea chemically ? What is its physiologic significance ? 
How does the amount of urea vary in health ? In disease ? What is the 
normal amount excreted in twenty-four hours in grains? In grams? 
What is the normal percentage of urea in urine ? Describe a test for the 
presence of urea in a liquid. How can the amount of urea be approxi- 
mately deduced from the specific gravity, and under what conditions ? 

What is the principle of the hypobromite method? 

Describe Doremus' apparatus. How is it used? What solution is 
employed? What precautions are observed in using it? What is 
Hinds' modification ? Describe the method of Huf ner. 

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Next to urea, the urine contains a group of nitrogenous 
compounds much more complex in structure, which are 
regarded as derived from a chemical group to which E. 
Fischer gave the name of "purin.*\ According to this 
author the purin bodies (also known as the xanthin or 
alloxur bodies) are derived from a hypothetic, chemical 
molecule, "purin," C5H4N4, containing carbon and 
hydrogen atoms arranged in a ring. The ring, which is 
called '' the purin ring,'' is the same for uric acid and the 
other members of this group, the differences being merely 
the substitution of one or more of the hydrogen atoms 
of the ring by different radicals. The purin ring has the 

N = CH 

I / 

HC C— NHv 

N - C N^ 

The purin bodies (including uric acid) are derived from 
this by the substitution of hydroxyl, amid, or alkyl groups 
for the various hydrogen atoms — e. g., uric acid is — 

HN — CO 

I I 

CO C— NHv 

I II >co. 

HN — C— NH^ 
10 145 

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Uric acid is the only constituent of this group that has 
sh'ght acid properties. All the other compounds are bases 
known, therefore, as purin bases (also xanthin bases or 
alloxuric bases). 


XJric acid (C5H4N^O^) is a nitrogenous compound form ed 
i p the body by the decomposition of nucleins of the nuc lei 
of both tissue cells and food-stuflf s! Normally, small 
amounts of uric acid ( 0.7 to 0.75 gm. in twenty-four hours) 
are excreted in the urine. The substance crystallizes in 
the shape ot rhombic, rectangular prisms, wedge or whet- 
stone shape, of a color varying from the palest yellow to a 
deep yellowish red (Plate 4). 

Pure uric acid is soluble in 16,000 parts of cold water 
and in 1600 parts of boiling water. Impure uric acid is 
more readily soluble in water. It is not acid in reaction in 
cold solutions when tested with litmus-paper. It is in- 
soluble in alcohol and ether, but soluble in warm glycerin, 
insoluble in strong mineral acids, but soluble in alkalis. 
It is more soluble in solutions of urea than in water. 
On boiling it reduces alkaline solutions of copper, first 
giving a white precipitate of cuprous urate. 

The Origin of Uric Acid. — As has already been s aid 
in the defi nition of uric acid ^ t^i<^ bndy w a pr oduct of ox i- 
dation of the nuclein bas es. Horbaczewski regarded it 
especially as derived from the nuclei of the leukocytes. 
It has been shown, however, that the other cells of the or- 
ganism containing nuclei and, therefore, nucleins, may also 
be the source of uric acid, and that, in fact, the leukocytes 
give origin to a very small fraction of the uric acid output. 
The greatest source of uric acid are the nuclein or the purin 

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Uric-acid Crystals; Normal Color [after Peyer), 

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compounds contained in the fo od. The amount of uric 
acid excreted is, indeed, to be measured only in the light of 
our knowledge of the amount of nuclein-containing food 
that is eaten. 

The old idea that uric acid is derived from all proteids 
of the food is wrong, for when very large amounts of proteid 
food containing no nuclein are given, there is no increase 
of uric acid. On the other hand, when large amounts of 
nuclein are given in the food (organs containing many 
nucleated cells, like the pancreas, brain, etc.) there is 
always an increase in the excretion of uric acid. 

T he term endof^enous uric acid is applied to the uric 
acid derived from the nucleins of body cells, while the term 
exogenous uric acid is used to designate that derived from 
~the nucleins of the food. There is also a very small amount 
of uric acid formed synthetically in the body, as is the case 
in birds and in certain reptiles. In these animals uric 
acid is the chief nitrogen compound excreted in the urine, 
and is probably derived from urea by synthesis. 

Two theories are held as regards the place where uric 
acid is formed: Garrod claims that uric acid is not only 
excreted, but formed in the kidneys, b ut the view generally 
held to-day is that it is formed in the tiss ues, especially 
in th e liver and spleen^ and merely excreted by the kid neysT 
T he latter view is supported by the following, facts : 
Uric acid is foimd in the blood normally and contin ues to 
be formed there after extirpation of the kidneys. It is 
greatest in amount dur ing digestion, when the liver and 

o p lPP fl pr^mr^cf ar-fi'irA^ nnH I'f n >.nni%<iilnf nn I'n fVin KlnnH 

apd tissues in goiit and anemia^ when the excretion is 
Pathologic Significance, — A great deal of nonsense 

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has been written about uric acid and its pathologic sig- 
nificance. The cause for the widespread misapprehension 
of the real significance of uric acid lay in the misunder- 
standing of its formation, and in confusing really normal 
conditions with pathologic states, or in attributing to uric 
acid symptoms which had quite a different origin. In the 
light of modern knowledge, an increased elimination of 
uric acid has a f ar less serious sigmticance than it had before 
moaern research had demonstrated the mechanism of uri c 
acid forma tion. No conclusion should be drawn from an 
increased excretion of uric acid without a previous knowl- 
edge of the patient's diet with reference to the presence of 
nucleins therein. Moreover, it has been shown (Croftan) 
that the kidneys can destroy uric acid and the urinary uric 
acid cannot always be considered as an index to the amount 
of uric acid in the circulation. The urinary uric acid 
merely represents the algebraic sum of the uric acid circu- 
lating in the blood and that destroyed by the kidneys. 

Uric acid is increased in the following^ conditions (Ser- 
kowski) : 

(i) After a proteid diet rich in nucleins. 

(2) After drinking coffee or caflein-containing beverages. 

(3) After the use of salicylic acid or sodium salicylate. 
Uric acid is diminished: 

(i) After a vegetable diet. 

(2) After eating yolks of eggs, milk, and dairy products. 

(3) After the ingestion of cherries and fruit containing 
quinic acid. 

(4) After the use of artificial proteid foods containing 
no nuclein. 

(5) After drinking saline and alkaline mineral waters 
(increase of alkalinity of blood and of oxidation). 

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(6) After the administration of a number of drugs, 
among which are colchicum, citric acid, potassium iodid, 
urotropin, etc. 

(7) In lead-poisoning. 

Uric acid is increased in fevers and in all conditio ns 
i n which there is rapid wasting of tissues. This incre ase 
is at the expense of the endogenous uric acid. Afte r 
severe muscular exercise, g rea t fatigue, and during the 
attacks i n gout there ma y be als o an increase of uric a cid. 
Whenever ther e is a leukocytos is (as after a full meal or 
in septic infection), the destruction of leukocytes leads to 
an increase of uric acid. In leukemia there is a mar ked 
incre ase of uric acid (4.2 gm. in twenty-four hours, Bar- 
tels), and the sa me is true of cirrhosis of the l iver (8 gm. 
in twenty-four hours, Bouchard). The cause of this 
increase may lie in the interference with the uric-acid- 
forming function of the liver. In pseudoleukemia there 
is no increase in uric acid. 

An increase of uric acid may occur in neurasthenia, 
together with a phosphaturia. In pernicious anemia the 
uric acid is increased (due to diminished metabolism and 
to leukocytosis), while in mild forms of anemia, chlorosis, 
etc., there is a diminution of uric acid. 

A decrease in the elimination of uric acid may be due to 
a retention of this product, owing to an insuflScient excre- 
tion or to an imperfect oxidation. In chronic kidney dis- 
eases and other conditions diminishing the amount of solids 
eliminated, after prolonged drinking of large amounts of 
water, after chronic wasting diseases in which metabolism- 
is lowered, the uric acid may also be diminished. 

The relation of uric acid to gout has been placed in 
a doubtful position by recent investigations. Gout has 

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been considered for a long time to be due to the increase of 
uric acid in the blood, but it has been found recently that 
such an increase does not always take place. The amount 
of uric acid in acute gout may be high, but is more often 
low, and never so high as in leukemia. The amount of 
u ric acid excreted in the urine is so variable that It js of 
practically little clini cal importance, especially with a 
mixed diet. A meal composed of food rich in nuclein 
will increase the uric acid in the urine more than an attack 
of gout. 

Apparent Increase. — It is important to apprehend 
properly what actually constitutes an increase of uric acid 
in the urine. A common error is to consider urine of high 
specific gravity, acid in reaction, which deposits uric-acid 
crystals and urates, as a specimen of increased elimination 
of uric acid. The presence of uric-acid crystals or of a 
deposit of urates does not by any means indicate necessarily 
an excess of uric acid; in fact, such deposits may occur 
when a urine is cooled and undergoes "acid fermentation." 
TTrineR of hi^h rnnrpntratinn (in persons who drink little 
water, etc.) an d of hi^h acidity are very apt to d eposit 
uric aci d. 

A true increase of the uric acid in the urine can be de- 
tected only by quantitative methods. While such an in- 
crease may be accompanied by a deposit of uric-acid 
crystals, this deposit alone is no evidence of an increased 
elimination of this substance. 

The cause of this seemingly paradoxic fact is that under 
ordinary conditions nearly all the uric acid exists in the 
urine in combination with sodium and other bases (see 
Urates, p. 154) as urates. Of these urates, those known as 
the neutral salts are readily soluble in the urine, while 

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Others, known as the acid urates, are much less soluble.' 
Uric acid itself is almost insoluble in urine. As a com- 
paratively slight influence — an increase in acidity — will 
convert the neutral urates into the acid, or even into uric 
acid, it will be seen that a deposit of urates or of uric acid 
depends not so much upon the amoimt of these substances 
as upon the solubility of the particular types found in a 
urine, a solubility affected by cold and the presence of 
high acidity. 

Normal urine contain s about 0.2 to 1.25 gm. of uric 
acid in twenty-four hours, the averag e being 0. 7 gm. 
The proportion of uric aid to urea is about i : 45. 

Detection. — (a) A few crystals of the material 
are placed on a slide and dissolved in dilute sodium hy- 
drate. A drop of dilute hydrochloric acid is added under 
the cover-glass, and typical crystals of uric acid will form. 

(6) Murexid Test. — A small quantity of the specimen is 
treated with nitric acid in a small porcelain dish, and gently 
warmed until a yellowish-red residue is left. A very small 
quantity of ammonia is added, when the color will change 
to a beautiful purple, changing to a deep blue on the addi- 
tion of a little sodium hydrate. The color disappears on 
warming and does not reappear on evaporating. In the 
case of xanthin and guanin, the color returns on evapora- 

(c) Silver Test. — ^Uric acid is dissolved in dilute sodium 
carbonate and dropped upon a paper moistened with silver 
nitrate. A dark spot of reduced silver is produced. 

(d) Copper Test. — ^Uric acid dissolved in dilute sodium 
hydrate and treated with Fehling's solution gives a precipi- 
tate of white cuprous oxid and, finally, of red cuprous 

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Quantitative Estimation of Uric 
Acid. — There is no convenient clinical 
method for the estimation of uric acid 
which is at the same time accurate. 
The following methods are described 
because they are less troublesome than 
any others devised: 

Heintz's Method. — To 200 cc. of 
filtered urine free from albumin add 10 
cc. of hydrochloric acid. Allow this 
to stand for twenty-four hours in a 
cold place; collect the uric-acid crys- 
tals on previously dried and weighed 
filter-paper; wash once or twice in 
cold distilled water; dry the whole 
at about 100° C, cool, and weigh. 
By subtracting the weight of the 
filter-paper the weight of the uric 
acid in 200 cc. of urine is obtained. 
This method is only approximate. 

Ruhemann's Method. — In 1902 
Ruhemann suggested a colorimetric 
method of estimating the amoimt 
of uric acid in urine based on the 
titration of uric acid with iodin 
with the aid of carbon disulphid. 
A graduated tube with a glass stopper, 
called the uricometer, is used for 
this test. One cm. above the bot- 
tom of this tube is a line marked S, 
and 2.7 cm. over this is another line 

Fig. 20. — ^Ruhemann's uricometer. 

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marked J, the distance between them being divided into 
two by another line. Above the line J is a scale indicating 
parts of uric acid per 1000, beginning below at 2.45 and 
ending above at 0.175 (^^g- 20). 

The tube is filled to S with pure carbon disulphid, the 
lower meniscus touching the line. The iodin solution 
(iodin, 1.5; potassium iodid, 1.5; absolute alcohol, 15; 
distilled water, 185) is poured over this up to the 
mark J, and enough urine is added to reach the mark 
2.45, and then, drop by drop, closing the tube and 
shaking it after each addition. The carbon disul- 
phid, absorbing the free iodin, becomes coppery-brown; 
the rest of the fluid assumes the color of urine. On 
the addition of further amounts of urine, drop by drop, 
the carbon disulphid becomes violet, pinkish violet, pink, 
pale pink, and finally milky white, the foam taking 
part in the color changes. The end-reaction is shown 
by a pale-pink color in the carbon disulphid. The 
stopper should be removed cautiously, and the foam got 
rid of by gently shaking the tube from side to side. The 
scale is read directly, showing the number of parts of uric 
acid per 1000 of urine, or grams per liter. If the urine has 
very little uric acid, then only half the amount of iodin 
solution should be used, the rest of the space up to J being 
filled with distilled water and the figures divided by two. 
If an excess of uric acid is present, twice the amount of 
iodin is used and the result multiplied by two. The 
urine must be acid and free from albumin. This method 
has been found in the author's hands to give a considerable 
percentage of error, but it is recommended by some clin- 
icians. There are a number of substances in the urine 
capable of forming compounds with iodin and interfering 

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with this test, especially bile, albumin, blood, antip3n:in, 
aspirin, and diacetic acid. Their presence should be ex- 
cluded by appropriate tests. 

Folin-Hopkin's Method. — To loo cc. of urine are added lo gm. of 
ammonium acetate, and ammonia is added, drop by drop, until a slight 
ammoniacal odor is perceived. The mixture is set aside for three hours 
and then filtered. The sediment is washed six to eight times with a satu- 
rated solution of ammonium carbonate and then transferred by means 
of hot distilled water to a beaker by means of a wash bottle. Then 15 cc. 
of concentrated HaSO^ are added (specific gravity 1,845) ^^^ the whole is 
titrated with ^^ potassium permanganate standard solution until the first 
appearance of pink, which diffuses throughout the liquid and persists for 
a few seconds. Each cubic centimeter of KMnO^ used equals 3.648 mg. 
of uric acid, the total product representing the amount of uric acid in 
100 cc. of urine. This is the most satisfactory method among the sim- 
pler ones thus far devised. 


As has already been mentioned, nearly all the uric acid 
of the urine is in combination with sodium, potassium, 
ammonium, calcium, and magnesium, in the form of urates. 
These are very soluble at body-temperature, but are pre- 
cipitated, on cooling the urine, in the form of amorphous 

Uric acid is dibasic, forming neutral and acid salts, 
and the acid salts are much less soluble than the neutral. 
They therefore form the bulk of the precipitate, while 
the neutral or less acid salts remain in solution. Urine 
which remains clear for some time on standing at room- 
temperature often contains a large proportion of the neutral 

When an acid is added to such urine, the urates become 
acid, consequently insoluble, and precipitate in a finely 
granular form, with the result that the urine becomes 
decidedly opaque. This is the cause of the opacity ob- 

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served with the nitric acid test for albumin and of the 
opaque zone occurring in Heller's test. Heat dispels this 
precipitate. If the urine mixed with acid be allowed to 
stand, the sediment falls to the bottom in the form of crys- 
tals of acid urates, and if the acid be allowed to act long 
enough, crystals of uric acid are deposited. 


We have already referred to the general chemical char- 
acters of these bases on p. 145. They are derivatives of the 
nucleins, form with uric acid a part of the purin bodies 
of E. Fischer, are present in very small quantities in normal 
urine, and have the tollowing composition (^Hammarsten) : 

Xanthin CgH^N^Oj 

Heteroxanthin and i-methylxanthin C^H^Nfi^ 

Paraxanthin C^HgN^Og 

Guanin C5H5N5O 

Hypoxanthin CgH^N^O 

Adenin CgHgNg 

Episarkin C^H^NgO (?) 

Camin C^HgN^Og 

Epiguanin CgH^NjO 

Origin of the Purin Bases.— Of these, xanthin, guanin, 
h)rpoxanthin, and adenin ^are the most important and are 
known as "the real nuclein bases." These have been 
shown by Kossel to be cleavage products of the nucleins. 
, They are, therefore, decomposition products of the nuclei 
of the body cells. 

The other purin bodies mentioned in the above list have 
not been so thoroughly studied, but three of them (hetero- 
xanthin, paraxanthin, and i-methylxanthin: Albanese, 
Bondzynski, etc.) which form the bulk of the purin bases 

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in the urine are derived from the theobromin, caflfein, and 
theophyllin, and their compounds occurring in food (tea, 
coffee, cocoa, etc.). 

The term endogenous purin bodies is used to designate 
those derived from tissue metabolism, while exogenous 
purins are derived from the food. 

Clinical Significance. — Inasmuch as the purin bases 
are closely related to the nucleins , they are increased in th e 
urine in all conditions in which there is either a greater 

Fig. 21. — Xanthin crystals (after the drawings of Horbaczewski, as repre- 
sented in Neubauer and Vogel). 

ingestion of nucleated tissue (certain foods containing 
many nuclei, see Uric Acid, p. 147) or a breakdown^ of 
nuclei in the bo dv. 

Normally, the purin bases _occur in the urine in very 
gmall q]]pptii^g (Flatow and Reitzenstein, quoted by 
Hammarsten), 15.6 to 45.1 mg. in twenty-four hours. 

They are increased in healthy persons by feeding upon 
food rich in nuclei and food containing derivatives of 
caffein, thepbromin, etc. 

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In diseases the purin bases are especially increased in 
leukemia (destruction of nuclei of leukocytes). 


The methods of quantitatively measuring the amount of 
uric acid and of purin bases are far too complex for routine 
clinical work, and, therefore, we shall content ourselves 
in describing an approximate clinical 
method which has become popular 
during the past few years. The method 
cannot replace the more accurate proc- 
esses of estimating uric acid and other 
purin bodies as such, but may be used 
for comparison. The method is chiefly 
of value in regulating the patient's diet, 
diminishing his purin intake (exogenous 
purin), and then watching the diminu- 
tion of the purin output. If this does 
not diminish in proportion within a 
reasonable time, we must conclude that 
there is an increase of endogenous purins 

Camerer*s Method. — An apparatus 
is made under the name of purinom- 
eter (Fig. 22), in which the amount of 
purin bodies as a whole may be approximately estimated 
as follows (the apparatus consists of a graduated cylinder 
divided into two parts by a glass cock) : 

The total quantity of the urine must be known and 
well mixed. It is, if necessary, freed from albumin by 
boiling in slightly acid solution. With the tap at right 

Fig. 22. — Purinom-' 

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angles to the tube, 20 cc. of No. i solution are added 
to 90 cc. of urine. The phosphates are at once precipi- 
tated and the tap is turned parallel to the tube. In ten 
minutes the phosphates will have passed into the lower 
portion of the tube, and the tap is again turned at right 
angles and No. 2 solution added up to 100 cc. The 
resultant precipitate of silver-purin should be pale yel- 
low. Incline the purinometer backward and forward 
until all the white silver chlorid is dissolved. If this 
does not occur, add a few drops of strong ammonia or 
use diluted urine. Place the apparatus in a cupboard 
away from the light, and read off the number of cubic 
centimeters occupied by the precipitate an hour later, 
although it is better to wait for twenty-four hours. 

Solution No, i consists of: 

Ludwig's magnesia mixture* loo cc. 

Ammonia (20 per cent.) 100 cc. 

Talcum 10 gm. 

Solution No, 2 consists of: 

Silver nitrate i gm. 

Ammonia (strong) 100 cc. 

Talcum 5 gm. 

Distilled water 100 cc. 

A table is given with the apparatus for converti^j^Nlfc 
reading in cubic centimeters to the amount of purin- 
nitrogen in twenty-four hours. 

* Magnesium chlorid crystals 100 gm. 

Water 1000 cc. 

Ammonia, enough to give strong odor. 

Ammonium chlorid, enough to dissolve the precipitate which forms. 

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This table shows the nitrogen percentage yielded by each 
cubic centimeter of the precipitate. Multiply this factor 
by the number of cubic centimeters contained in the 
twenty-four-hour urine divided by 100. 

Cubic Percentage 

centimeters. Purin-nitrogen. 

4 0.0078 

5 0.0097 

6 0.01 17 

7 0.0136 

8 0.01 56 

9 0.0175 

10 0.0185 

II 0.0195 

12 0.0205 

13 0.0218 

14 0.0225 

15 0.0234 

16 0.0249 

17 0.0260 

18 0.0265 

19 0.0270 

20 0.0275 

21 0.0283 

22 0.0286 

23 0.0299 

24 0.0312 

25 0.0325 

Example. — The precipitate yielded lo cc. This contains 0.0185 
nitrogen. The total daily urine was 1120 cc. 10.0185 X 11. 2 = 0.2072 
pffifflfiTrogeri.*--''*- *'--«fK--- m*.*^ 


T he normal urine invariably contains small quantit ies 
of ammonia (NH,) , the amount averaging 0.7 gm. in twen ty- 
four hours on a mixed diet, an d r epresen ting from 3.5 to 
5 per cent, of the total nitrogen (see p. 1377; 

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Ammonia is normally present not only in the blood but 
also in the tissues, and is changed to urea in the liver and 
other organs. Xli£J^l^^^ ^^ a mmonia to the total n i- 
trogen is a fairly constant one in health. In disease iF is 

increased when the WlUlULiuu Of uiea is interfered with, as 

^^ __^ 

in cirrhosis ot the liver. It furthermore seems to serve as 
the neutralizer of excessive acidity with w hichTthe bo dy 
defends itseij a^ai nt;f the o verproduction of aci ds (acid- 
emia and acid intoxication), t hus maintaining the alka- 
linity needed to sustain life. 

I'he organic acids against which ammonia rises in this 
way are increased in persons living on a very abundant 
proteid diet (diabetics), in diseases accompanied with fever, 
in certain types of insanity, in diabetes (oxybutyric acid, 
diacetic acid), and in the toxemias of pregnancy (probably), 
especially the cases accompanied by persistent vomiting 
and those of "the pre-eclamptic state" and eclampsias. 
In all these conditions, therefore, there may be a more or 
less marked increase of ammonia, usually at the expense 
of the urea — i. e.y with a comparatively diminished urea 



Creatin and creatinin (C^H^NgOg and C4H7N3O) are 
found in normal urine, creatinin containing one molecule 
less of water than creatin. They are both derived from 
muscle-tissue of the body^^HflWBBaHHMfliHHMBi^. 
The amount varies according to the waste of muscle and 
the meat ingested. 

Normally, 0.6 to 1.5 gm. of creatinin are excreted daij; 

JNormaiiy, 0.0 to 1.5 gm. ot creatinin are excretea aaiyt^ ^ t 
^ ^ h^ this amount being probably formed in the kidne^ y^Ser- / 
^^y^ kowski). To excrete i.o gm. of creatinin one must eat / 
about 330 gm. of meat. , ^ 




The amount of creatinin is increased in fever, 


iHMittBMIiHBI- It 

Fig. 23. — Crystals of creatinin-zinc chlorid (Salkowski). 

diminished in cachexias, starvation, muscle-atrophy, and 
in chronic nephritis (Serkowski). 


Allantoin (C4H6N4O3) is found in the urine of new- 
bom infants and also in adults, but in the latter in mere 
traces. It is increased by meat diet, by taking tannic acid, 
and in cases of diabetes insipidus and hysteria. 

Allantoin is obtained from uric acid by oxidation — e, g,j 
with potassium permanganate — and is decomposed by 
heat and hydrochloric acid into allanturic acid and urea: 

Allantoin. Allanturic acid. Urea. 

Moemer found nucleic acid in very small quantities in 
the urine. Larger amounts appear in combination with 

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albumin as nucleo-albumin. These acids are interesting 

physiologfcally, as iiygy* ai gj ' c^M ' pcm Bds^af plaospboric acid, 

xanthin bases, and non-nitrogenous substances. They 

may contain as much as 9 or 10 per cent, of phosphorus. 

They do not give the reactions of proteids, but when some 

of them are boiled with dilute mineral acid, a carbohydrate 

substance is produced which gives the reduction test with 



Hippuric acid (C^H^NOg) occurs in normal urine of man 
in quantities of from o.i to i gm. in twenty-four hours, 
varying largely according to the amount of vegetable food. 

Fig. 24. — Hippuric-acid crystals (Jakob). 

It is absent in the urine of carnivora and is very abundant 
in that of herbivora. 

It crystallizes in fine needles or in four-sided prisms and 
pillars with ends beveled in two or four planes (Fig. 24). 

^ Hippuric acid is classified chemically as one of the aromatic group of 
substances in the urine. It is placed here for convenience of study. 

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The typical crystals are vertical rhombic prisms. Hip- 
puric acid is soluble in wqjter„ajid alcohol, and ij;s solutions 
are strongly acid in reaction. It combines with alkalis and 
alkaline earths to form soluble salts, but its silver, copper, 
and lead compounds are sparingly soluble in water. 
Strong acids precipitate it from solutions of its salts. On 
boiling with an alkaline hydrate hippuric acid decomposes 
into benzoic acid and glycocoU. This is clinically inter- 
esting because the same decomposition takes place in 
alkaline fermentation, especially in urine containing al- 
bumin, so that such urine is found to contain benzoic acid 
instead of hippuric. Hippuric acid is probably formed 
in the kidneys by the union of benzoic acid and glycocoU. 
Clinically it has no very great significance, its amount de- 
pending chiefly upon the diet. It is increased by vegetable 
diet and by the use of benzoic acid, salicylic acid, and their 
congeners; also in acute fevers, diseases of the liver, and 

Detection. — Add concentrated nitric acid to the urine 
and evaporate it to dryness. The residue heated in the 
test-tube gives the odor of bitter almonds, due to nitro- 
benzol. When an excess is present, hippuric acid may be 
separated in crystals by evaporating the urine to one- 
fourth its volume and adding some hydrochloric acid. 


What are the purin bodies? What is the "purin" molecule? What 
purin body is an acid ? 

What is uric acid ? Give an account of its origin. When is uric 
acid excretion increased ? Diminished ? What is its clinical significance ? 
What can you say of the relation of uric acid to gout ? 

Give the general properties of uric acid. How is it detected ? Describe 
Heintz's method; Ruhemann's method; Folin-Hopkins' method. 

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In what form does most of the uric acid occur in urine ? What two 
varieties of uric acid salts occur in the urine ? Which are the less soluble ? 

What causes the opacity observed on adding an acid to urine rich in 
neutral urates ? How is the precipitate affected by heat ? 

What are the purin bases f Name some of the most important mem- 
bers of this group. What is their clinical significance ? Describe the 
method of estimating the total amount of purin bodies. 

How much ammonia appears normally in the urine? When is this 
amount increased? Decreased? 

Whence are creatin and creatinin derived, and what causes their 
variations in urine? 

Under what conditions has allantoin been found in the urine ? 

What element do the nucleic acids contain that is of interest, and in 
what amount ? What do these acids form when boiled with dilute mineral 
acids ? 

What causes the variations in the amount of hippuric acid ? What 
are the general properties of this acid? 

Into what constituents does hippuric acid decompose on fermenta- 
tion ? 

How is hippuric acid probably formed ? When is it increased in the 
urine? How is it detected? 

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Acetone (CsHgO) is a volatile compound belonging 
to the group of ketones, and may be present in large 
amounts in urine in disease. In health the urine contains 
traces of it, especially after the use of alcohol and of food' 
rich in proteids. 

Clinical Significance. — According to von Jaksch, 
pathologic acetonuria occurs as follows: (i) Febrile 
acetonuria . in scarlet fever, typhoid pneumonia, measles, 
small-pox, etc.; (2) diabetic acetonuria ; (3) i n certa in 
forms of canc er, independently of inanition; (4 ) in starva - 
tioi\. especially in gastric ulcer and after the use of rectal 
feeding; (5) i n mental diseases; (6) in auto-intox ication; 
(7) in derang e ments of diges tion; (8) in chloroform na r- 

Acetonuria is common in fevers. In diabetes its ap- 
pearance shows an advanced stage, but it must be remem- 
bered that the predominance of nitrogenous food in diabe- 
tics tends to produce acetone. Cerebral irritation may 
give rise to persistent acetonuria. 


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Preparation of Urine for Acetone Tests. — The first requisite for 
accurate tests for acetone is that the urine be freshly voided. There should 
be no preservatives in such urine, especially no thymol^ as this interferes 
with acetone reactions. 

If the urine proves negative to the ordinary acetone tests it should be 
distilled and the distillate tested again. Without testing the distillate 
no negative acetone reaction should he accepted as final. This especially 

Fig. 25. — Simple apparatus for distilling urine (Sahli). 

applies in cases of diabetes and of the toxemia of pregnant women. 
Small traces can be detected with the distillate when the urine proves 
negative. An easy method of distilling the urine is described by Sahli as 
follows, and can be used by the practitioner without any trouble: 

"About 50 cc. of urine acidified with a little phosphoric acid (sufficient 
for a marked Congo reaction, to prevent foaming) are poured into a 
fractionation flask (Fig. 25) and heated to gentle boiling, preferably over 
a water-bath or over a wire gauze. A test-tube is then slipped over the 

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projecting arm for a receiver and fastened with a piece of string or wire. 
The upp)er, open end of the flask is closed with a cork. The distillate 
will now collect in the test-tube without any special cooling apparatus. 
Within a few minutes several cubic centimeters will have distilled over, 
and the acetone test can then be performed upon the distillate." 

" Hoppe-Seyler claims that if diacetic acid is also present the distilla- 
tion will produce acetone artificially, so that in such an event another 
method must be selected. Instead of being distilled the urine is rendered 
slightly alkaline, and then extracted with pure ether, the ether shaken with 
water, and the test performed upon the aqueous solution." 

Detection. — Legal's Nitroprussid Test. — This is 
not a delicate test, but suffices for clinical purposes, as a 
rule. It should be repeated with the distillate if the urine 
is negative. To the urine or the distillate a few drops of 
concentrated watery solution of sodium nitroprussid are 
added. (The latter should be freshly prepared.) Then 
a solution of sodium hydrate is added till strongly alkaline. 
A ruby-red color changing to yellow is seen, which may be 
due to acetone or to creatinin. If due to acetone, the ad- 
dition of glacial acetic acid to excess will turn the fluid to a 
purple red and finally to a violet color. If creatinin 
caused the reaction, the red turns to yellow and to green, 
finally to blue. The test is not positive for acetone unless 
a purple-red color is obtained. 

Jackson-Taylor's Modification of Legal's Test. — 
Jackson-Taylor* modified the above test as follows: 
Equal parts of urine and of the sodium nitroprussid solu- 
tion are mixed in a test-tube. Over this mixture strong 
ammonia is layered by pouring it along the side of the tube 
(see Heller's Albumin Test, p. 61). When no acetone is 
present there will be no ring, or only a faint orange- 
brown ring at the point of contact of the two fluids. The 
presence of acetone is evidenced by a magenta or petunia- 

* "Lancet," 1907, iii, 23. 

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red ring, which may spread upward in the ammonia. 
This test has proved most satisfactory in the hands of the 
present writer, and is to be recommended for routine work. 
No acetic acid is used in this test. 

Lieben's lodofonn Test* — ^This is best applied to the 
distillate of the urine. Half a liter of urine is treated with 
phosphoric acid or hydrochloric acid in the proportion of 
3 to ICO cc. The mixture is partly evaporated into the 
distilling apparatus, and the process completed in a retort. 
The acid is added to prevent the evolution of gases. 
Lieben's test consists in adding a small amount of potas- 
sium hydrate, solution to the distillate, and then a few 
drops of a solution of iodin and potassium iodid (iodin, 
i; potassium iodid, 2; distilled water, 50). Acetone, if 
present, gives a yellowish precipitate of iodoform at once. 
Alcohol gives the same precipitate, but more slowly. 
For this reason Gunning uses ammonium hydrate and 
tincture of iodin, which react only with acetone, and not 
with alcohol. The crystals are recognized under the 
microscope by their characteristic shape (flat hexagons, 
often arranged in star-like groups — Fig. 26), and the odor 
of iodoform also helps in detecting acetone. 

Gunning's Iodoform Test. — This is a modification 
of Lieben's, designed to avoid confusion of acetone with 
alcohol in the urine. An alcoholic solution (tincture) 
of iodin and a little ammonia water are added to the dis- 
tillate or to the urine itself (the latter is not so satisfactory). 
If alcohol is present, no precipitate will occur, while ace- 
tone produces a precipitate of iodoform and of iodin, the 
latter falling as a black sediment even if there be no acetone 
present. A large amount of acetone in the urine will cause 
the disappearance of the black iodin sediment after a while, 

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but if there be little acetone, the iodin sediment is found at 
the bottom of the test-tube, with a layer of iodoform in 
yellow crystals lying over it in a thin stratum (Fig. 26). 
The mixture must not be warmed while there is any 
nitrogen iodid in it — i. e., for twenty-four hour§ — on ac- 
count of the danger of an explosion. 

Reynold's Test. — ^Acetone dissolves freshly precipitated 
mercuric oxid. Yellow mercuric oxid is precipitated from 
a solution of mercuric nitrate in a test-tube by the addition 

Fig. 26. — Crystals of iodoform. 

of an alcoholic solution of potassium hydrate. The urine 
is added and the mixture shaken. The liquid is filtered 
until it passes through clear. To the filtrate ammonium 
sulphid is carefully added. If acetone is present, some 
mercuric oxid has been dissolved, and is shown in the 
filtrate by a dark ring of mercuric sulphid at the contact 
of the two liquids. 

Frommer's Test. — Ten cc. of urine in a test-tube are 
treated with i gm. of potassium hydrate (the solid sub- 

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stance) and without waiting for a solution to take place 
from 10 to 12 drops of a 10 per cent, alcoholic solution of 
salicylaldehyd (salicylous acid) are added. The mixture 
is heated gently to 70° C. (not boiled). In the presence of 
acetone there appears a deep red ring at the bottom of the 
tube, at the line of contact of the two substances. This 
reaction is very delicate and does not take place with other 
substances than acetone. 


Diacetic acid (aceto-acetic or ethyldiacetic acid, CgH^jOg) 
is probably derived from beta-oxybutyric acid (see p. 172). 
Diacetic acid is readily converted into acetone, alcohol, and 
carbon dioxid by the action of alkalis, a similar decomposi- 
tion possibly taking place in the blood. It is a colorless 
liquid, which gives a deep-red color with ferric chlorid. 

Clinical Significance. — Diacetic acid is now regarded 
as the most important body, c linically, ot the acetone group. 
Folin^ finds that diacetic acid is much more abundantly 
and more commonly present in urine than acetone, and 
that the tests for the latter really show diacetic acid. This 
acid should always be looked for in diabetes and in 
toxemias, in addition to, or even in preference to, acetone. 

A mere trace of diacetic acid occurs normallv in uri ne. 
It occurs also in starvation and in persons on a rigid non- 
carbohydrate diet. When carbohydrates are given, it 

T he presence of diacetic acid is usually a serious svm p- 
tom. It occurs in t he urine in toxemias^ and espe cially 

^ Journal A. M. A., May 2, 1908. 

^ This test of diet should be used in diabetics before drawing conclu- 
sions as to the significance of diacetic acid. 

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in diabetes and in fevers^ In children with fever its pres- 
ence is not of grave import. In diabetes its appeara nce 
i s a poor prognostic sig n. Ajform of a uto-intoxication a c- 
companied by diaceturia i s sometimes rapidly ffltal w ithout 
any definite lesions. 

Detection. — ^Von Jaksch's method is trustworthy. 
A solution of iron perchlorid is cautiously added to the 
urine. If phosphates precipitate, they are removed by 
filtering, and some more of the reagent is added. A char- 
acteristic Bordeaux-red color appears, but this color may 
be produced with the same reagent in the presence of 
salicylic acid, carbolic acid, and other substances. If the 
urine be previously boiled, diacetic acid does not give the 
reaction, or gives a much fainter color, while the other sub- 
stances continue to give it. If the deep Bordeaux-red 
color develops, therefore, when a portion of the original 
urine is boiled, the reaction is negative. 

Another portion of the urine may be acidulated with 
sulphuric acid and extracted with ether. The ether 
extract is shaken with water and FcjCLg added. A violet 
color appears in the layer of water if diacetic acid is present. 
If the color pales after standing for one or two days, 
diacetic acid was present. If the color reaction with the 
ethereal extract does not fade, the substance is probably 
beta-oxybutyric acid (see below), of which diacetic acid is 
a further oxidation. The urine to be tested should be per- 
fectly fresh, as diacetic acid decomposes readily into 
acetone, etc., in urine on standing.^ 

^ This process is attributed to Gerhardt by Purdy. 

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Beta-oxybutyric acid (C^HgOg) sometimes accompanies 
diacetic acid and acetone in urine. It is the substance from 
which diacetic acid is derived. Acetone, in turn, is formed 
from diacetic acid. It forms an odorless, colorless, trans- 
parent syrup with aqueous vapor, and rotates polarized 
light to the left. It gives no reaction with ferric chlorid, but 
is easily convertible into acetone and diacetic acid by oxi- 

Clinical Significance. — This substance is met with 
in large amounts in severe forms of diabetes and in small 
amounts in scurvy, scarlet fever, measles, in the starving, 
the insane, in cancer patients dying from coma, and in 
persons living exclusively on meat and fat. In diabetes 
it is probably the cause of the acid intoxication which 
usually precedes and accompanies diabetic coma. Herter 
found that the persistent appearance of more than 25 gm. 
of this acid indicates impending coma. 

It is found in the blood of diabetic patients and is a 
homologue of lactic acid. It is formed from diseased mus- 
cle as lactic acid is from healthy, but the steps by which it 
is formed are unknown. Its presence in the blood has 
given rise to the alkaline treatment of severe diabetes, which 
is supposed to neutralize the acid in the blood. 

Detection. — There is no simple reaction for this 
member of the acetone group. If the urine is fermented 
with yeast and tested for its polarity, a strong left-hand 
rotation indicates the probable presence of this acid. A 
better way is to ferment the ether extract of urine, then 
to acidify the fermented fluid with phosphoric acid, to ex- 
tract with ether, and to test the extract with the polariscope. 

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If levorotatory, /?-oxybut)n-ic acid is quite surely present 
(Emerson). The process of isolation is tedious. 


What is acetone ? Is it present in healthy urines; if so, under what 
conditions? What is its significance in disease? How should urine be 
prepared for acetone tests? 

Describe Legal's test for acetone; Jackson-Taylor's modification; 
Lieben's test; Gunning's test; Reynold's test; Frommer's test. 

What is diacetic acid and when does it occur in the urine ? What does 
it augur in diabetes ? How is is detected ? 

How do we differentiate the iron reaction of diacetic acid from that of 
salicylic acid, etc. ? 

Describe beta-oxybuiyric acid. What is its clinical significance in the 
urine ? From what tissues is it probably formed ? How is it detected ? 

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Indican (indoxyl-potassium-sulphate, CgH^NO-SOj . KO) 
is formed from indol (CgH^N), a product of intestinal 
putrefaction of albuminous substances. The indol is 
absorbed from the intestine and becomes oxidized to in- 
doxyl (CgHgNO), immediately combining with "potassium 
sulphate (and also to a slight extent with sodium), form- 
ing indoxyl potassium sulphate, which is eliminated in 
the urine.^ 

Indigo-blue is formed by the oxidation of indoxyl-potas- 
sium-sulphate, thus: 

2C8HeNKS04 + 03= 2C8H5NO = 2HKSO4. 

Indoxyl potassium Indigo-blue. Potassium hydra 

sulphate. sulphate. 

Indigo-red, which has the same formula as indigo- 
blue, is also a product of oxidation of indican. 

Clinical Significance. — Putrefaction goes on con- 
stantly in the normal intestine, except in the newborn, 
and so indoxyl is a constituent of normal urine. The 
quantity separated from the urine as indigo-blue is between 
0.005 ^^d 0.0025 gm. in twenty-four hours in normal man 
on a mixed diet. A milk diet gives very small amounts, 

^ For further data on the chemistry of indican, see p. 224. 

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while a liberal meat diet gives the largest amounts excreted 
in health. 

Indicanuria has been the subject of study since 1853, 
when it was first described by Hill-Cassel. Many con- 
fusing and conflicting statements concerning excessive 
excretion of indican have appeared and are still appearing 
in medical literature. In the following the author intends 
giving the student a concise summary of the important 
facts to be borne in mind in this connection. 

An excess of indican merely shows that there is putre- 
faction of proteids somewhere in the body. Usually this 
putrefaction takes place in the intestines, but in a smaller 
number of instances it may occur in other parts of the body. 

Indicanuria may, therefore, be at once divided into two 
groups: (i) Inteslinal 3ind (2) extra-intestinal. The latter, 
which is the less important, may be dismissed briefly. 
It may occur as the result of proteid putrefaction in such 
conditions as putrescent cancer, pulmonary gangrene, 
empyema, putrid bronchiectasis, pulmonary tuberculosis 
with cavities, etc. In these conditions indol is formed and 
absorbed into the blood and is excreted as indican. 

Intestinal indicanuria is dependent upon the putre- 
faction of proteids by the bacteria of the intestine. Tryp- 
sin has also something to do with this favoring putre- 
faction; for when the pancreatic duct is obstructed, in- 
dican greatly diminishes or disappears from the urine. 

The experiments of Jaffe and of EUinger and Prutz 
showed that indican is formed largely if not entirely in the 
small intestine, especially in its terminal portion, and not in 
the large gut. These observers tied the end of the small 
intestine in animals and produced a rapid and marked in- 
dicanuria. When this small gut was tied high up, where 

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there is comparatively little bacterial putrefaction, in- 
dicanuria was absent. These observers also state that 
obstruction of the large intestine does not produce indi- 
canuria unless indirectly affecting the small intestine. 
Basing their ideas upon these researches, Leube, Jaksch, 
Senator, and especially Nothnagel insist that there is 
an important difference between the large and the small 
intestine in regard to the production of indican, and that 
obstruction or even ligation of the large intestine does not 
produce indicanuria. The influence of trypsin probably 
has to do with this difference in the behavior of the small 
and the large intestines, for trypsin acts in the former, but 
is destroyed by the time the food remnants reach the large 

Indicanuria is, therefore, present in a variety of condi- 
tions associated with increased intestinal putrefaction 
(especially in the small intestine) and with occlusion of 
the bowel, such as mechanical obstruction of the in- 
testines, ileus, acute and chronic peritonitis, appendicitis, 
ulcers of the intestine leading to scar-formation and con- 
traction (tuberculosis, typhoid), gastroptosis, enteroptosis 
and lead-poisoning, cholera, intestinal auto-intoxication, etc. 

Anything that will increase intestinal putrefaction will, therefore, give 
rise to indicanuria, especially if the putrefying material is retained suffi- 
ciently long to allow absorption of indol to take place. The study of 
intestinal putrefaction belongs to other treatises. In this connection we 
might mention two factors which have been brought forward as in- 
fluencing intestinal putrefaction, the functions of the stomach and of the 
liver respectively. 

It has been claimed by Carles and others that the secretion of HCl has 
something to do with indicanuria, and when HCl is low there is an in- 
creased bacterial putrefaction in the stomach. This has been shown to 
be incorrect by Enriquez and Binet, who claim that both hypo-acidity 
and hyperacidity may be accompanied by indicanuria. 

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The liver cells, when incapacitated by disease, are held reponsible 
for a type of indicanuria due to hepatic insufficiency by Gilbert and Weil. 
This was also proved false by Enriquez and Binet, who produced liver 
lesions in dogs and found no indicanuria. On the other hand, the 
flow of bile, when impeded or when diminished, will increase intestinal 
putrefaction and hence indicanuria may be due to biliary insufficiency 
or to a stenosis of the bile-duct. The bile, it will be remembered, acts 
both as an antiseptic and a stimulant of peristalsis. 

The Relation of Constipation to Indicanuria. — This is a most important 
question. The older writers, especially Nothnagel, insisted that habitual 
constipation alone could not give rise to indicanuria. These authors 
pointed to the fact that indicanuria is often present in intestinal diseases 
accompanied by diarrhea. Recent observations have shown, however, 
that constipation, especially when chronic, may be the sole cause of indi- 
canuria (Emerson, Enriquez, and Binet). Some observers even found 
that they could produce indicanuria by giving patients astringent drugs. 
On the other hand, indicanuria is rare in simple diarrhea, or even in ty- 
phoid fever accompanied by severe diarrhea. In false diarrhea, which 
indicates fecal retention, there is indicanuria, e. g., in mucomembranous 
colitis, but not in conditions in which the diarrhea acts as a thorough 
evacuant of the tract. By giving purgatives, especially castor oil, an 
indicanuria due to constipation may be markedly diminished or made to 

In interpreting indicanurias the student should, therefore, never fail 
to consider the presence of constipation. The patient's diet should also 
be inquired into. People "living high," on a rich proteid diet, who over- 
eat habitually, are apt to have an excess of indican, which is easily 
removed by appropriate dietetic measures. 

Detection. — Indican is in itself a colorless substance 
or a brown syrup easily soluble in water, alcohol, and ether, 
and having a bitter taste. With acids and heat it is easily 
converted into indigo-blue (Heller's uroglaucin) and indigo- 
red (Heller's urrhodin). This conversion is the basis of 
the tests for indican. 

Ordinarily, indoxyl does not alter the color of fresh urine, 
but sometimes it may *be partially or completely oxidized 
in the body, giving the urine a blue color, due to the deposit 
of indigo-blue. The same may take place outside of the 

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body on ammoniacal decomposition. Calculi of indigo 
have rarely been found in the urinary tract as the result of 
the separation of indigo. 

Heller's Test. — ^This is a very convenient and practical 
test. Into a small conic glass or wineglass pour 4 cc. 
(i dm.) of hydochloric acid (c. p.), and add one drop, or at 
most two, of pure nitric acid. The latter makes the test 
more delicate, but an excess of nitric acid is fatal to the 
test, as the oxidation will be so rapid that the reaction can- 
not be seen and a yellow color results. To these acids 
add fifteen drops of the urine and stir. Within from five 
to twenty minutes an amethyst color appears. Under 
these conditions the mixture may be colored a pale-yel- 
lowish or pinkish tint, showing that indican is diminished. 
A distinct amethyst color, which is not intense and which 
appears rather slowly, indicates a normal amount. A deep 
violet color appearing quickly indicates an increase of 

It is best to perform this test always in the same sized 
receptacle, and to use exactly the same proportions of urine 
and acids, although the quantities may be varied to suit 
the observer. Some definite rule should be observed al- 
ways, frequently controlling oxidations with normal urine. 
In this way one can easily learn to distinguish increase of 
indican at a glance. 

Jaffa's Test. — To about 10 cc. of urine in a large test- 
tube add an equal amount of fuming hydrochloric acid, and 
then, with constant shaking, a perfectly fresh saturated 
solution of calcium hypochlorite, drop by drop, until the 
blue color ceases to deepen. Instead of this solution a 0.5 
per cent, solution of potassium permanganate may be used. 
Shake with some chloroform, which dissolves the indigo, 

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and allow to stand, the chloroform separating as a blue 
fluid, the color being more or less deep according to the 
amount of indican. Dark urines, whose other coloring- 
matters are decomposed by hydrochloric acid and hypo- 
chlorite, should first be decolorized with basic acetate of 
lead solution. This may be done by adding i cc. of lead 
acetate solution to 10 cc. of urine and filtering. The 
filtrate should be tested for indican. 

Obermeyer's Test. — The reagent is composed of strong 
hydrochloric acid, to which are added 4 parts per 1000 of 
ferric chlorid, the combination forming a fuming yellow 
liquid which keeps indefinitely.* The urine should pref- 
erably be decolorized with a small amount of lead acetate 
solution, as its pigments prevent the recognition of the blue 
colc^. Equal parts of urine and of Obermeyer's reagent 
are mixed in the test-tube, and a small quantity of chloro- 
form is added. The tube is corked and inverted several 
times without shaking. The chloroform becomes blue in 
proportion to the indican present, increasing on standing. 
Normal urine becomes faint blue, while an increase of 
indican gives a deep blue color. 

Approximate Quantitative Estimation. — Robin's Method. — ^The 
accurate methods of quantitative estimation of indican being too complex 
for chemical use, the following approximate method may be employed with 
advantage. The solutions required are: (i) Obermeyer's reagent (HCl, 
1000; FegClg, 4); (2) a 25 per cent, solution of lead acetate; (3) a solution 
of potassium chlorate containing i per cent, of available CI, or 34.6 gm. 
of the salt per liter. 

"To 10 cc. of the urine add i cc. of the lead acetate solution, and filter 
through a double filter. Put 5 cc. of the filtrate into a test-tube, add 5 cc. 
of Obermeyer's reagent and 2 cc. of chloroform, and invert the tube about 
ten times, or until the color of the chloroform ceases to become more in- 
tense. The latter will assume a violet or blue color according to the 
amount of indican present. Now add from a dropper the potassium 

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chlorate solution, shaking the mixture after each addition until the blue 
color of the chloroform disappears. The potassium chlorate liberates 
chlorine in the presence of a strong mineral acid and oxidizes the indigo 
formed by the addition of Obermeyer's reagent. If the amount of indican 
is normal, one or two drops will cause discoloration. In recording 
results write: * Indican = x gtt. KCIO3 solution' " (Boardman Reed). 
This method has given very satisfactory comparative results in the 
hands of the present writer. The progress of an indicanuria can be con- 
veniently watched by this simplified process. 

Precautions in testing for indican with any of these 
tests should include the removal of albumin, as the latter 
develops a blue color with hydrochloric acid on standing for 
a long time. A red color obscuring the blue due to any 
indoxyl develops when iodin is present in patients 
who had been taking iodids. In this case a small 
quantity of a strong solution of sodium hyposulphite 
should be added to the test-tube and the mixture shaken. 
When the chloroform has settled again, the blue of the 
indigo will appear. It is important to note the specific 
gravity of the urine to be tested for indican. If an intense 
reaction is obtained with urine of low specific gravity, 
there is far more indican excreted relatively than when 
the same tint is obtained with a urine of high specific 

Rosenbach's Burgundy-red Reaction. — ^This is a 
color-reaction observed in severe intestinal disturbances 
in which there are a high degree of decomposition and a 
large amount of indican. The urine is reddish in color to 
start with, and on the addition of nitric acid, drop by drop, 
and boiling, it gives a deep. Burgundy-red color. 

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Besides indican, there are several products of decom- 
position eliminated in the urine which appear in the form 
of sulphates of sodium and potassium. These, together 
with indican, are grouped chemically as the ethereal sul- 
phates. The amount of these bodies in the urine varies 
with the extent of putrefaction in the intestine. It is 
said that the best criterion of the occurrence of the amount 
of putrefaction in the body is the relation of the ethereal 
sulphates to the total sulphates, the normal proportion 
being about i to lo, the relative amount of ethereal sul- 
phates rising as putrefaction increases. The two ethereal 
sulphates besides indican that are of importance are 
skatoxyl potassium sulphate and phenol potassium sul- 
phate. For further details, see Sulphates, p. 224. 

Skatoxyl potassium sulphate (CgHgNO.SOzK) is formed 
from skatol under the same conditions as indican is from 
indol. It is present in the urine as a colorless compound, 
and when oxidized gives a red color. When the indican 
test gives a purple-red color, the presence of skatol may 
be surmised. This red color cannot be removed by shaking 
the urine with chloroform, but it is extracted by amyl- 
alcohol. Normally it occurs in smaller quantities than 
indican, and clinically it is of little interest, except in con- 
nection with indoxyl. 

Phenol Potassium Sulphate (C,H50S03.K).— Phenol 
is a product of intestinal putrefaction, and is probably in- 
termediate as to the place where it is developed between 
indol, which arises high up in the intestine, and skatol, 
which is formed low down in the tract. It is absorbed 
from the intestine, enters the blood, and combines with 
potassium sulphate to form an ethereal sulphate, phenol 

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potassium sulphate. This is present in normal urine in 
amounts averaging about 0.03 gm. in twenty-four hours, 
and constitutes the form in which all the phenol or carbolic 
acid of the body exists. 

Clinical Significance. — ^When there is an excess of 
indican there is usually an increased amount of phenol, 
but the reverse is not true. In albuminous putrefaction 
in other parts of the body than the intestine — as, for 
example, in empyema, etc. — there may be an increase of 
phenol alone, indican remaining normal. The use of car- 
bolic acid, lysol, and other phenol compounds may increase 
the amount of phenol potassium sulphate. When phenol 
compounds are taken, the urine becomes smoky, dark 
brown, or black on standing exposed to the air, as the result 
of the splitting up of phenol into pyrocatechin and hy- 
droquinon. Clinically any condition that causes increase 
of indican also causes an increase of phenol, especially 
increased putrefaction in the lower part of the small in- 
testine and in the upper part of the large intestine. 

Detection. — ^To detect phenol, add some nitric acid to 
the urine and boil, when the urine will give an odor of bitter 
almond oil. After cooling, add some bromin water, causing 
a precipitate of tribronitrophenol. To another portion of 
the original test add sodium hydrate to excess, and observe 
an orange-red color, due to the formation of sodium nitro- 
phenol. Other tests are too elaborate, as they require 
the distillation of the urine. 

In 1882 Ehrlich described a reaction in the urine, which 
has taken his name, and which depends upon the presence 
of certain aromatic substances which form anilin colors in 

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ehrlich's diazo-reaction 183 

the presence of diazosulphobenzol. The latter is formed 
by the union of sulphanilic acid (amidosulphobenzol) and 
HNO2. In order to obtain a fresh solution of diazosul- 
phobenzol, a solution of sodium nitrite is added to a solution 
of sulphanilic acid containing 5 per cent, of hydrochloric 
acid. When the two solutions are mixed, HNOj is set 
free, and diazosulphobenzol is formed. The reagents 
used in Ehrlich's diazo-reaction, therefore, are as follows: 

Solution I : 

Sulphanilic acid i part 

Hydrochloric acid (c. p.) 50 parts 

Distilled water 1000 " 

Solution 2 : 

Sodium nitrite i part 

Distilled water 200 parts 

The solutions should be kept in separate well-stoppered 
bottles of amber glass, and should be mixed when needed 
by combining 50 cc. of No. i and i cc. of No. 2. The 
sodium nitrite solution does not keep well and should be 
prepared freshly at frequent intervals. 

The test is performed by mixing equal bulks of the 
freshly voided urine and the mixed reagents; quickly adding 
one-tenth volume of ammonia water, and shaking.^ A 
deep cherry-red color indicates a positive reaction, and 
if the reaction is marked, the foam will appear salmon- 
pink or even deep-red in color. On standing for twenty- 
four hours a green precipitate is formed, which is a further 
proof of the true reaction. 

^Another way is to mix 15 cc. of urine and 15 cc. of solution No. i, 
shaking gently, adding 5 drops of solution No. 2, and shaking well with 

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Clinical Significance. — ^The chief clinical value of 
the diazo test is in the diagnosis of typhoid fever. It is 
present very constantly in severe types of typhoid fever, 
with an intensity running usually parallel to the severity 
of the infection (Wood). The clinical value of the diazo- 
reaction is, however, greatly lessened by several facts: 

1. It often does not occur in the milder forms of typhoid 
fever until the acme of the disease has been reached, and at 
times is wholly absent in such cases. 

2. It occurs in many other diseases, notably in tuber- 
culosis, pneumonia, pleurisy, many acute fevers (measles, 
scarlet fever, diphtheria, erysipelas, etc.), in syphilis, 
cancer, septicemia, pyemia, rheumatism, etc. In practice 
the chief diseases in which it puzzles the diagnostician are 
tuberculosis and septicemia. In pulmonary tuberculosis 
its presence is of bad prognostic import and its persist- 
ence indicates an advanced stage of the disease. 

3. The reaction occurs in the urine of persons who 
have been taking certain drugs — e. g,, naphthalin, chrysa- 
robin, etc. This reaction is, however, distinguished from 
the true diazo-reaction by the absence of a green precipitate 
occurring on standing for twenty-four hours, and by the fact 
that the color does not disappear on the addition of acids. 

Other drugs — e, g,, gallic and tannic acids and their 
compounds, iodin, and the iodids — inhibit the appearance 
of the reaction. This is especially to be noted in tuberculo- 
sis, where tannates are frequently given for the diarrhea. 


What is indican ? How is it formed ? 

How is indigo-blue formed ? 

What is the clinical significance of indican? 

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ehrlich's diazo-reaction 185 

What does diminution of indican imply ? When is it increased ? 

What weight should be given to indicanuria in clinical work? 

What is the principle of all indican tests? Describe Heller's test; 
Jaffa's test; Obermeyer's test; Robin's quantitative method. 

What precautions should be taken in testing for indican ? 

How does indican give the urine voided a blue color? 

What are indigo calculi? 

What are the other chief ethereal sulphates besides indican in the urine ? 

What does the relation of ethereal sulphates to the total sulphates 
indicate? What is the normal proportion? 

What is skatoxyl potassium sulphate ? How is it detected ? 

What is phenol potassium sulphate ? Where is it formed probably ? 

Why does urine containing phenol turn dark on standing exposed to 
the air ? 

What is the clinical significance of phenol potassium sulphate in urine ? 
How is its presence detected? 

Describe Ehrlich's diazo-reaction. On what principle is it based? 
What is its clinical significance? What are its limitations? In what 
diseases does it occur? 

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Two pigments are always present in normal urine 
— urochrome and hematoporphyrin. Two other pigments — 
uroerythrin and urobilin — ^may be present, especially on 
sanding. Urochrome gives the yellow color to the urine. 
Hematoporphyrin is present in small amounts, is red in 
color, and is considered under the head of Blood Coloring- 
matters. Uroerythrin gives the pink color to urate deposits 
and urobilin gives urine a dark-brown color. Of the nor- 
mal pigments the only one that has any clinical significance 
is urobilin, an increase of which is noted in certain diseases. 

Urobilin (C32H40N4O7; urophaein. Heller; hydrobilirubin 
Maly) was first isolated by Jaffe in 1868. It is present in 
the urine chiefly as a chromogen — urobilinogen — and its 
color is set free only when this chromogen is decomposed. 
In some diseases there is an increased amount of free 

It is derived partly through the decomposition of the 
hemoglobin of the blood, but chiefly through the decom- 
position of the biliary pigments (bilirubin) which takes 
place in the intestine as the result of bacterial action. 
Urobilin may be formed either from bile-pigment or from 

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blood-pigment. Conditions accompanied by destruction 
of red blood-cells give an increased amount of urobilin^ and 
this amount is a measure of the destruction of blood-pig- 
ment. Normal urine contains 0.08 to 0.20 gm. of urobilin 
in twenty-four hours, the excretion being greater in tropic 

Clinical Significance. — ^Urobilin is absent: (i) In new- 
bom children. (2) In obstruction of the bile-ducts (jaun- 
dice). (3) In phosphorus-poisoning. (4) In severe 

Urobilin is increased (Serkowski) : (i) In conditions of 
intestinal putrefaction (in which it is parallel to indican). 
(2) In hemorrhages into the organs or cavities of the body. 
If no excess of urobilin occurs there could not have been 
any bleeding. (3) In atrophic cirrhosis of the liver. (4) 
In scarlet fever. (It is not increased in diphtheria.) (5) 
In appendicitis. (6) In malaria. (7) In cancer. 

Detection. — ^Urobilin is best detected by examining 
the urine directly by means of a small pocket-spectroscope.^ 
The urine may have to be diluted if it is deeply colored. 
The characteristic absorption-band is between the green 
and the blue parts, between the lines b and F (Fig. 28). 
These bands are rendered sharper on adding a few drops 
of tincture of iodin to 10 cc. of urine. 

When no spectroscope is available, an old test, which 
is very useful, the so-called urophaein test of Heller, may 
be employed. To about 7 cc. of concentrated sulphuric 
acid add twice the amount of urine in a conic glass, pouring 
the urine into the acid from the height of about 4 inches. 
If the amount of urobilin is normal, a garnet-red color ap- 
pears, which is so intense that but little light passes through 

^ For the method of using this instrument, see page 197. 

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the mixture; if increased, the mixture is opaque, and if 
diminished, it is transparent. This test is not of any value 
as a specific test of urobilin, for other coloring-matters and 
such abnormal constituents as bile, sugar, etc., give this 
reaction. It is frequently used, however, as a test for uro- 
bilin after excluding the presence of sugar, bile, etc. 

Harlefs Test. — ^Dilute the twenty-four-hour urine with 
water until it measures 1800 cc. (60 oz.), or, if the quan- 

Fig. 27. — I, Acid urobilin; 2, alkaline urobilin (after Neubauer and 


tity exceed this amount, concentrate it to this measure. 
To 4 parts of it in a test-tube add i part of pure nitric 
acid, and allow the mixture to stand for some minutes. 
If the quantity of urobilin is normal, the mixture will 
change but slightly in color. If there is an excess, it will 
become pink, red, or purple, according to the amount. 
The acid liberates the coloring-matter which may be con- 
cealed, so that a pale urine often contains a large amount 
of pigment. 

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The presence of bile in the urine is represented by the 
occurrence of biliary pigments and biliary acids. Both 
groups will be considered here together for the sake of 

Bilirubin. — Bile-pigments occur in the urine in the form 
of a combination of bilirubin with alkalis. When urine 
rich in bile-pigment is allowed to stand exposed to the air, 
bilirubin becomes oxidized to the green biliverdin. Bili- 
rubin itself is orange colored and is an intermediate prod- 
uct in the body between hemoglobin and urobilin. The 
oxidation products of bilirubin are, in the order of im- 
portance, biliverdin, already mentioned (green), bili- 
cyanin (blue), bilifuscin, biliprasin, and choletelin. 

Bilirubin occurs in a free state in urine, but the color 
of a bile-containing urine, though almost always abnor- 
mally deep, varies greatly between a yellowish brown to a 
nearly pure green, according to the presence of oxidation 
products. On shaking, the froth is persistently yellow or 
greenish yellow. The urine permanently stains filter-paper 
a yellow color, and usually contains an excess of urobilin 
and of indican. A bile-containing urine always gives a 
reaction for albumin, especially for nucleo-albiunin, and the 
nitric acid test with such urines is unsatisfactory on account 
of the masking of the white zone by the coloring-matter. 

For this reason a urine containing much bile should be 
tested preferably by the heat test for albumin. The sedi- 
ment of such urines often contains many epithelial cells 
from the kidneys, casts, blood-cells, and crystals of bili- 
rubin. The organized sediment may be stained yellow. 

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Clinical Significance. — Bile-pigments occur in the 
urine in nearly all forms of jaundice. In the severer 
types bile-acids are also present, especially, however, in 
catarrhal jaundice or in obstruction of the bile-ducts. In 
congestion of the liver due to organic heart disease, in 
cancer of the liver (pressure on hepatic duct), acute yellow 
atrophy of the liver (with leucin and tyrosin). In hyper- 
trophic cirrhosis the urine contains bile-pigments (and in 
severe cases, bile-acids), but in atrophic cirrhosis there may 
be no jaundice, consequently no bile in the urine, though 
both may be present in the later stages (Serkowski). Bile- 
pigments may also appear in severe infectious diseases, 
phosphorus-poisoning, and other conditions in which there 
is a destruction of red cells. 

Detection. — On inspection the urine containing bile 
may show the characteristics already described as regards 
its tint, when viewed by reflected light, and the color of its 

Gmelin^s test consists in overlaying concentrated fuming 
"yellow" nitric acid with the urine. This nitric acid, also 
known as crude or nitroso-nitric acid, contains HNOj. It 
should not contain too much of this acid, but enough to show 
a distinct yellow color. By placing a small piece of wood 
(match-stick) in nitric acid and heating, HNO2 is developed, 
and the fluid can be used for this test. There is always 
some resin in wood and a green ring appears at the point 
of contact; below this a blue ring, and next to this a red one. 
The green ring is characteristic of bile; the others may 
come from urobilin or from indican. At times a beautiful 
play of colors — green, blue, violet, red, and yellow, in the 
order named — is seen with this test. This test may also 
be. applied by placing a drop of urine on a porcelain plate 

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and allowing a drop of fuming nitric acid to mingle gradu- 
ally with the urine, giving the same play of colors. 

MarichaVs Test. — About a dram of an alcoholic solu- 
tion of iodin of moderate strength is poured into a test- 
tube, and the urine is allowed to flow down the sides of 
the inclined tube so as to underlie the reagent. A green 
color appears just below the point of contact of the two 

Rosenbach^s test is based on the fact that when a large 
amount of urine containing bile passes through white 
filter-paper, the bilirubin is retained in the paper, and when 
a drop of nitric acid is placed on the inner surface of the 
filter, a green spot is produced, changing to red. 


Bile-acids can he divided into two groups — the glyco- 
cholic and the taurocholic acid groups. The former are 
acids containing nitrogen, but no sulphur, and on the ad- 
dition of water can be split into glycocoU and cholic acid. 
The taurocholic acids contain nitrogen and sulphur and are 
split into taurin and cholalic acid. 

Clinical Significance. — Bile-acids are found in the 
urine in the same conditions as are bile-pigments, but 
their determination is much more difficult than that of 
the pigments. According to von Leyden, the urine of 
hematogenous jaundice contains only bile-pigments, while 
that of hepatogenous jaundice contains both bile-pigments 
and bile-acids. This is not always true, however, although 
the presence of a considerable amount of bile-acids shows 
the existence of hepatogenous jaundice, while their ab- 
sence does not show the absence of this form of icterus. 
The question as to whether bile-acids occur in normal 

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urine has not been settled. Bile-acids are present in he- 
patic congestion, cirrhosis, tumors of the liver, and severe 
acute catarrhal jaundice, anemia, scurvy, and splenic leu- 
kemia. Their clinical significance is important. 

Detection. — ^The tests for biliary pigments are usually 
sufficient to show the presence of bile without testing for 
the acids separately. Bile-acids are not usually tested for 
in routine examinations. They must first be isolated by 
concentrating the urine and extracting the residue with 
strong alcohol, removing the alcohol by evaporation, and 
precipitating with basic lead acetate and a little ammonia. 
The precipitate is washed with water and again extracted 
with warm alcohol, evaporated to dr)aiess after the addi- 
tion of a few drops of sodium carbonate solution. The 
residue is extracted for the third time with alcohol, and 
the acids precipitated by the addition of ether to the alco- 
holic extract. The following test is then carried out with 
the precipitate: 

Pettenkofer's Test. — ^A small amount of watery 
solution of bile-acids is treated in a test-tube with 5 
drops of a 10 per cent, solution of cane-sugar, and this 
mixture carefully layered over concentrated sulphuric acid. 
A red or purple ring will appear at the point of contact. 
(The tube is dipped into cold water and shaken gently. A 
small amount of the purple fluid is poured into one tube 
containing glacial acetic acid, and into another containing 
alcohol. The spectrum of the first shows an absorption- 
band in green, while the second, after a few moments, 
becomes brown and then shows two bands, one between 
D and E and the other at F.) 

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The presence of blood in small quantities does not change 
the color of the urine, but larger amounts give rise to 
cloudiness and to a reddish sediment if the hemorrhage 
is recent. If the blood has been mixed with the urine for 
any length of time within the body, or if ammoniacal fer- 
mentation has occurred, the bloody urine is of a dirty 
brownish-red or dark-brown color, sometimes with a tinge 
of green. 

The coloring-matters of the blood which occur in the 
urine are hemoglobin and its derivatives, oxyhemoglobin, 
methemoglobin, and hematin. Hemaiin is a reduced 
hemoglobin, and the latter is converted into hematin and a 
coagulated albuminous substance by means of heat. 
Methemoglobin is intermediate between hemoglobin and 
hematin. Oxyhemoglobin is obtained by shaking hemo- 
globin with air. These different substances are all dis- 
tinguished by special absorption-bands in their spectra. 

Blood coloring-matters can enter the urine either by 
direct excretion by the kidney or by the disintegration of 
the blood-cells after they have entered the urine from differ- 
ent sources. The color of such urines differs according 
to the amount of hemoglobin or methemoglobin, the former 
giving a bright color, the latter a dark brownish-red. 
Recent hemorrhages from the larger vessels give more 
hemoglobin, while capillary bleeding gives more methe- 

Clinical Significance. — Hemoglobinuria means the 
direct passage of the blood coloring-matters into the urine 
without any red blood-corpuscles. This occurs in a large 
variety of general diseases, such as scurvy, purpura, scarlet 
fever, malarial poisoning, etc. The comparative absence 

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of blood-corpuscles and the presence of a small amount of 
albumin (or even the absence of albumin) distinguish 
hemoglobinuria from hematuria. It must be remem- 
bered, however, that blood-corpuscles are rapidly dis- 
solved, especially in alkaline urine, and, therefore, that red 
cells may have been present in the specimen. Urine con- 
taining dissolved corpuscles is apt to be alkaline, while 
the urine of hemoglobinuria is acid and contains a much 
smaller amount of albumin. It is of lower specific gravity 
and deposits less sediment than the blood of hemoglo- 

Hematuria is a term applied to urine containing both 
blood-corpuscles and blood-pigments. The causes of 
hematuria are very numerous, for blood may come from 
the kidney, from the renal pelvis, from the ureter, bladder, 
prostate, or urethra. Blood from the kidney may be due 
to acute congestion, acute nephritis, or to acute axacerba- 
tions of chronic kidney disease. In acute parenchyma- 
tous and in chronic diffuse nephritis, in interstitial neph- 
ritis as the result of changes in the vessels, and in amyloid 
kidney hematuria is not uncommon. 

Hematuria is very common in tuberculosis, tumors of the 
kidney, and stone in the kidney. It occurs also after the 
administration of certain drugs, such as turpentine, and 
following injuries to the kidney. In the tropics it is often 
caused by parasites, to which allusion will be made later on 

(P- 337)- 
Bleeding from the lower urinary tract may be due to 

tuberculosis, stone or tumor of the bladder; acute or chronic 

inflammations of the bladder; traumatism; acute urethritis, 

urethral chancre, or surgical operations for strictures, etc. 

(See Table of Causes of Hematuria, p. 278.) 

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Relation to Albuminuria. — The presence of blood 
coloring-matters in very minute quantities may be observed 
in urines that are in every way normal. Very small amounts 
of hemoglobin without any albumin may be found in 
scarlet fever just before the onset of albuminuria, thus 
giving warning of the impending danger to the kidney. 
The blood-pigment disappears when the albumin becomes 
copious, and reappears as it diminishes. Hemoglobin is not 
found, however, in albuminuria due to fevers; as in typhoid, 
pneumonia, etc. 

Detection of Blood-pigments.— Guaiacum Test.— The reagents 
needed are: (i) A freshly prepared tincture of guaiacum. Take a pen- 
knife-pointful of the powdered guaiac resin and mix with 3 to 5 cc. of 
95 per cent, alcohol; shake for a minute, allow to stand, and after a few 
minutes filter 5 drops into a test-tube; (2) to this add 20 drops "seasoned" 
oil of turpentine. This is made by allowing commercial turpentine 
to stand exposed in an open dish and in a light room till thick, and 
diluting with about five volumes of ordinary turpentine (Schumm). 
To about 5 cc. of urine add the mixed reagents (turpentine and guaiac) 
and shake repeatedly. A little alcohol now added brings out the color 
better. On standing a short time a blue or bluish-green color develops 
in the presence of blood. Or the urine to be tested is layered under this 
mixture, and a bluish-green and then a brilliant blue contact-ring is 
produced when blood-pigments are present. Pus also gives this ring, but 
in this case the ring disappears on heating the mixture. The blood ring, 
however, stays. Before using this test an alkaline urine must be made 
acid. This test is very delicate. 

Benzidin Test. — A test similar to the guaiacum test, but still more 
delicate. The reagent consists of J cc. of a fresh solution of Merck's 
pure benzidin in glacial acetic acid and 2 or 3 cc. of 3 per cent, hydro- 
gen peroxid. To 10 cc. of urine add 0.5 to i.o cc. of glacial acetic acid, 
and shake well. Then add one-third volume of ether and shake thor- 
oughly. Allow to stand a little while and add 5 to 10 drops of absolute 
alcohol. Shake gently and pipet off the cleared ethereal layer. The 
latter is added to the benzidin reagent in another test-tube and the mix- 
ture is well-shaken. If small amounts of blood are present, a green color 
develops; if larger amounts, a blue color. The reaction is about twenty 

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so if 5p so 7p m sip ,m sjo m j50 m ibo m tro 
















. 1 



IP ' m^^^^^^i 







Ji; a* 


Fig. 28. — Spectra : I dt, Oxyhemoglobin ; by oxygen-free hem<^lobin. 
2, Methemoglobin : a'y in neutral solution ; b\ in alkaline solution. 3, 
Hematin in acid alcoholic solution ; ^, in ammoniacal solution ; ^, reduce^ 
hematin (after Neubauer and Vogel). 


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Blood-pigments 197 

times more delicate than Heller's. It can be used both in hematuria and 
hemoglobinuria, and is not interfered with by pus, sugar, bile, iodide, 
senna, or rhubarb (Schlesinger and Hoist). 

Heller's Test. — ^The earthy phosphates are precipitated from the urine 
by means of caustic potash solution and gentle heat. The precipitate 
of earthy phosphates carries with it, as it sinks, the blood coloring-matters 
and appears not white, as in normal urine, but blood-red. In alkaline 
urine the phosphates may be precipitated by a few drops of the magnesium 
fluid (see p. 218) on the application of heat. Heller's test is not nearly so 
delicate as the above tests. It is open to the objection that it reacts with 
hematoporphyrin and with certain vegetable drugs, iodids, iron salts, and 

Teichmaxm's Hemin Crystal Test. — The precipitated earthy phos- 
phates obtained in the preceding test are filtered out and dried on a slide. 
A minute granule of common salt is thoroughly mixed with the dried 
mixture of hematin and earthy phosphates. Any excess of salt is re- 
moved, the mixture is covered with a cover-glass, a hair is intersposed, and 
a drop or two of glacial acetic acid is allowed to pass under the cover- 
glass. The slide is carefully warmed until bubbles begin to appear. On 
cooling, crystals of hematin hydrochlorate will form. Gentle heat only 
should be used in precipitating the earthy phosphates with caustic potash 
(see Heller's Test) and the urine filtered quickly. Bubbles appearing 
under the cover-glass before heat is applied are carbonic acid, and 
should be allowed to pass away. 

Spectroscopic Test. — ^The urine is placed in a test-tube or small 
trough with plate-glass sides, and examined with a small pocket-spec- 
troscope. Water may be poured on the surface of the urine without mix- 
ing, thus obtaining a mixture graduated from pure water to pure urine. 
Observe the absorption-bands of oxyhemoglobin, two in number, between 
lines D and £; or the single line of reduced hemoglobin between D and E\ 
or the four bands of methemoglobin, the latter giving a dark band in the 
red between C and D if the reaction of the urine is acid (Fig. 28). 

The spectrum of hematin is rarely seen, and is difficult to distinguish 
from that of methemeglobin. If the urine is rendered strongly alkaline 
by ammonium hydrate, and if ammonium sulphid be added, the spectrum 
of reduced hemoglobin will appear with two bands between D and £, 
like oxyhemoglobin, only a little nearer to the green. 

Hematoporphyrin (CieHigNjOg), discovered in 1871 
by Hoppe-Seyler, is a derivative of hemoglobin and is 
present in traces in normal urine. It is identical with 

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iron-free hematin. A urine containing this substance is 
opaque and almost black, or, in a thin layer, reddish- 
brown. Clinically it is important when present in large 
amounts. It has been seen in increased quantities in 
leprosy, acute articular rheumatism, pulmonary tubercu- 

C£ /3 

Fig. 29. — Spectrum of hematoporphyrin : a, Acid; 6, alkaline; c, neutral; 
d^ metallic spectrum. 

losis, pleurisy with effusion, etc. It is increased by the use 
of large doses of sulphonal, trional, or tetronal; in lead- 
poisoning; in intestinal tuberculosis, and in certain nervous 
diseases. It can be detected only by the spectroscope, the 
alkaline solution presenting a four-banded spectrum which 

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is most characteristic (Fig. 29). Its isolation is trouble- 

Melanin is a pigment sometimes found in urine in 
cases of melanotic cancer or sarcoma. It occurs usually 
in solution of the urine or in small black particles. Urine 
containing this pigment is normal in appearance when 
freshly voided, but on exposure to air it becomes brown or 
black. The pigment is eliminated in the form of a chro- 
mogen — melanogen — which becomes oxidized to melanin, 
probably in the liver, although this is still a matter of dis- 
cussion. Melanin has also been observed very rarely in 
severe wasting conditions and in chronic malaria. It 
must be noted that melanin may be entirely absent from 
the urine in cases of actively progressing new growths 
of the melanotic type. 

Detection. — On adding nitric acid to the cold urine, 
the latter turns black. Zeller^s test consists in the addition 
of bromin water, causing a yellow precipitate that gradually 
blackens. The addition of ferric chlorid will cause a gray 
precipitate soluble in an excess of Fe^Clg, constituting von 
JaksMs test, which is much more delicate than Zeller's 
and should always be used to detect melanin.^ 


What two pigments are always present in normal urine? What 
two other pigments are usually present and especially on standing ? 

What pigment gives the yellow color to urine ? The dark-brown color ? 
The pink color to the urates? 

In what form is urobilin present in normal urine? 

What are the theories of origin of urobilin? 

* For other conditions causing black urine, see under alkapton, pyro- 
catechin, hydroquinon, phenol, etc. 

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What relation does the amount of urobilin bear to the destruction of 
the blood-pigment in the body? 

In what conditions is urobilin increased ? 

How is urobiiin detected by the pocket-spectroscope? By Heller's 
urophaein test ? What is the value of the latter test ? Describe Harley's 

What two classes of substances represent bile in the urine ? 

How do bile-pigments occur in the urine ? What is their significance ? 

What is the difference between bilirubin and hiliverdinf 

What are the characteristics of a bile-containing urine? What al- 
bumin test should be used in such urines, and why? 

In what conditions does bile appear in the urine ? Describe Gmelin's 
test; Marechal's test; Rosenbach's test. 

What is said of bile-acids in jaundice ? 

In what conditions are bile-acids present in the urine? 

What is Pettenkofer's test for bile-acids? 

What is the appearance of urine containing fresh blood ? Old or de- 
composed blood? 

What coloring-matters Trom the blood may occur in the urine ? How 
do they enter the urine ? 

What coloring-matter is found chiefly in recent hemorrhage ? 

Define hemoglobinuria; hematuria. How does the urine of the first 
differ from that of the second condition? 

When does the hemoglobinuria occur? 

In what diseases is hematuria seen? 

What warning of an impending nephritis do we get in the urine of 
scarlatina ? 

What is the relation of albuminuria to hemoglobinuria in scarlatina? 
In typhoid and other fevers? 

Describe the guaiacum test; the benzidin test; Heller's test; Teich- 
mann's test; the spectroscopic test. 

What is hemaioporphyrin? What is its clinical significance? 

What is melanin, and what does its presence imply? 

What is Zeller's test for melanin ? Von Jaksch's test ? 

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(C«Hi3N02 and C9H11NO3) 

These substances are products of retrograde changes 
of nitrogenous substances, and occur in certain fetid secre- 
tions of the skin, as in the axilla. They can be produced 
from the tissues of some glands, as the liver, pancreas, or 
spleen. They are found in the urine chiefly in diseases in 
the liver, especially in rapidly destructive processes, such as 
acute yellow atrophy or phosphorus-poisoning, and in 
smaller quantities in acute infectious diseases, such as 
typhus and smallpox. These urines always contain a 
large amount of biliary coloring-matter and albumin. 
When present in large amounts, leucin and tyrosin deposit 
spontaneously in the sediment. Leucin and tyrosin usu- 
ally, if not always, occur together in the urine, and although 
some authors claim that they are present in minute traces 
in normal urine, their presence in any urine is very rare. 
The urea is very much diminished in such urines. 

Detection. — If the crystals are not deposited spontan- 
eously, the urine should be evaporated in order to display 
them. If this does not suffice to demonstrate them, the 
method of Frerichs may be used. A large quantity of 
urine is treated with basic lead acetate, filtered, the excess 
of lead removed from the filtrate by sulphuretted hydrogen, 
and the filtrate evaporated to a small volume over a water- 
bath. Tyrosin needles will crystallize in twenty-four 

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hours, but leucin spheres do not appear until later, as 
leucin is much more soluble. If a mixture of leucin and 
tyrosin is extracted with alcohol, the leucin will dissolve 
and leave a more or less pure tyrosin. After separating 
the two in this way the following chemic tests may be ap- 

Tests for Tyrosin. — (i) Hoffmann^s Test. — A bright 
pink or crimson color is produced when a solution of 
tyrosin that has been boiled in an excess of water is heated 
with Millon's reagent. (See p. 80.) 

(2) Piria^s Test. — Tyrosin heated with a few drops of 
sulphuric acid, diluted, and boiled with barium carbonate 
will give a filtrate which strikes a violet color on the addition 
of a dilute solution of ferric chlorid. An excess of iron 
should be avoided, as it destroys the color. 

(3) A hot solution of tyrosin acidified with i per cent, 
acetic acid turns bright red on the addition of a little sodium 

(4) Von Udrdnszky^s Test (Furfurol), — A small crystal 
of tyrosin is dissolved in i cc. of water; one drop of a 0.5 
per cent, solution of furfurol is added. Underlie this 
with concentrated sulphuric acid, keeping the temperature 
of the mixture not over 50° C. The fluid is colored rose 

Tests for Leucin. — (i) A little leucin heated on a 
platinum sheet with a little nitric acid melts and forms an 
oily drop which rolls about on the platinum and does not 
adhere to it. 

(2) On the addition of a trace of quinon and a few drops 
of sodium hydrate to a cold aqueous solution of leucin, a 
deep- violet color appears. (This reaction occurs also with 
certain proteids.) 

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The microscopic appearances of leucin and tyrosin 
crystals are characteristic and will be found described on 
page 267. 


A trace of fat is present in solution in normal urine, and 
abnormal quantities have been found in disease, as in cases 
of chronic nephritis which give fatty epithelium, fatty casts, 
and free oil- drops; in fatty kidney, phosphorus-poisoning, 
and diabetes mellitus, and in cases of cystitis and vaginitis 
in which fatty epithelium is present. 

In chyluria (see p. 2ti) the fat in the urine is in the form 
of a molecular emulsion, while in lipuria it is present in the 
urine in the form of a clear fluid oil. Chylous urine may 
result from leakage of a lymph- vessel into some part of the 
urinary tract, as in filariasis. In this disease the lymphatic 
vessels in the bladder-walls become filled with the embryos 
or mature worms of Filaria sanguinis 2Sid rupture, allowing 
the escape of lymph into the urine. Chyluria may occur, 
however, without the presence of these parasites and without 
definite cause. Fat in the form of oil has been found in the 
urine in pregnancy, fractures of the long bones, eclampsia, 
diabetes, pulmonary tuberculosis, and after large doses 
of cod-liver oil (Roberts); in cystic cheesy degeneration 
of the kidney; in abscesses communicating with the ureter; 
in heart disease, and in calculous disease of the pancreas. 
The admixture of fat from lubricants of catheters or from 
fatty material used in the vagina for examinations must not 
be mistaken for fat in the urine. 

Cholesterin (Cj^H^^O) is a monatomic alcohol, normally 
present in bile, blood-corpuscles, nerve tissues, and else- 
where in the body. In disease it occurs in gall-stones, in 

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pus, in tuberculous and cheesy masses, in old transudates, 
tumors, etc. It may be present in urine under pathologic 
conditions, in such cases as cheesy cystic kidney, but this is 
of very rare occurrence. Extensive fatty degeneration 
of some part of the urinary tract, as subacute or chronic 
nephritis or the fatty stage of acute nephritis, may rarely 
give cholesterin crystals in the urinary sediment. Choles- 
terin crystallizes in large plates, the appearance of which 

Fig. 30. — Cholesterin crystals (Jakob). 

is characteristic (Fig. 30). It is insoluble in water, but 
readily soluble in alcohol, ether, chloroform, etc. Choles- 
terin is detected by means of the microscope. 


Besides the organic substances already described, very small amounts 
of a number of organic bodies may occur in normal urine and are some- 
times increased pathologically. They may be divided into five groups: 

(a) The non-nitrogenous organic acids, e. g.^ oxalic, lactic, succinic, etc. 

(b) The fatty acids, including formic, acetic, butyric, and propionic. 
{c) The aromatic oxyacids — hydroparacumaric and paraoxyphenylacetic, 
etc. (d) Aromatic substances present as ethereal sulphates, e. g.y phenol, 
etc. {e) Ferments. 

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Oxalic acid (CjHjO^) is probably present in very small quantities 
in normal urine. Whenever there is an interference with oxidation in 
the body, as in diabetes, diseases of the liver, heart, or lungs, it may be 

Most of the oxalic acid in the urine exists as calcium oxalate^ a salt 
that crystallizes and is deposited in the urinary sediment when it is present 
in excess. The crystals are described on page 259, where the subject 
of oxaluria is further discussed. 

Lactic acid (CgHgOj) is not found in normal urine, but its salts have 
been found in advanced disease of the liver (acute jrellow atrophy, cir- 
rhosis), in phosphorus-poisoning, in diseases of the muscles (trichinosis), 
and after severe muscular efforts. In the latter case it occurs in the form 
of sarcolactic acid. The detection of lactic acid will be found described 
in the larger text-books. 

Succinic acid (C^H^O^) has been found at times in normal urine, 
usually in combination with sodium. It is increased by eating asparagus. 

Glycerophosphoric Acid (C3H703.PO(OH)2).— A portion of the 
phosphoric acid which is present in the urine in organic combination 
is contained in the nucleic acid of this fluid. (See p. 161.) It is said by 
some authors (Sotnitschewsky, 1880) that another portion of the organic 
phosphoric acid is present as glycerophosphoric acid. The amount of 
phosphoric acid united to organic compounds in the urine is i per cent, of 
the total phosphoric acid, according to Lupine, Eymonet, and Aubert 
(1884). Glycerophosphoric acid is a dibasic substance, syrupy in con- 
sistence, and forms salts soluble in water. 

Benzoic acid (C^HgOj) has been at times found in normal urine, and 
is interesting as the mother-substance of hippuric acid {q. v.). It is in- 
creased by the ingestion of benzoic acid or benzoates, etc., and in decom- 
posing urine it is derived from hippuric acid. In the human body, ac- 
cording to Baumann, benzoic acid is formed from the decomposition of 
proteids in the intestine. 

Chondroi tin-sulphuric acid (CigHg-NOjg-SOg.OH) was found con- 
stantly in normal urine by Moerner (1895). This substance has been 
mentioned when speaking of nucleo-albumin. Moerner considers the sub- 
stance described as nucleo-albumin as a compound of a proteid with 
chondroitin-sulphuric acid, and also with nucleic and taurocholic acids, 
the latter being present especially in urine of jaundice, 

Oxyproteic acid (C^gHgjN^^SOgj) is regarded as an intermediate 
oxidation product of the proteids and is said to be a normal constituent 
of human urine (Topfer, Bondzynsky, and Gottlieb). 

gulphocyanic Acid (CN.SH.); Hydro|;en $ulpbpcyanid.--Accord- 

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ing to Gscheidlen, sulphocyanids occur in normal urine as constant con- 
stituents, 0.035 g"^- o^ potassium sulphocyanid being found per liter. 

Volatile Fatty Acids. — Traces of acetic, butyric, formic, and pro- 
pionic acids have been found in the urine. The amounts grow larger 
during alkaline fermentation, and are increased in some diseases of the 
liver; in fevers; in diabetes (von Jaksch). They have no special clinical 
significance, and are produced by the same conditions that cause aceto- 
nuria. Von Jaksch gave the name lipaciduria to the presence of an in- 
creased amount of volatile fatty acids. 

Aromatic Ozyacids. — Normal urine contains small amounts of 
hydroparacumaric and paraoxyphenylacetic acid in the form of potassium 
salts. These substances are probably products of intestinal proteid de- 
composition, and occur in larger amounts whenever indican is increased. 
Paraoxyphenylglycolic and oxyamygdalic acids are two other substances 
of the same class (Huppert) that have been found in the urine, and still 
another set of acids of this sort are uroleucic and homogentisic (Kirk, 
Baumann and Wolkoff), wh'ich constitute alkaptoriy described separately 
on page 127, on account of its more marked clinical significance. 

Aromatic Substances. — A series of aromatic substances occurring 
in the urine in combination with sulphuric acid are parakresol, pyrocate- 
chin, and hydroquinon. 

Pyrocatechin is said to occur very frequently in urine. These urines' 
are light colored when passed, but become dark on standing or on the 
addition of KOH solution. Hydroquinon occurs in urine after carbolic 
acid poisoning, giving the urine its dark color. It is present as an ethereal 

There are methods for the isolation and quantitative estimation of all 
these ingredients, but these are too complex and not sufficiently import- 
ant to be described here. 

Ferments. — Pepsin and trypsin have been found in urine. Leo 
found that normal urine possesses digestive powers for fibrin, and Neu- 
meister has shown that true pepsin occurs in urine. Trypsin has been 
found by Sahli, though its presence is doubted by some authors. 

Accidental Organic Constituents. — There are a large number 
of organic substances which may be present in urine when they are taken 
internally or absorbed from the skin or mucous membranes. The dis- 
cussion of these belongs properly to pharmacology and toxicology, but a 
few of the more important ones may be mentioned: alcohol, glycerin, 
chloroform, chloral, iodoform, sulphonal, salicylic acid, salol, resorcin, 
guaiacol, thymol, naphthol, copaiba, santonin, aloin, phenacetin, acc- 
tanilid, ahtipyrin, quinin, morphin, etc. 

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What are leucin and tyrosin f When are these substances found in 
the urine? What is their relation to the occurrence of albumin, and of 
biliary pigments and of urea in the urine? What is the frequency of 
their presence in urine? How may the crystals be obtained? Which 
crystallizes first ? How do we separate the two by means of a solvent ? 
What is Hoffmann's test? Piria's test? The furfurol test? What 
is the platinum-foil test for leucin ? 

In what form does jat occur in the urine ? What is lipuria ? 

What is chyluriay and what is it due to? 

In what conditions has fat in the form of oil-globules been found in the 

What extraneous fat must be guarded against in urinary examination ? 

What is cholesterin ? Under what conditions may it be present in the 
urine ? What are its properties, and how is it detected ? 

Name some of the organic acids present in urine? 

Where has phenol been found increased in the urine ? Where pyro- 
catechin ? What ferments occur in urine ? 

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The principal inorganic constituents of the urine are 
the chlorids, phosphates, and sulphates occurring in com- 
bination with sodium, potassium, ammonium, calcium, 
and magnesium. There are also traces of carbonates of 
the alkalis, and also minute quantities of iron, fluorin, and 
silicic acid, as well as free gases, including carbonic acid, 
nitrogen, and oxygen. The total amount of inorganic 
substances excreted in twenty-four hours is between 9 and 
25 gm. 



The chlorids, next to urea, are the chief solid constituents 
of the urine. Most of the chlorin in the urine exists as so- 
dium chlorid, and small amounts are combined with potas- 
sium and ammonium. The chlorids in the urine are 
derived from the food, and most of the salt ingested is 
eliminated in the urine as such. Normally, from 10 to 15 
gm. of NaCl are excreted in twenty-four hours, but if 
salty food is eaten, the amount may reach 40 to 50 gm. 
In starvation the chlorids almost entirely disappear from 
the urine. The tissues need a certain amount of sodium 
chlorid, and if salt-containing food is given after a period of 
starvation, some of the salt is retained in the body until the 
tissue fluids have enough NaCl, when the original equilib- 

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rium is restored. An increased excretion of chlorids takes 
place when large amounts of water are taken. The amount 
of chlorids in the urine is lowered at night and increases 
in the afternoon, especially upon a vegetable diet (Serkow- 
ski). Usually the amount of chlorids eliminated is parallel 
to that of urea, but an exception must be made in excessive 
muscular work, when urea is increased and chlorids are 

Clinical Significance. — The chlorids are diminished 
in all acute diseases, especially those in which there is a 
serous exudation or transudation (dropsy), vomiting, or 

The test for chlorids is, therefore, often of considerable 
clinical value in determining the progress of an exudative 
process or of an effusion into one of the serous cavities. In 
pneumonia the chlorids are very low or even absent in the 
acute stage, but as the exudate becomes absorbed and con- 
valescence sets in, the chlorids increase and may exceed the 
normal for a time. In differentiating between acute menin- 
gitis and typhoid fever this test is also useful, as the serous 
exudation in acute meningitis causes a marked diminution 
in the chlorids, while in typhoid these are only moderately 
diminished. Other acute diseases in which chlorids are 
diminished or absent are cholera, septicemia, pyemia, 
puerperal fever, and acute articular rheumatism. In 
the acute diseases mentioned, especially in pneumonia, a 
persistent decrease of chlorids is of bad prognostic import, 
while an increase is a good omen. The chlorids increase 
rapidly after the crisis in pneumonia. After operations 
Guyon found that a low percentage of chlorids was a bad 
prognostic sign and that patients with very low NaCl in the 
urine (less than i.o per liter) would probably not survive. 

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In chronic diseases ax:companied by dropsy the chlorids 
may be absent from the urine, and if the fluid be absorbed 
they gradually rise to near the normal. When there is 
no exudation or transudation in chronic diseases, the 
amount of chlorids is in proportion to the amount of salt 
in the food — i. e.y the amount of chlorids is a measure of 
the appetite. 

The following table (Serkowski) shows the conditions 
in which chlorids are increased or decreased: 

Chlorids are increased: 

1. After a vegetable diet. 

2. After massage. 

3. After chloroform anesthesia. 

4. In prurigo. 

5. In rickets. 

6. After taking digitalis. 

7. During the absorption of ex- 7. 

udates and transudates. 

8. After the crisis in acute fevers. 8. 

9. In tertian malaria (destruc- 9, 

tion of red cells). 

10. In cirrhosis of the liver. 

11. In poisoning by p3n-ogallol, 

etc. (destruction of red blood- 

Chlorids are diminished: 

1. At night; during repose. 

2. In gastric diseases (insufficient 

3. In fevers, especially lobar pneu- 

4. In nephritis (chronic). 

5. In chyluria. 

6. In cancer (insufficient nutri- 

7. In dropsy, exudates and trans- 
udates. (During the rapid 
formation of these.) 

In many cachexias, in anemia, 

and in starvation. 
In diarrhea or vomiting. 

Detection. — Silver Nitrate Test. — Before applying 
this test, if more than a trace of albumin is present, it 
should be removed by heat, as albuminate of silver forms 
and interferes with the reaction. The test may be applied 
by acidulating the urine in a test-tube with nitric acid, 

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shaking, and adding a drop of a i : 8 silver nitrate solution. 
A solid flocculent mass of precipitate falling rapidly in- 
dicates normal or increased chlorid; a diffused cloudy 
precipitate indicates a diminution. The addition of nitric 
acid is necessary to prevent the formation of silver phos- 

Quantitative Test. — If a more accurate determination 
is wanted, Volhard's method as modified by Salkowski 
should be used (quoted from Boston, Clinical Diagnosis, 
2d ed., p. i8o): 

The reagents required are: 

(i) Pure nitric acid, sp. gr., 1.2. 

(2) Concentrated solution of double sulphate of iron and ammonia, 
free from chlorin (if necessary, free from chlorin by recrystallization). 

(3) Saturated solution of silver nitrate (29.075 gm. of the crystals 
per liter). Of this i.o cc. corresponds to 0.0 1 gm. NaCl. 

(4) Ammonium sulphocyanid solution 6f gm. in enough water to 
make 400 cc. Of this solution 2.5 cc. correspond to 10 cc. of the 
standard silver solution. 

The following method may be employed for standardizing the sul- 
phocyanid solution: 

Ten cc. of the silver solution (3) are placed in a flask and 90 cc. 
of water added. Four cc. of nitric acid (1) are now added, and finally 
5 cc. of the double sulphate solution (2). After the mixture is well 
shaken, the sulphocyanid of ammonium solution is carefully added 
from the buret until a slight red color appears. This process should 
be repeated often, noting each time the quantity of sulphocyanid solu- 
tion necessary and the mean obtained. Based upon these results the 
sulphocyanid solution is diluted to a point so that 2.5 cc. correspond 
to 1.0 cc. of the silver solution. Should the reaction (red color) 
appear after 20 cc. of the sulphocyanid solution are added, the fol- 
lowing formula serves to determine the quantity of water to be added 
to I liter; 

^TT^ 20 ; 25 : : 1000 ; x. .*. {x =5 1250). 

fh^Fefore, 250 cc. of water are added in order that 25 cc. shall cor- 
respond JQ 10 cc, of the gilver §olutiont 

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Method of Testing. — (l) Ten cc. of the urine, previously freed from 
albumin, are placed in a loo-cc. flask. (Il) Fifty cc. of water are 
added. (Ill) Four cc. of the nitric acid (i) are added, and then an 
excess (15 cc.) of the silver nitrate (3) solution. (IV) The mixture 
is thoroughly shaken till the precipitation is completed and the fluid 
begins to clear, and then enough water is added to make 100 cc. 
(V) The resultant mixture is filtered through dry filter-paper into an 
80-CC. flask. (VI) The 80 cc. of fluid obtained are now poured into 
a 250-cc. flask. (VII) Five cc. of the solution of the double sulphate 
of iron and ammonia (2) are added. (VIII) The sulphocyanid 
solution (4) is slowly added from a buret till the end reaction (red 
color) is obtained and does not disappear on shaking. 

The excess of silver solution not needed to precipitate the chlorids 
from 10 cc. of urine is now estimated as follows: Of the sulphocyanid 
solution 2.5 cc. corresponds to i.o of silver solution. Therefore 
should, for example, 12.5 cc. of the sulphocyanid solution be required 
to produce the end reactign, then there were 5 cc. of the silver solu- 
tion not employed in precipitating the chlorids from the 10 cc. of 
urine. Since 15 cc. of silver solution have been added, and 5 cc. 
were found to be in excess, it required 10 cc. of AgNOg solution to 
precipitate the chlorids from 10 cc. of urine. As i cc. of the AgNOj 
solution corresponds to 0.0 1 gm. of NaCl, 10 cc. of the AgNOg solu- 
tion will correspond to o. i gm. of NaCl in 10 cc. of urine, or to i.o 
gm. of NaCl in 100 cc. of urine and of the total output of urine for 
twenty-four hours was 800 cc, the quantity of NaCl excreted in that 
period would be 8.0 gm. 

Purdy*s Centrifuge Method. — This has been described 
in general under the heading of Albumin Tests. The 
percentage tubes of the apparatus are filled to the 10 cc. 
mark with the urine. From 15 to 30 drops of nitric acid 
are added to prevent the precipitation of silver phosphate, 
the amount of acid varying with the specific gravity of the 
urine (the higher the latter, the more acid is used), and the 
tubes are filled to the 15 cc. mark with a 1:8 solution 
of silver nitrate. The tubes are closed and the contents 
thoroughly mixed. The tubes are placed in the standard 
centrifuge and revolved at the rate of 1500 revolutions a 

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minute for three successive periods of five minutes each, 
when the quantity of bulk-percentage is read off on the 
scale of the tube. This bulk-percentage is converted 
into weight-percentage of NaCl with the aid of the follow- 
ing table: 


Normally from \ to 1 per cent.y or 10 to 15 gm. in 24 hours. 


Per Cent. 


Per Cent, 
of NaCl. 

Gram per 


per Ounce 



Per Cent. 


Per Cent, 
of NaCl. 

Gram per 


per Ounce 










■ ; 





1. 1 



\ ■ 





1. 17 


































































































































10. i; I 
















II. 2 








II. 51 


























What are the principal classes of inorganic constituents in the urine ? 

What inorganic substances occur in minute quantities? 

What gases occur in the urine? 

What is the chief group of solids in the urine next to urea? 

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Whence are the chlorids of the urine derived ? 

How much NaCl is eliminated normally in twenty-four hours? 

What eflFect has starvation upon sodium chlorid elimination. In- 
creased amounts of water drunk ? 

What does increase of chlorids mean in diabetes insipidus? 

When are chlorids diminished ? Of what value is this in diagnosis ? 

How does dropsy affect the amount of chlorids ? Absorption of drop- 
sical fluid? 

How are the chlorids estimated approximately? How are they de- 
termined accurately? 

Describe Purdy's centrifuge method for the estimation of chlorids. 

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The phosphates of the urine are derived partly from the 
food and partly from the decomposition of proteids con- 
taining phosphorus, particularly nuclein and lecithin from 
the tissue cells, especially from the brain and nerves. 
Organic phosphorus compounds (from eggs, milk, etc.) 
are much more readily assimilated than inorganic. In- 
soluble compounds of phosphoric acid with earthy salts are 
formed in the intestines and are excreted in the feces with- 
out being absorbed. These compounds are formed 
especially when the diet is rich in calcium (and mag- 
nesium) salts. 

Normally the average excretion of phosphates is repre- 
sented by from 2.5 to 3.5 gm. of phosphoric acid (P2O5) 
in twenty-four hours, or 1.7 to 2.6 gm. per liter. Of this 
amount about two- thirds (2.0 to 4.0 gm. in twenty-four 
hours) are represented by the alkaline phosphates (Na,K), 
while the remaining one-third (i.o to 1.5 gm. in twenty- 
four hours) is derived from the earthy phosphates (Ca,Mg). 

Earthy phosphates are insoluble in water, but soluble 
in acids. In acid urines they occur as a^id phosphates 
in solution, although occasionally a faint precipitate of acid 
calcium phosphate (CaHPO^ -h 2H2O) is seen in acid 
urines. When urine becomes alkaline the acid phosphates 
are converted into normal phosphates and precipitate as 
a heavy, amorphous, whitish sediment. On heating a 
faintly acid, neutral, or alkaline urine (see Albumin Tests), 


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a similar precipitate is often obtained, because this converts 
the acid phosphates into normal phosphates, which are 
precipitated, and into superphosphates, which remain in 

4CaHPO, = CaH,2PO + Ca32PO,. 

The addition of a few drops of acid quickly dissolves 
the earthy phosphate precipitate. When ammoniacal 
fermentation occurs, the ammonia combines with the mag- 
nesium phosphate to form ammoniomagnesium phosphate 
or "triple phosphate." (See Description of Crystals, p. 

Alkaline phosphates are soluble in water and alkalis. 
The sodium compound is chiefly responsible for the acidity 
of the urine (monosodic acid phosphate, NaHzPOJ. 
The alkaline phosphates are more abundant in the urine 
than the earthy, the proportions being usually as twp is 
to one. 

Clinical Significance.— The amount of phosphates in 
the urine varies normally with the amount of food absorbed 
containing phosphorus. On a mixed diet the amount of 
phosphoric acid excreted should not exceed 3.5 or, at most, 
4 gm. in twenty-four hours. Normally the relative pro- 
portion of phosphoric acid to the total nitrogen is from 
17 to 20 : 100 (average 18.9: 100). This ratio p^^^^ is 
known as Ziieltzefs coefficient. 

I. Trti£ Phosphaturia. — A true excess of phosphoric acid excreted 
beyond the normal limit stated above (3.5 to 4.0 gm. in twenty-four hours) 
or an increase in the PjOg as compared to the nitrogen (15 urea = 7 
nitrogen [SahliJ constitutes trtie phosphaturia. This is not a definite 
condition, but merely a symptom that may occur in a variety of condi- 
tions in which there is either (a) an increased amount of phosphorus ab- 
sorbed in the food, or {h) an increased metabolism of the phosphorus- 
containing tissues of the body (brain, nerves, etc.). 

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2. Clinical Phosphaturia, — This is quite a different conditioni and is 
the "phosphaturia" commonly spoken of when no qualification is made. 
This is an apparent increase of the phosphates which is due to a tendency 
on the part of the urine to precipitate phosphatic deposits. This pre- 
cipitation is, in turn, due to a change in the acidity of the urine from acid 
to neutral or alkaline. The change depends either (i) upon alkaline 
fermentation in the urinary tract; (2) upon a lowered acidity as the result 
of a predominantly vegetable diet, or the drinking of alkaline mineral 
waters, or the ingestion of alkaline diuretics, etc. (We have already 
referred to the subject of phosphatic turbidity, etc., on p. 215.) Clinical 
phosphaturia, therefore, does not mean an increase in the amount of 
P2O5. excreted, but a diminished acidity or an increased amount of the 
earthy elements, especially calcium. Naturally, both clinical phospha- 
turia and true phosphaturia may coexist, but this is comparatively rare. 

Clinical phosphaturia is especially typical of neurasthenia. In hysteria 
the proportion of earthy phosphates rises as compared to that of the al- 
kaline phosphates, until the two groups may be as 1:1 (Gilles de la 
Tourette and Cattelineau). 

Phosphatic Diabetes. — This is said to be an independent disease of 
metabolism (Teissier) in which large amounts (30 to 35 gm. P2O5 in 
twenty-four hours) of phosphates are excreted. It has nothing to do with 
true or glycosuric diabetes, but phosphatic diabetes (a badly chosen 
term, because confusing) may lead to or end in diabetes mellitus. 

The following tabular statement sums up the clinical 
significance of changes in the amount of phosphates ex- 
creted. The conditions followed by a question mark are 

Phosphates increased : Phosphates decreased : 

1. In active metabolism. i. In starvation (slightly). 

2. With a diet rich in nuclein. 2. In chronic diseases with lowered 


3. In bone diseases, e. g., rickets, 3. In chronic renal diseases (renal 

osteomalacia (?). insufficiency). 

4. In destructive pulmonary dis- 4. In pregnancy (formation of fetal 

eases, e. g., tuberculosis(?). bones). 

5. In nervous and mental diseases, 5. In gout (may be imchanged). 

e. g.j insanity (mania); neuras- 
thenia; organic nervous dis- 
eases; meningitis. 

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Phosphates increased : Phosphates decreased : 

6. In "phosphatic diabetes" (see 6. In acute yellow atrophy (phos- 

text). phates disappear completely). 

7. After mental strain, excitement. 

8. In diabetes mellitus (proteid 

diet, etc.). 

Detection. — Earthy Phosphates. — Render half a 
test-tube full of filtered urine alkaline with ammonia, and 
warm gently, causing the precipitation of earthy phosphates 
in the form of a whitish cloud that settles to the bottom of 
the tube. The precipitate is dissolved on the addition of 
acetic acid. 

This test may be also made to serve approximately for 
quantitative estimation, according to Ultzmann: A test- 
tube 2 cm. wide is filled with the urine to the depth of 5§ 
cm., and a few drops of strong ammonia are added. The 
mixture is warmed over an alcohol lamp until the earthy 
phosphates separate. The depth of the sediment is 
measured after standing for fifteen minutes. Normally, 
the layer will be i cm. high; a greater depth indicates an 
increase, while a less abundant precipitate means diminu- 

Alkaline Phosphates. — After the earthy phosphates 
have been separated as shown above, the mixture is filtered. 
To the filtrate add one-third of its volume of magnesium 
fluid (magnesium sulphate, ammonium hydrate, am- 
monium chlorid, of each, i part; water, 8 parts). The 
white precipitate consists of alkaline phosphates. To 
make this test available for approximate estimation, ac- 
cording to Ultzmann, 10 cc. of the urine are treated with 
3 cc. of the magnesium fluid. A precipitate of crys- 
talline ammoniomagnesium phosphate is formed, together 

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With an amorphous mass of calcium phosphate. If a 
milky turbidity permeates the entire fluid, the alkaline 
phosphates are normal in amount. If an abundant pre- 
cipitate gives the fluid the appearance of cream, they are 
greatly increased, and if a slight turbidity follows, or if the 
fluid remains transparent, they are decreased. 

Estimation of Total Phosphoric Acid. — The following 
method is based upon the fact that, when a solution of a 
phosphate acidulated with acetic acid is treated with a 
solution of uranium nitrate or acetate, a precipitate of 
uranium phosphate occurs, and when a soluble salt of 
uranium is added to a solution of potassium ferrocyanid, 
a reddish-brown precipitate is formed. The solutions 
required are: 

I. A standard solution of uranium nitrate or acetate, con- 
sisting of 35.5 gm. of pure uranic nitrate or acetate in 
1000 cc. of distilled water. One cc. corresponds to 5 mg. of 
phosphoric acid (phosphoric anhydrid, PzOg).^ As the 
salts of uranium are apt to be contaminated with uranium 
oxid, the following method (Tyson) is recommended in 
preparing the standard uranium solution: 

Dissolve 20.3 gm. of yellow uranic oxid in strong acetic 
acid previously diluted to nearly a liter. To determine 
the strength of the solution place 50 cc. of the standard 
solution of sodium phosphate in a beaker with 5 cc. of the 
solution of sodium acetate and heat on a water-bath to 
90° or 100^ C. The uranium solution is then allowed to 

* Standard solutions for quantitative analysis may be bought already 
prepared, and the rather high prices of these will often appear insignificant 
when the time required in making such solutions at one's office is con- 
sidered. The standard solutions should preferably be made by a com- 
petent pharmacist or analytic chemist, as they require testing by titration 
methods which are often tedious. 

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run from a buret into the warm mixture until precipitation 

Then a drop of the mixture is carried on a glass rod into 
contact with a drop of the potassium ferrocyanid solution 
or a porcelain dish, and if the reddish-brown uranium 
ferrocyanid does not appear, cautiously continue the addi- 
tion of the uranium solution until the eolor responds to the 
test. The quantity used is then read off, being that which 
is sufficient to decompose sodium phosphate corresponding 
to O.I gm. of P2O5. From this is calculated the amount 
of distilled water to be added to make i cc. of the uranium 
solution correspond to 0.005 S^- ^^ phosphoric acid. 

2, Sodium Acetate Solution, — One hundred gm. of 
sodium acetate are dissolved in 900 cc. of distilled water, 
and to this 100 cc. of acetic acid are added. 

3. A saturated solution of potassium ferrocyanid to be 
used as an indicator. 

Method. — To 50 cc. of the urine in a glass beaker add 
5 cc. of sodium acetate solution, and warm the mixture 
over a water-bath to 80° C. Drop the standard solution 
of uranium from a buret into the hot urine slowly, as long 
as the precipitate forms, or until a drop of the mixture, 
removed by means of a glass rod and placed on a portion 
of the plate, gives a distinct brown color with a drop of the 
indicator. This point indicates the end-reaction; the 
number of cubic centimeters used is read off and, multi- 
plied by 0.005, gives the amount of phosphoric acid in 50 cc. 
of urine, from which the quantity in twenty-four hours is 
calculated. The end-reaction, shown by the brown color 
on the porcelain dish, takes place when the uranium solu- 
tion has precipitated all the phosphoric acid and the mix- 
ture in the beaker contains pure uranium. 

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Cochineal tincture is also used instead of potassium 
ferrocyanid as an indicator. A few drops of it are added 
to the urinie before heating, and the standard uranium 
solution is added until a faint but distinct and permanent 
green color appears^that is, until all the phosphoric acid 
has been precipitated and there is a slight excess of 

Phosphoric Acid with Earthy Phosphates. — To 
determine phosphoric acid which is in combination with 
lime and magnesia, 200 cc. of urine are treated with am- 
monia, the precipitate is collected after twelve hours on a 
filter, and washed with ammonia water (1:3). The filter 
is broken at its point, the precipitate washed into a beaker, 
and dissolved while warm with as little acetic acid as pos- 
sible. Add 5 cc. of sodium acetate solution, dilute to 50 
cc, and treat as in the preceding method. The difference " 
between the total phosphoric acid and that combined with 
the earths represents the quantity combined with the 

Purdy's Centrifugal Method. — Fill a Purdy centrif- 
ugal percentage tube to the 10 cc. mark with the urine 
and add 2 cc. of 50 per cent, acetic acid, shake, and add 
3 cc. of a 5 per cent, solution of uranium nitrate. The 
tube is closed, inverted several times until the urine and 
reagent are well mixed, allowed to stand for three minutes 
to secure complete precipitation, placed in the Purdy cen- 
trifuge (a centrifuge with an arm measuring 6f inches is 
essential), and made to revolve at the rate of 1500 revolu- 
tions a minute for three minutes. The bulk-percentage of 
uranyl nitrate is read at the level of the precipitate and is 
converted into the corresponding per cent, of P0O5 (by 
weight) by the use of the following table, which is that 

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of Purdy, with the addition of a column showing the num- 
ber of grams of PjOg per liter of urine. 

Purdy's method is a rapid and convenient one, and is 
sufficiently accurate for comparative clinical estimations: 


Normally: 0.17-0.26 per cent.y PzO^; or 1.7-2.6 grams per liter ; or 
2.5-3.5 grams in twenty-four hours. 

Per Cent. 


Per Cent. 


per Liter 



per Ounce 


Per Cent. 


Per Cent. 


per Liter 



per Ounce 




























































































1. 00 







0.1 1 

1. 10 























What is the origin of the urinary phosphates? In what amounts is 
P2O5 normally excreted? 

In what condition is the amount of phosphoric acid increased? 

What is phosphaturia ? What is clinical phosphaturia ? True phos- 
phaturia ? 

What is phosphatic diabetes? 

When is phosphoric acid diminished in the urine? 

How do you detect and approximately estimate earthy phosphates? 
Alkaline phosphates ? Total phosphoric acid ? 

What is the most rapid clinical method for the latter? 

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The sulphates of the urine are derived from two sources: 
(i) The food; (2) the tissues whose proteid molecules bum 
up, giving up their sulphur contents. 

The sulphates in the urine occur in three distinct forms 
of compounds: 

(i) The mineral or preformed sulphates, which occur as 
compounds of Na, K, Mg, and Ca; (2) the conjugate, 
ethereal, or aromatic sulphates, indol, skatol, phenols 
(cresol, pyrocatechin, hydroquinon), occurring usually as 
K or Na salts of the ethereal sulphates; and (3) the neutral 
sulphates (incompletely oxidized sulphur) — e. g., cystin, 
taurin, thiosulphates, sulphocyanids, etc. 

The relations between each of these groups and the total 
sulphur in the urine is shown by the following table from 

Total sulphur 

Acid sulphur 
80 to 86 per 

Neutral sulphur 
sulphur, 1 4 to 
20 per cent.). 

1. Preformed (mineral) sulphates. 

2. Conjugate (ethereal, aromatic) 
sulphates (nominally one-tenth of 
total sulphates). 

Cystin, taurin, thiosulphates, sulpho- 
cyanids, etc. 

The mineral or preformed sulphates of the food form a small part of the 
total sulphur excreted in the urine. The bulk of the urinary sulphates is 
derived from the metabolism of proteids, both from food and tissues. It 
is not surprising to find, therefore, that the excretion of total sulphur 
varies usually as the excretion of nitrogen (the ratio of H3SO4 to N. being 


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normally 1:5), and that this ratio is a fairly constant one. [About four- 
fifths of all the sulphur in albuminous food is excreted in the urine, but 
some foods give ofiF more sulphur than others, the average being i per 
cent, sulphur, so that 100 gm. albumin in food give off 2.5 gm. HjSO^ in 
twenty-four hours.] 

The total sulphate otUput is, therefore, an index to proteid metabolism 
(though not as accurate as the nitrogen output). The amount of total 
sulphates by itself has little clinical value, but is useful in determining 
the diflferent sulphate groups by subtraction (see below). Normally the 
total sulphur, as SO3, is equivalent to from 1.5 to 3 gm. in Iwenty-four 
hours (= 2.5 gm., average, HaSOJ on a mixed diet. 

The total sulphates are increased in all conditions tending to increase 
proteid metabolism, and diminished in the reverse conditions. The 
following table sums up the principal causes of total sulphur variations: 

Total sulphates increased : 

Total sulphates decreased : 


On a meat diet. 


On a proteid-free diet. 


After exercise. 


In diminished metabolism. 


In fevers. 


In convalescence from fevers. 


In acute diseases. 


In nephritis (usually varies as 
urea). ' 


In acute articular rheumatism. 


In jaundice (relative increase of 
neutral sulphur, taurin, etc.). 


In chorea. 


In rickets (?). 


In diabetes mellitus (meat diet). 


In anemia, cachexia. 


In acute gastro-enteritis. 


In many skin diseases, e. ^., 

The ethereal sulphates (conjugate sulphates, aromatic sulphates) have 
received partial consideration under the heading of Indican, etc. (p. 174). 
The constitution of these compounds is illustrated by the following graphic 

/OH .OH 


^OH ^ORi 

HgSO^ = Sulphuric acid. Ethereal sulphate. 

The ethereal sulphates are, therefore, compounds of sulphuric acid in 
which an aromatic radicle is substituted for one of the hydrogen atoms. 
The principal compounds of this group are indol (the source of indican), 
skatol, phenol, cresol, pyrocatechin, and hydroquinon. They occur in 
the urine as the potassium or sodium salts of the corresponding ethereal 

^ R = aromatic radicle in ethereal sulphates. 

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sulphates. This means that the remaining H atom in the above graphic 
formula is substituted by an atom of K or Na. Indol and skatol, further- 
more, are not excreted as such, but after oxidation, as indoxyl and ska- 
toxyl respectively. The potassium salt of the ethereal sulphate of indoxyl 
(clinically known as indican) has been the following graphic formula: 

/b . K 


\0 . CsH^N 
Indoxyl-potassium sulphate (indican). 

The ratio of ethereal sulphates to the total sulphates is said to be i : lo; 
but this is not at all constant, and this ratio has no clinical value, for the 
simple reason that the total sulphates represent largely albumin-break- 
down in food and tissues, while the ethereal sulphates represent largely 
intestinal decomposition and putrefaction. The absolute amount of 
ethereal sulphates is of greater clinical value, and corresponds to from 
0.15 to 0.3 gm. of SO3 in twenty-four hours. 

The amount of ethereal sulphates may be considered as a quite accu- 
rate indication of the degree of intestinal putrefaction. The following 
table* shows the principal causes afifecting the amount of ethereal sul- 
phates excreted: 

Ethereal sulphates increased : Ethereal sulphates decreased : 

1. By a rich meat diet; by eating i. Starvation; milk diet (casein [?] 

putrid food. inhibits intestinal putrefac- 


2. After taking drugs furnishing 2. After taking calomel or other 

phenol and other aromatic intestinal antiseptics, 


3. In constipation (not constant). 3. In acute intestinal catarrh. 

4. In chronic intestinal catarrh and 4. After acid (HCl) medication ; in 

conditions accompanied by hyperchlorhydria, and a diet 

same. (Carcinoma of liver; rich in NaCl. 

acute yellow atrophy, etc.) 

5. In typhoid fever, tuberculous 

enterocolitis, peritonitis, chol- 

6. After alkaline medication ; in 

hypochlorhydria, and a diet 
low in NaCl. 

* Arranged by the author from data furnished by Emerson, Clinical 
Diagnosis, 1908, p. 139. 


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The neutral sulphates (suboxidized or unoxidized organic sulphur) 
constitute from 14 to 20 per cent, of the total sulphur in health. The 
exact mechanism underlying the failure of this sulphur to become oxi- 
dized is obscure, but normally the neutral sulphur in the urine is derived 
chiefly from (i) the bile (taurocholic acid partly reabsorbed from bowel); 
(2) the saliva (sulphocyanids reabsorbed from bowel); (3) the putrefac- 
tion of albumin in the intestine, and (4) the incomplete oxidation of tissue 
albumins (Croftan). 

Pathologically there may be an increase of neutral sulphur compounds 
in a number of conditions, the exact reason not being understood as yet 
in some of them. 

Neutral sulphur is increased in inanition, in asphyxia, dyspnea (de- 
ficient oxidation). It is said to be increased after muscular fatigue and 
as a result of tissue waste, and after the ingestion of sulphur and its 
compounds, e. g., sublimed sulphur, sul phonal, and also after taking 
chloral and inhaling chloroform. Large amounts of neutral sulphates are 
excreted in some febrile conditions, such as pneumonia and typhoid (in 
the latter, thiosulphates have been found). 

The biliary origin of neutral sulphur (taurin, taurocholic acid) ac- 
counts for its increased elimination in jaundice (sometimes as high as 
60 per cent, of total sulphur) and in biliary stasis (gall-stones, diseases 
of the liver, bile-ducts, etc.). (Neutral sulphur is diminished in bile- 
fistula.) A special condition known as cystinuria^ in which neutral sul- 
phur is markedly increased, will be discussed on page 268. This condition 
seems to be an unaccountable metabolic freak, the chief interest of which 
clinically lies in the danger of possible formation of cystin stones. 

Detection. — For ordinary purposes the following test 
is sufficient: To 10 cc. of filtered urine add about 3 cc. 
of barium solution (barium chlorid, 4 parts; concentrated 
hydrochloric acid, i part; distilled water, 16 parts), a little 
at a time, shaking after each addition. When less sul- 
phates than normal are present the fluid shows opalescence; 
when normal, it becomes opaque, milky; when in excess, it 
grows thick and creamy. The precipitate normally fills 
one-half of the concavity of the test-tube. 

Quantitative Determination of Total Sulphates. — 
(a) Purdy*s Centrifugal Method. — A convenient clinical 

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test for determining with a fair degree of accuracy the 
total sulphates is that of Purdy. (Compare: Phosphates, 
Chlorids, Albumin.) A graduated centrifuge tube is filled 
to the 10 cc. mark with urine; 5 cc. of a solution of 
barium sulphate are added. The solution is made up of 
4 parts barium chlorid, 16 parts distilled water, i part 
HCI. Mix the contents of the tube well, inverting several 
times, and allow to stand for about five minutes, and centri- 
fuge at a uniform speed of 1500 revolutions per minute for 
three minutes, employing a centrifuge with standard arm- 
length of 6J inches. The bulk-percentage of BaS04 is 
read oflf on the tube. The following table shows the equiv- 
alents in weight-percentage of SO3, in grams per liter, and 
in grains per ounce. 

Normally : 0.1-0.2 per cent.^ or 1-2 grains per liter 


Per Cent. 


Per Cent. 


per Liter 



pci Ounce 



Per Cent. 


Per Cent. 


per Liter 



per Ounce 
























































































1. 21 



(&) The gravimetric method, according to Salkowski, consists in 
weighing the precipitate of barium sulphate, obtained by adding barium 

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chlorid to a known volume of urine. Fifty cc. of diluted or filtered urine 
are acidified in a beaker with 5 cc. of hydrochloric acid and heated to 
boiling for about fifteen minutes to break up the. ethereal sulphates. 
Barium chlorid is then added until no more precipitation occurs. The 
precipitate is collected on a small filter the weight of whose ash is known, 
and washed with hot distilled water imtil no more barium chlorid is found 
in the filtrate — i. e., until the filtrate remains clear after the addition of a 
few drops of sulphuric acid. The precipitate is washed with hot alcohol 
to remove resinous matter and then with ether. The filter is removed and 
burned with its contents in a platinum crucible. It is cooled over sul- 
phuric acid in a drying-oven to 100° C, weighed, and the weights of the 
crucible and filter-ash are deducted.* The remainder is the weight of 
the barium sulphate formed, from which the sulphuric acid is calculated 
as follows: One hundred parts of barium sulphate correspond to 34.33 
parts of SO3. 

Quantitative Estimation of Ethereal Sulphates. — Mix 100 cc. of urine 
with an equal volume of alkaline barium chlorid solution (BaCl saturated 
solution, I part; BaOH saturated solution, 2 parts) in a beaker, stir well, 
allow to stand for ten minutes, and filter until the filtrate reaches 100 cc. 
Add dilute HCl J;ill strongly acid and boil on a water-bath till all the 
BaSO^ precipitate has been deposited, leaving supernatant liquid clear. 
Filter ofiF this sediment; wash on the filter with distilled water, dry, and 
weigh. Multiply the weight by 2 to get the amount of ethereal sul- 
phates in 100 cc. of urine. 

Quantitative Determination of Preformed or Mineral Sulphates. — The 
amount of preformed sulphates is obtained simply by subtracting the 
quantity of ethereal sulphates from that of total sulphates. (The presence 
of preformed sulphates is demonstrated qualitatively by acidifjdng some 
urine in a test-tube with acetic acid and adding BaCl solution, see above, 
p. 226.) 

Quantity of Neutral Sulphur. — The amount of total sulphur is deter- 
mined and from this the amount of total sulphates (total sulphuric acid, 
see above) is deducted, giving the amount of neutral sulphur. To deter- 
mine the total sulphur the following method is used: 

Fifty cc. (25 cc. if there is cystin) of urine are evaporated to dryness in 
a silver crucible. To the residue is added a mixture of potassium nitrate 
4 parts, sodium carbonate i part (chemicals to be free from sulphur), 

* To correct for a slight error due to the formation of a small amount 
of barium sulphid, a few drops of pure sulphuric acid are added after the 
platinum crucible has cooled, thus converting the sulphid into sulphate. 
Heat again to redness to drive off the excess of sulphuric acid. 

Digitized by VjOOQIC 


and the resultant mass burned till white. The residue is thoroughly 
washed out with water and the watery solution carefully poured into a 
porcelain dish. In this the fluid is evaporated three times, adding HCl 
each time. The HCl is added to take up the nitric acid, all of which 
must be removed. The residue is dissolved in water and allowed to 
stand to see if any AgCl separates. If it does, filter (Emerson). In 
the filtrate the neutral sulphur is precipitated by adding BaCl. The 
precipitate of BaSO^ is filtered out, dried, and weighed, as described 
under total sulphates. 


Minute quantities of carbonates and bicarbonates of 
sodium, ammonium, calcium, and magnesium are found in 
fresh urine of alkaline reaction. Ammonium carbonate 
may occur in large amounts, owing to alkaline decomposi- 
tion. The carbonates in urine are derived from the food, 
especially from vegetable acids, such as lactic, tartaric, 
malic, succinic, etc. 

They are, therefore, most abundant in the urine of her- 
bivora. An excess of carbonates renders the urine turbid 
when passed or on standing, and, as a rule, the sediment 
is mixed with phosphates. 

. Detection. — On the addition of an acid the presence of 
carbonates is detected by the evolution of gas-bubbles, and 
this gas, when passed into baryta water, renders the latter 
turbid. The determination of the amount of carbonic acid 
will be foimd described in the larger text-books. 


Gases in the Urine. — One liter of human urine normally yields about 
100 to 200 cc. of gases, which consists of from 83 to 95 volumes of COj, 
0.5 volume of oxygen, and from 6 to 16 volumes of nitrogen. These 
gases exist in solution and are separated by means of a vacuum-pump. 
They have no clinical significance. 

Iron. — Traces of iron are found in the residue of urine after evapo- 
ration. The amount in a healthy urine varies between 0.003 ^^^ 0.00 11 
gm. in a liter. The exact combination in which iron occurs is still un- 

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known. The presence of iron is detected from the ash of the evaporated 
residue, which is dissolved in a little hydrochloric acid, and the solution 
divided into two parts: the first part is boiled with a drop of nitric acid 
and treated with some potassium sulphocyanid solution, which produces 
a blood-red color in the presence of ferric oxid. The other half of the 
solution is boiled with nitric acid and diluted. On addition of potassium 
ferrocyanid a precipitate of Prussian blue is formed after standing a 

Hydrogen Peroocid. — Schonbein found this substance in the urine in 
very small amounts, but so far as is known it has no significance. Dilute 
indigo solution is bleached by hydrogen peroxid in the presence of a solu- 
tion of iron sulphate. The urine must be perfectly fresh. 

Fluorin. — Hydrofluoric acid was discovered in urine by Berzelius 
(London, 181 2), but occurs in urine only in faint traces. Berzelius 
found enough, however, in a considerable volume of urine to etch lines 
on a glass plate. 

ThiostUphuric acid does not normally occur in human urine (Sal- 
kowski, Presch), but was found in a case of typhoid fever by Strumpell. 
It is present in the normal urine of cats and dogs. Its isolation and de- 
tection will be found described in Neubauer and Vogel, 1898, page 20. 

Hydrogen sulphid (sulphuretted hydrogen) is rarely present in freshly 
passed urine. It is not found in diseases accompanied by putrefaction, 
after the ingestion of sulphids, or after sulphur baths. It may pass 
into the urine through a rectal fistula. The chief importance of this gas 
lies, however, in the fact that it is formed during decomposition of purulent 
urine (pyelitis, cystitis). Hydrogen sulphid putrefaction has been 
ascribed (Miiller, von Jaksch, etc.) to a special coccus, and, according 
to Salkowski, the unoxidized sulphur of albumin is the source of this 
sulphid in albuminous urine. The presence of hydrogen sulphid may be 
detected by its odor (see Odor of Urine, p. 28) and by hanging in the acid 
urine a strip of blotting-paper moistened with lead acetate solution and 
then with a drop of NaOH solution. The paper turns black, owing to a 
deposit of lead sulphid. 

Silicic acid is present in normal urine in minute traces, and presents 
no clinical interest. 

Nitric and Nitrous Acids. — According to Wulffius and Schonbein 
every normal urine contains small amounts of nitrates derived from food 
and drinking-water. Nitric acid was found in traces in normal urines 
freshly passed, while nitrous acid occurs in urines after long standing, 
through the reduction of nitric acid. It disappears as putrefaction in- 

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A number of inorganic substances may be present accidentally in the 
urine, which may otherwise be normal or may show evidences of disease. 

Metals. — Mercury, arsenic, antimony, lead, silver, thallium, cadmium, 
and lithium have been found in urine under various circumstances. The 
study of their absorption, elimination, and detection belongs to toxicologic 

Halogens. — lodids and bromids appear in the urine after they have 
been taken internally. They are of sufficient clinical interest to merit 
a few words as to their detection. 

When the nitric acid test for albumin is performed, the elimination of 
iodin may be detected by the appearance of a reddish-brown zone (free 
iodin) at the border-line between urine and acid, the brown color gradually 
spreading downward into the acid. 

lodids are detected by adding chloroform to urine, then a few drops 
of yellow HNO3, and shaking. The acid sets free the iodin and the 
chloroform becomes pink or purple. 

Bromids are detected in the same manner, but more of the acid is added, 
and the chloroform is tinted a brownish-red. 


What varieties of sulphates are present in the urine ? 

What is meant by "preformed sulphuric acid"? 

What is "conjugate sulphuric acid" ? How much is excreted daily in 
health? What is meant by "neutral sulphur"? 

Whence are sulphates in the urine derived ? 

What is the clinical significance of sulphates? With what other 
constituents do they run parallel usually? 

When are sulphates increased ? Decreased ? 

Describe the ordinary test for sulphates. 

How is total sulphuric acid determined ? What methods are used for 
determining the amount of ethereal sulphates ? The preformed sulphates ? 
The neutral sulphur? 

What carbonates are found in fresh urine? In decomposing urine? 
Whence are they derived? 

What is a simple test for carbonates? 

How is the presence of iron detected? 

In what amounts does healthy urine contain iron? 

How is hydrogen peroxid in the urine detected ? 

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Concretions are termed sand, gravel, stones (or cal- 
culi), according to their size. They are either primary or 
secondary. Primary concretions are deposited from urine 
that has undergone no decomposition, either as a result of 
an excess of some normal constituents or as the result of 
some foreign additions to the urine. Secondary concretions 
are due to decomposition of the urine with the resulting 
precipitation of compounds of ammonia, etc., produced 
by such decomposition. 

The classification into primary and secondary is, how- 
ever, not practical and has no clinical value, as the pres- 
ence of decomposition, inflamimation, and suppuration in 
the urinary tract can always be detected from other ele- 
ments in the examination of the sediment. 

The most common calculi are those of — (i) Uric acid and 
its compounds; (2) calcium oxalate; (3) mixed phosphates. 
Rarer forms are made up of calcium carbonate, xanthin, 
cystin, and urostealith. Besides the urinary calculi, there 
are prostatic calculi and fibrin or blood concretions. 

Uric-acid calculi are the most common. They are 
brown or some shade of red, usually smooth, but may be 
irregular. They leave only a trace of residue after igni- 

Calcium-oxalate calculi are quite common; are usually 
dark brown or dark gray, typically irregular, with more or 
less sharp points, and are sometimes called "mulberry 

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On Heating the Powder on Platinum Foil, it 

Does not burn 

The fwwder when treated with HCl 

Does not effervesce 

The gently heated powder 

• -ici 

with HCl 

The powder when 
moistened with a little 

(0 a" 









*< D 





P9 O 


o {» 

c o 

■O S3 



Does burn 

With flame 










X 3 














»> ^ 






p •-< 

































Without flame 


3 CO 



The powder 
gives the murex- 
id test 

The powder 
when treated 
with KOH gives 


Digitized by VjOOQIC 


calculi." They may be small and smooth ("hemp-seed 
calculi"). They give a considerable residue after ignition 
and are soluble in acids without effervescence. 

Mixed- phosphate calculi or " fusible calculi " consist of 
calcium phosphate and of triple phosphates of ammonium 
and magnesium. Phosphates may form the outer layers 
of other calculi of various compositions, but rarely form 
the nucleus of a calculus alone. Mixed-phosphate calculi 
are white, very brittle, melt in the blow-pipe flame, and 
are soluble in acids, but insoluble in alkalis. 

As a rule, calculi are of mixed composition if large in size, 
and show on section several concentric layers around a 
nucleus. The latter may consist of a foreign body, organic 
matter, such as blood-clots, or of a dense mass of calcium 
oxalate or uric acid. 

Analysis of Calculi. — A portion of the calculus 
should be powdered, and when the stone is of any size it 
should be sawed across, so that each layer may be ex- 
amined separately. A portion of the powdered calculus 
is exposed on a platinum foil to dull-red heat for a consider- 
able time. The table on p. 233 from Heller is a conve- 
nient guide to the examination of calculi. 

What designations are applied to concretions according to their size ? 
What are primary concretions? Secondary? 
What are the most common varieties? Name some rarer forms. 
Describe uric-acid calculi ; calcium-oxalate calculi ; mixed-phosphate 

What do most calculi show on section ? 
How is a calculus prepared for analysis? 

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The microscopic examination of urinary sediments 
should form part of the routine analysis, and should sup- 
plement the chemic tests. Very often the microscopic 
findings give more important clues as to the clinical con- 
ditions present than does the chemic analysis. 

The microscopic examination should be made as soon as 
possible after the urine has been voided. On standing, 
decomposition and fermentation take place, which alter 
the microscopic picture materially. The most important 
change which occurs in urine on standing, however, is the 
disintegration of casts, epithelia, etc. A specimen of urine 
should never be violently shaken, as this also contributes 
to the breaking up of casts and other delicate structures. 


By Gravity. — This consists simply in placing the urine 
in a suitable glass, covering with a glass plate in order to 
keep out dust and foreign matter, and allowing to stand, 
preferably in a dark cool place, for about twelve hours. 


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The edges of the glass should be ground flat and the cover 
should be made of ground glass. 

The time required for the urine to settle is a serious 
objection to this method, and the decomposition which 
the urine undergoes on standing so long renders it unfit 
for microscopic examination. Casts may become disin- 

F^g- 3^' — Urine or sediment 

Fig. 32. — Hand centrifuge. 

tegrated, chemic deposits altered and dissolved, and cells 
may change beyond recognition in decomposing urine. In 
order to prevent this, the addition of a crystal of thymol 
or of a small quantity of saturated solution of boric acid or 
a drop or two of formalin may be added to the urine. Of 
these, thymol is as satisfactory as any other preservative, 

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but some workers prefer chloral, salicylic acid, chloroform, 
etc. The writer would warn against the use of formalin, 
especially in excessive quantities, as it seriously interferes 
with the examination (see p. 24). 

Centrifugal Method.— For accurate work, the use of a 
centrifuge for obtaining urinary sediments is almost in- 
dispensable. In this method the urine is placed in glass 

33. — Ball-bearing water- 
motor centrifuge. 

Fig. 34. — The Purdy electric cen- 

tubes which are drawn out to a point, and revolved at 
high speed in a centrifugal apparatus, thus depositing all 
solids at the bottom of the tube in a few minutes. Imme- 
diate microscopic examination is then possible, and not only 
is there no danger of decomposition, but the sediment is 
more concentrated, and thus one is sure to have all the 
elements deposited, irrespectively of the specific gravity of 
the urine or the character of the sediment. 

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The simplest centrifuge is operated by hand (Fig. 32) 
and is satisfactory for ordinary purposes when only a 
few examinations are to be made daily. It gives a speed 
of 3000 revolutions a minute at the maximum. A water- 
power centrifuge which can be con- 
nected to the ordinary faucet is an 
excellent form of this apparatus 
(Fig. 33) . It is very easy to operate, 
giving a smooth and rapid motion 
without much noise, and its price is 
moderate. The most satisfactory 
centrifugal machine is operated by 
electricity. There are numerous 
types, but Purdy's electric centri- 
fuge (Fig. 34) is unquestionably the 
most serviceable. It can be oper- 
ated either by batteries or with the 
street current, and is capable of all 
grades of speed, from 500 to 10,000 
revolutions a minute. With this 
centrifuge from three to five minutes 
are sufficient to precipitate all the 
elements of a sediment, and ap- 
proximately the same time is re- 
quired with the simpler centrifuges 
worked by hand or water power. 
Purdy's apparatus has arms of such 
lengths that the tips of the tubes describe a circle of a 
standard diameter of 13^ inches (Fig. 34), and can also 
be used for quantitative estimations of chlorids, etc., that 
have been described in previous chapters. All these 
centrifuges have aluminum shields which carry the glass 

Fig. 35. — Purdy's tubes 
for the centrifuge: a, Per- 
centage tube; bf sediment 

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tubes and are supported on elastic cushions to prevent 
breakage during rotation. The tubes hold about 15 cc. 
each, and are made either plain or graduated (Fig. 35). 
It is important that a worker who examines urine 
should become accustomed to using one centrifuge at a 
certain rate of speed for a certain length of time, so as to 
be able to compare the relative amounts of sediment 
and the relative proportions of the microscopic elements 
thereof in different specimens. A great difference as re- 
gards these points will be noted if different speeds are 
used for different lengths of time, or still more if the 
gravity method be used for some specimens and the 
centrifuge method for others. 


The sediment having been obtained in one of the ways 
described, a drop of it is drawn into a pipet and deposited 
on a slide. The pipet should consist of a simple glass tube 
J inch in diameter, drawn to a fairly fine point at one end. 
The opening at this end must not be too small, lest the tube 
be clogged. The upper end may have smoothed or ground 
edges, as the worker prefers. In drawing up the necessary 
sample of the sediment the pipet is to he held in the right 
hand, with the index-finger closing the upper opening 
firmly. It is passed into the urine glass or centrifuge tube, 
and should almost touch the bottom thereof, then be slowly 
withdrawn, the pressure of the index-finger being gently re- 
laxed until the upper stratum of the sediment is reached. 
In this way the pipet will contain parts of every layer of the 
sediment. It must be remembered that the elements of a 
urinary deposit are thrown down in a certain order, the 
lightest coming last. Casts, mucus, and the smaller cells 

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are among the lightest elements. The sediment is often 
so dense that it is better to dilute it slightly with a few drops 
of urine, which are allowed to get into the pipet from the 
supernatant portion. After depositing the sediment 
upon the slide, the pipet should not be blown out with the 
mouth, as is commonly done. It should be preferably 
at once immersed in a solution of liquid soap and cresol 
and then rinsed in running water. A cylinder with the 
antiseptic solution mentioned can be kept for cleansing 
such pipet. Urine frequently contains typhoid bacilli 
and other pathogenic germs, and after the top of the pipet 
has 'been closed with the finger which has previously 
handled urine, the mouth should not be applied to the glass 
tube. Nipple pipets may be used, but are not so con- 

Two or three slides should be in readiness, perfectly 
clean and free from grease and scratches. [Slides should 
be immersed at once after using in a solution of antiseptic 
soap in a wide-mouth glass-stoppered jar. They can be 
used over and over again (till they become scratched) for 
examining urine sediments and before using need only be 
rinsed in hot water and thoroughly dried on a soft cloth. 
The soap solution should be frequently renewed. For 
bacterial work (staining) slides should be taken out of the 
soap solution and washed with distilled water and then 
with alcohol, and passed through a flame repeatedly before 
applying the sediment.] 

The sediment is deposited at first in the center of the 
slide and then spread in as thin a layer as possible over the 
entire slide by means of the pipet held flat against the glass. 
If too much urine is on the slide, the mass of fluid will bulge 
on account of the power of cohesion, which confines it to the 

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glass surface. In such cases it is better to drain oflf a drop 
or two from the slide, and so secure a thin layer of urine. 

The next step is to place the slide on the stage of the 
microscope and to examine its entire surface with a low- 
power objective. 

The low power enables one to search systematically, pref- 
erably with the aid of a mechanical stage, the surfaces 
of several slides in a few minutes, and suffices to detect all 
the larger elements, including casts, crystals, large epithelia, 
and pus. The higher power (Leitz No. 7) should be used 
only for the minute study of casts, renal cells, and red blood- 
cells, etc. The exclusive use of the liigh power frequently 
makes one miss casts and other important elements which 
are found on a general survey with the low power. 

In using high power (No. 7 Leitz or J Bausch and 
Lomb) a drop of the sediment is placed on the center of 
the slide and is carefully covered with a clean cover-glass. 
The excess of fluid must be absorbed with filter-paper, 
as the cover-glass should rest firmly, not float, on the 

In searching for casts the fine adjustment should be kept 
constantly changing by very slight turns of the screw. 
This brings different planes of a cast into view, and as casts 
are cylindric and often twisted, some parts are brought into 
focus in one position of the screw, while others are not seen 
until the focus is changed. If strong diffuse white light 
is available, the search for casts is facilitated by the use of 
the flat mirror; the reduction of the diaphragm aperture to 
the minimum, and the elimination of the Abbe condenser. 
In this way the faintest hyaline casts become visible. 
Ordinarily, however, the concave mirror and the Abb^ 
condenser may be used for urinary examination by workers 

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who must content themselves with the comparatively 
uncertain light available in a large city. 

As regards the microscope, no description is here needed, 
as the student is supposed to be familiar with its features. 
For urinary work a moderate-sized microscope of medium 
price is sufficient, and the objectives most useful are the 
Leitz's No. 3 or Zeiss' objective AA for low power, while 
Leitz's No. 7 or Zeiss' objective D is sufficient for the higher 
magnifications. An oil-immersion objective of ^ inch 
diameter is not absolutely essential, but is necessary in 
bacteriologic work in connection with urinalysis. 

The microscopes made by Bausch and Lomb and by 
Spencer are excellent for urinary work, and may be had at 
lower prices than the corresponding imported instruments. 
In these instruments eye-piece I, and objectives § inch and 
J or J inch are the most useful for urinary work. 

In microchemic reactions, as in testing pus-cells with 
iodin or acetic acid, a drop of the reagent should be 
dropped close to one edge of the cover-glass, and drawn 
under the latter by applying blotting-paper to its opposite 


In order to preserve a sediment we must prevent de- 
composition, the growth of bacteria, and other changes. 
This is done by allowing the sediment to settle thoroughly 
and by washing it in such media as will remove the soluble 
urinary constituents. 

Crystalline sediments may be most conveniently and almost in- 
definitely preserved by the dry method recommended by A. S. Del^pine. 
The sediment is first washed by placing the urine in a centrifuge tube, 

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thoroughly centrifuging the deposit, decanting the fluid portion, filling 
the tube with distilled water, and centrifuging again. The process of 
washing and centrifuging is repeated three or four times till all soluble 
parts of the urine have been removed. The sediment is then dried at a 
temperature below 40° C. on a water-bath. (If the sediment is insoluble 
in alcohol, it may first be washed in absolute alcohol and then quickly 
dried with moderate heat.) The dry sediment may be kept in sealed glass 
tubes. When needed for microscopic examination it may be mixed 
with a drop of water and covered with a cover-glass. In this way phos- 
phates, calcium oxalate, uric acid, cholesterin, cystin, hematin, indigo, 
calcium carbonate, urates, etc., may be preserved. 

The dry sediment may also be mounted in Canada balsam. This is 
done by placing a drop of water on a cover-glass, mixing a little dry sedi- 
ment, and drying in the air. As soon as dry, the cover-glass is placed face 
downward upon a drop of thick Canada balsam in the center of a slide 
and gently pressed down. Enough water must remain in the crystals to 
prevent the balsam attacking them while it is still soft, so the drying must 
not be too complete (Delepine). This method preserves uric acid, cystin, 
hematoidin, indigo, calcium carbonate, and urates, but is not suitable 
for calcium, oxalate, or phosphate crystals. 

These crystals (calcium phosphate, sulphate, oxalate, triple phosphate) 
may be preserved in cells of varnish made by "ringing" slides on a turn- 
table with shellac varnish, covering with a cover-glass, and sealing with 
more of the varnish. The crystals are thoroughly washed in the manner 
described above, and the final washing is allowed to become perfectly 
saturated with the substance to be preserved. This is done by keeping 
the sediment in contact with a small amount of water for several weeks, 
then mounting a drop in a cell, as described. Triple phosphate is best 
mounted in a saturated solution in ammonia, which may be kept in a 
varnish cell for a year or two, but which ultimately attacks the varnish. 

CastSy epithelia, and other organized sediments must be first treated 
with a preservative solution before mounting. The sediment is thor- 
oughly centrifuged, the supernatant fluid decanted, and from five to ten 
times the bulk of a preservative solution is added. 

For casts the best preservative is Mliller's fluid (potassium bichromate, 
2 parts; sodium sulphate, i part; water, 100 parts). This is diluted with 
an equal volume of water, the sediment is mixed (without shaking) with 
the dilute fluid, and is allowed to settle. The fluid is decanted and fresh 
fluid is added. This is repeated three times, when undiluted MuUer's fluid 
is added. The sediment remains in this for two weeks, the fluid is de- 
canted, and the deposit washed well with 50 per cent, alcohol. The lat- 

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ter is poured off and the following "glycerin solution" added: Alcohol, 
glycerin, and water, of each, lo parts; carbolic acid, i part. In this the 
casts keep for years if the bottle is kept well closed and if only a small 
amount of glycerin solution is allowed to moisten the deposit. To 
mount the casts a drop of the deposit is mixed with a drop of fresh glycerin 
solution and is preserved in a cell, or simply examined under a cover-glass. 
For epitkeliaj puSy tisstie fragments^ etc., the sediment may be simply 
washed four or five times with the glycerin solution and then mounted in 
the same medium. 


The staining of urinary sediments is difficult and usually unsatisfactory 
because of the interference of urinary constituents with the action of the 

The Author's Method. — In order to get the best results the sediment 
should be repeatedly washed with distilled water, with the aid of the 
centrifuge. The washed sediment is then spread upon slides and dried in 
the air. The slides are covered with equal parts of absolute alcohol and 
ether, and the fluid allowed to evaporate. If crystalline frost appears on 
the slide it should be rejected and the sediment washed more thoroughly. 
The sediment thus fixed is stained with dilute eosin-hematoxylin 
or with Unna's polychrome blue or with the following staining method 
employed in preference by the author: 

Saturated alcoholic solution of eosin i part 

Water 4 parts 

Stain for thirty seconds and wash thoroughly in distilled water; 
then add: aqueous solution of methylene-blue, 2 per cent, (or saturated 
alcoholic solution of methylene-blue i part to 4 parts distilled water). 
Stain for from two to five minutes, according to the thickness of the 
film. Wash well in distilled water. The nuclei of the epithelia and pus- 
cells appear blue or purple, the cell-bodies a faint pink, the bacteria a 
deep blue or purple. 

Collodion Film Method. — Instead of fixation ^fdih. alcohol and ether 
the film may also be fixed to the slide by pouring over it a very thin solu- 
tion of collodion (collodion 2 drops to 3 ounces of alcohol and ether, equal 
parts) and allowing to dry. Staining may be carried out then as above, 
but the collodion film tends to take up the stain and thus to interfere with 
the microscopic picture. Collodion films are more useful, however, when 
the sediment has been stained in the centrifuge tube and then fixed on 

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the slide. This method has not proved satisfactory in the author's 
hands, and is too tedious for clinical investigation. 

Centrifugal Staining. — The best method of staining sediments in the 
centrifuge is that of Elise Wolfif.* The sediment is allowed to deposit 
spontaneously, the urine is decanted and replaced with 10 per cent, 
formalin solution, and after twenty-four hours the fluid is again decanted 
and replaced with alcohol. The latter is removed with the aid of the centri- 
fuge, and dilute eosin-hematoxylin or some other suitable stain is added. 
The stain is allowed to act for twenty-four hours, the sediment centri- 
fuged, the stain decanted, and the sediment spread upon a slide. Then 
the excess of dye is removed with alcohol, the film cleared with xylol, and 
mounted in Canada balsam. 

Casts do not stain well with any of these methods and are best studied 
unstained, either fresh or in preserved sediments. The above methods 
are applicable chiefly to the study of bacteria, urinary epithelia, pus-cells, 
shreds, etc. 


It is important to know and to recognize various extra- 
neous matters occurring in the sediment, as they often lead 
to errors. The admixture of these matters is derived from 
exposure to the air, from unclean bottles, from the feces 
and the external genitals, as well as the clothing of the 

The fibers of textile fabrics — of cotton, linen, silk, and 
wool — are often found in the urine. Cotton fibers are 
coarse, wavy, or twisted, with edges more compact in the 
center; the center is wrinkled and shows irregular striations. 
They are highly refractive. Linen fibers are less refrac- 
tive and are composed of finer fibrillae. Irregular trans- 
verse breaks appear at diflferent parts of linen fibers, and 
the outer fibrillae are often broken off and branch irregularly 

* Deutsche med. Wochenschrift., No. 24, 1906. 

2 I am indebted for most of the following data to Heitzmann's hand- 
book, which contains a detailed description of the foreign materials found 

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from the main fiber. Silk fibers are smooth, shining, 
homogeneous, with jagged ends. Wool fibers are coarse 

Fig. 36. — Cotton fibers. 

and have serrated outlines, like the scales on some am- 
phibia. They are finely striated. 

Fig. 37. — Linen fibers. 

Hairs are often found in urine, and are distinguished 
by their pigment, their central medullary canal, and their 

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regular, straight outline. Particles of feathers show a 
characteristic formation, beginning with a fine quill from 
which branch the barbules composed of different sized 

Fig. 38.— Fibers of silk. 

links, gradually tapering toward the end. The scales of 
insect wings appear as delicate, transparent plates with 
little stems. 

'^'^Z- 39- — Wool fibers. 

Starch globules are seen in the urine, owing to the use of 
starch powders for dusting purposes. They are oval or 
round, highly refractive, with a central hilum and con- 

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centric striations. Lycopodium, also used for dusting, 
consists of round shells filled with many spherical particles. 

Fig. 40. — Feather. 


Fig. 41. — Scales from moth-wings. 

Fig. 42. — Globules of starch: 
a, Rice-starch; 6, corn -starch; 
c, wheat-starch. 

Cellulose appears usually in the form of a framework of cells 
with straight lines bounding the individual cells, which are 
angular or rectangular and contain large oblong nuclei. 

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Fig. 43. — Globules of lycopo- 

Cork appears in yellowish or reddish-brown particles of 
irregular size, which are highly refractive and often 
grouped in masses. 

Oil globules are yellowish, 
highly refractive, while air bub- 
bles have sharply defined double 
contour and a bluish-black 
refraction. Flaws in the glass, 
scratches in the slide, etc., are 
faint blue in refraction, and do 
not move when the fluid under 
the cover-glass is set in motion 
by a gentle tap at the side of the 
microscope stage or by inclining 
the latter backward. Rust particles may resemble hema- 
toidin crystals, but are more irregular. 

Fecal matter varies greatly in appearance. It consists 
of different forms of vegetable matter, such as spiral fibers 
from the air-vessels of plants; vegetable fibers, hairs of 
plants, cellulose, starch-globules, fat-globules, and crystals, 
spores, etc. Partly digested muscle-fibers, yellowish or 
brown in color, with their striations, also appear in fecal 
matter. There may be also connective-tissue threads, 
mucus threads, epithelia, pus-cells, and crystals of triple 
phosphate. The epithelia are usually of a flat variety, 
but columnar epithelia are sometimes found. Various bac- 
teria, fungi, yeasts, etc., from the feces will also be seen. 
The importance of recognizing fecal material lies in the 
possibility of a fistula between the rectum and the urinary 
tract. In a specimen of urine examined by the author the 
presence of fecal material and of masses of tumor cells and 
of pigmented intestinal epithelia has led to a diagnosis of a 

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rectovesical fistula due to carcinoma of the rectum. The 
patient was operated upon on the strength of the urinary 

Fig. 44. — Cellulose. 

Fig. 45.— Cork. 

diagnosis and a cancerous tumor found which had ulcerated 
into the bladder. 


The simplest classification of urinary sediments is into 
the unorganized and the organized. The following table 
from Tyson presents this classification in the most con- 
venient form: 

I. Uric acid (crystalline). 

' {a) Acid sodium urate (amorphous, 
occasionally crystalline). 
(6) Acid potassium urate (amorphous), 
(c) Acid calcium urate (amorphous). 
\_ ((f) Acid ammonium urate (crystalline). 
III. Calcium oxalate (crystalline). 

II. Uric acid compounds: - 

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' (o) Ammoniomagnesium phosphate 

IV. Earthy phosphates: j /,x ^^i^.^^^^^^^J?^^* u . / u a 

J ^ ^ (J)) Calcium phosphate (amorphous and 

t crystalline). 

V. Calcium carbonate (crystalline). 

VI. Calcium phosphate (crystalline). 

VII. Leucin and tyrosin (crystalline). 

VIII. Cystin (crystalline). 


I. Mucus and pus. V. Spermatozoa. 

II. Epithelium. VI. Fungi and infusoria. 

III. Blood. VII. Elements of tumors. 

IV. Casts. VIII. Entozoa. 

Another classification divides sediments into those 
occurring in acid urines and those present when urine 
becomes alkaline. Uric acid, urates, calcium oxalate, 
cystin, leucin, and tyrosin are usually found in acid urine; 
triple phosphate, calcium phosphate, ammonium urate, and 
calcium carbonate, in alkaline urine. 


The gross features of urinary sediments have already 
been considered in Chapter III, under the heading of 
Transparency, and the changes occurring in urine as the 
result of fermentation have been spoken of under the title 
of Selection of a Specimen of Urine, page 21. It is very 
important that the student should understand the chemistry 
of alkaline fermentation and of the so-called acid fermenta- 
tion, so as to be able to interpret the sediments occurring 
in normal urine. 

A normal urine, freshly passed and of acid reaction, 
contains no sediment save the faint cloud of mucus al- 
ready spoken of (p. 29) and a few epithelial cells. An 
occasional leukocyte, a few cylindroids, and a few crystal- 
line fragments, usually of the uric-acid type. In the urines 

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of women there are often a larger number of epithelia 
(from the vagina) and, as a rule, crystals are remarkably 
few in number. Urine of alkaline reaction, which is often 
normally seen three or four hours after a meal, may be 
more or less cloudy when passed, and may rapidly deposit 
flocculi of earthy phosphates, composed of amorphous 
granules which quickly disappear on the addition of a few 
drops of acetic acid. 

Acid urines on standing, especially in the cold, precipitate 
granular amorphous matter of considerable bulk, whitish, 
pinkish, or reddish in color, readily soluble by heat, and 
consisting of urates of potassium, sodium, ammonium, 
calcium, and magnesium. The same urine may show, on 
standing still longer, crystals of uric acid of a yellow or 
yellowish-red color, and often the octahedral crystals of 
calcium oxalate. These deposits are caused by what is 
sometimes called acid fermentation. According to Scherer, 
this is caused by the action of the mucus of the bladder as a 
ferment, producing lactic and acetic acid from the coloring- 
matters of the urine. These acids combine with some of 
the bases of the neutral or alkaline urates which are in 
solution in normal urine, then first produce the more in- 
soluble acid urates, which are thrown down, and later 
combine with the residue of the bases, leaving the crystal- 
line uric-acid sediment. 

Another explanation of the occurrence of urate deposits 
is that the. excess of phosphoric acid in the acid sodium 
phosphate unites with the basic urates, rendering them 
acid, less soluble, and, therefore, precipitates them. The 
same process going on further, according to the length of 
time and the amount of acid sodium phosphate present, 
converts the acid urates into uric acid. 

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The acidity of the urine is diminished in the course of 
these changes, and it may become neutral or alkaline be- 
fore the next stage — of alkaline fermentation — sets in. 

If urine is allowed to stand still longer, or if it is kept 
in a warm place, especially in an open vessel, it undergoes 
alkaline fermentation. In this the urea is converted into 
ammonium carbonate through the action of decomposing 
mucus, which has a fermentative effect, or, according to 

Fig. 46. — Deposit in ammoniacal urine (alkaline fermentation): 
a, Crystals of ammoniomagnesium phosphate (triple phosphate); 6, 
crystals of ammonium urate (after Neubauer and Vogel). 

some authors, through the action of a mould which multi- 
plies within the urine and deposits with the salts in the form 
of a white sediment at the bottom of the vessel. 

The results of the conversion of urea into ammonium 
carbonate are a great increase in alkalinity and a series of 
changes in the sediment. At the beginning of the reaction 
the uric-acid crystals begin to dissolve and to become frag- 
mented, and prismatic crystals of sodium urate and dark, 

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spheric crystals of ammonium urate adhere to the frag- 
ments of uric acid. The latter disappear altogether as the 
urine grows alkaline; masses of granules of amorphous 
calcium phosphate and triangular prisms (cofl&n-lid shaped) 
of triple phosphate (ammoniomagnesium phosphate) 
crowd the field together with a number of opaque black 
spheres of ammonium urate, some of which show spicules. 
In addition there are numerous spores, bacteria, infusoria, 
and granular matter, fragments of cells, etc. 

In pathologic conditions the sediment characteristic 
of either acid or alkaline urine may be deposited within 
the body, in the pelvis of the kidney, or in the bladder, and 
when urine freshly voided shows either of the sets of sedi- 
ments described, we have to deal often with uric-acid gravel 
or stone, or with an obstructive inflammatory or sup- 
purative condition somewhere in the urinary tract. 


How are sediments obtained? Describe the gravity method; the 
centrifuge method. 

Describe the method of preparing sediments for examination; the 
preservation and mounting of sediments. 

What extraneous materials may be found in the sediment? 

What is the importance of recognizing fecal elements? 

What sediment is found in normal urine of acid reaction ? Normal 
urine of alkaline reaction? 

What is acid fermentation ? What changes does it produce in urine ? 

What is alkaline fermentation and what sediment is found in the 
urine in this process? 

What may be inferred when acid fermentation goes on in the urine 
before it is voided ? If alkaline fermentation occurs so ? 

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Sediment of Alkaline Fermentation {^after Hof7nann and Ultzmann). 

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Uric Acid. — Uric acid occurs as a heavy sediment of 
small bulk, sinking to the bottom or sometimes adhering 
to the sides of the glass. The crystals are often large 
enough to be seen with the naked eye, and often form 
masses of yellowish-red color known as "gravel " or *^sand." 
These crystals are frequently seen in normal urine, espe- 
cially after a diet rich in meat and after exercise. They 
often occur at the end of the so-called acid fermentation 
(see p. 23); also in concentrated urine in fever, etc., and 
in any diseased condition in which there is an increase in 
the production of uric acid. It must be remembered that 
the occurrence of uric-acid crystals in urine is not neces- 
sarily a sign of the uric-acid diathesis, and before this diag- 
nosis is made the diet of the patient and other conditions 
modifying the urine must be studied. The only safe basis 
for a conclusion as to the elimination of uric acid is in a 
quantitative chemic test. 

Uric-acid crystals vary greatly in shape, but the typic 
forms are the rhombfc or six-sided plate^ Variations of 
this form are very often found (Fig. 47)6*^' Thus, whetstone- 
shaped crystals, alone or in stellate groups, and crystals 
resembling a comb with teeth on two sides, etc., are fre- 
quently met with. All these crystals are a more or less 
deeply tinted yellow, although perfectly colorless, diamond- 
shaped, and pointed crystals often occur. In cases of 

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uric-acid calculi, uric-acid cry tals often occur in masses 
of considerable size and irregular form. Microchemically 
these crystals are distinguished by adding a small amount 
of alkali, such as potassium hydrate solution, while the 
specimen is under the microscope. The crystals will 
readily dissolve and will soon reappear if a drop or two 
of acetic acid be added. Another method is to use the 
murexid test (see p. 151). 

Fig. 47. — Various forms of uric acid. 

In most instances, however, the characteristic shape and 
color of the crystals leave no doubt as to their character on 
microscopic examination. 

Uric^acid Compounds. — Sodium Urate.— This is 
usually amorphous, and forms the greater bulk of the heavy 
powdery deposit of mixed urate known as "brick-dust" 
or "lateritious" sediment. The color of this sediment 
varies with the color of the urine from which it is deposited, 
pale urines giving an almost white sediment, while high- 

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Plate 7 


U^!- ■ '^ L^' 



Uric-acid Crystals with Amorphous Urates ^(afier Pry er). 

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colored urines give a red sediment. Sodium urate and the 
other urates are found in the first stages of acid fermenta- 
tion, also in urine that has stood in the cold, and in fevers; 
after physical and mental exertion; in disorders of the 
stomach and intestine; on the first day of menstruation, 
and in various conditions where there is defective oxidation 
or assimilation. 

Most commonly sodium urate is seen under the micro- 
scope in the form of groups of light or dark brown, fine, 
amorphous granules, in moss-like masses which easily 
adhere to any larger elements of the sediment. Rarely, 
sodium urate occurs in pointed crystals (Fig. 48), which 

Fig. 48. — Acid sodium urate crystals (Ogden). 

are fan shaped, pointed toward the center, and broader 
toward the periphery, or arranged like sheaves of wheat. 
These crystals are striated in a characteristic manner. 

Potassium Urate. — ^This is found in acid urine in the 
form of amorphous granules, forming a part of the mixed 
urate sediment. This deposit is insoluble in cold, but 
soluble in hot water. 

Calcium urate is rarely found, and usually in small 
amounts, in the amorphous deposit of urates in acid urine. 
It has the same solubility as potassium urate. 

Ammonium Urate. — This occurs in the form of yel- 
lowish-red or dark-brown spherules studded with fine 

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sharp thorns, which have given rise to the term " thorn- 
apple crystals" and "hedge-hog" crystals. These thorns 
01 spicules are sometimes curved or branched and vary in 
length. The salt also often crystallizes in clumps of 
needles arranged in sheaves. In the center of these a 
small spherule may be found. The crystals of ammonium 
urate are soluble in hot water and in acids. On addition 
of the latter they are transformed into uric-acid crystals. 
On addition of potassium hydrate the odor of ammonia is 
evolved. According to some observers, the spherules are 
really sodium urate, while the thorns are composed of uric 
acid (Beale, Hassall, and Thudichum). Still others 
claim that sodium urate undergoes a change in the urine, 
on standing, from the amorphous form into small dumb- 
bells, and finally into the globules of ammonium urate, the 
change marking the transition of the acid sediment into an 
alkaline. Rarely ammonium urate occurs in the shape of 
highly refractive colorless or yellowish needles or prisms. 
In old urines it may occur as tufts of needles, sheaves, or 
stars. On addition of HCl they dissolve and uric acid 
crystals appear, a reaction which distinguishes them from 

Method of Dealing with Amorphous Urates. — ^A 
sediment, consisting largely of amorphous urates, is diffi- 
cult to examine, as many of its other elements are obscured 
by the abundant granules of urates. The latter may be 
eliminated in the following manner: The urine is allowed 
to settle thoroughly, is decanted, and the amount of urine 
decanted from the sediment is replaced by an equal amoimt 
of warm water. This dissolves the urates, and the sedi- 
ment may now be allowed to settle again or is clentrifuged, 
and may be examined for elements other than urates. 

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Ammonium Urate, showing Spherules and Thorn-apple- shaped 
Crystals {after Peyer), 

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The warm water also swells and renders colorless any 
normal blood-cells present. Boiling water should not be 
used for fear of coagulating any albumin present and thus 
rendering the sediment unfit for examination. A method 
which saves time, but which is not applicable to albuminous 
urines, is as follows: The sediment containing urates is 
very gently heated on a slide over an alcohol flame, and, 
if necessary, a few drops of warm water are added. The 
urates dissolve, leaving the other elements visible. 

Clinical Significance of Urates. — Deposits of amor- 
phous urates are often found in highly acid or highly con- 
centrated urines, as, for example, in acute fevers. They 
are often seen also in diseases of the heart, liver, and kid- 
neys. Ammonium urate is frequently found in the urine 
of newborn children. Before drawing any conclusions 
as to the meaning of a deposit of urates we must know 
the length of time the urine has stood and the temperature 
to which it has been subjected. Urine which deposits 
urates on standing in the cold may be perfectly normal, 
and amnionium urate is found in normal urine on alkaline 
fermentation. It is the only urate found in alkaline urine. 

Calcium Oxalate. — Normally, calcium oxalate is kept 
in solution in urine by acid sodium phosphate. When this 
solvent has become transformed to a neutral phosphate, 
calcic oxalate becomes deposited. This substance is often 
foimd in crystals in acid urine, and occurs frequently in 
urine on standing twenty-four hours. Calcium oxalate 
crystals are often of very small size. They can be scarcely 
seen with the § objective and a high-power (No. i) 
eye-piece. They are often mistaken for pus-cells when 
seen with this low power, and are distinguished only by 
careful focusing and by noting the square corners and the 

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X -figure in the center. Calcium oxalate crystals occur in 
two typical forms— the octahedral and the dumb-bell 
shapes — but there are several variations of these (Fig. 49) . 
The octahedral crystals consist of two four-sided pyramids 
placed base to base, and when seen from the apex of one of 
the pyramids appear like squares crossed obliquely by 
two lines, something like the outline of a square envelope. 
If the long axis of the crystal is turned toward the observer, 
the crystal appears as a long and very sharply pointed 

Fig. 49. — Calcium oxalate crystals (Jakob). 

octahedron. If several octahedra are joined, they may 
give the appearance of an opened umbrella. These crystals 
are sometimes adherent to renal casts and sometimes 
coalesce into larger masses. 

The dumb-bell shaped crystals of calcium oxalate are less 
frequently foimd, but are very characteristic (Fig. 50). 
They may be crossed, forming double dumb-bells, and 
should not be mistaken for the yellow and brown dumb- 
bells of uric acid and of ammonium urate. The latter are 

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easily soluble in alkalis, while those of calcium oxalate are 
soluble with difficulty. The dumb-bells of uric acid are in- 
soluble in dilute hydrochloric acid, while those of calcium 
oxalate are soluble. Small circular fragments of dumb-bells 
of calcium oxalate are sometimes mistaken for red blood- 
cells. They are distinguished by the fact that they are 
highly refractive, colorless, and unaffected by acetic acid. 

Fig. 50. — Atypical forms of calcium oxalate dumbells, crosses, rosets, 
multiple crystals, etc. 

The deposit of calcium oxalate crystals may be primary 
— i, e,, formed inside the body — and in this case the larger 
octahedra. and dumb-bells are found. After the urine has 
been standing, secondary crystals of smaller size but similar 
shapes are foundy often accompanied by uric acid. The 
large crystals may be deposited secondarily on the addition 
of acetic acid to the urine. 

Clinical Significance. — Calcium oxalate, when present 
in small amounts, has no clinical significance, as it occurs 

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in normal urines, especially after eating certain fruits and 
vegetables, such as apples, oranges, grapes, bananas, toma- 
toes, rhubarb, asparagus, spinach, and turnips, on account 
of the amount of oxalic acid contained in these substances. 
It is often increased in digestive disturbances, after an 
abundant diet of carbohydrates or of meat, and especially 
when the oxidizing power of the system is diminished. 
Oxalic acid is an intermediate product of metabolism 
between uric acid and urea, and when oxidation is dimin- 
ished, oxaluria is the result. In diseases of the nervous 
system oxaluria is commonly observed, and some authori- 
ties claim that an excess of oxalic acid in the blood is 
poisonous and causes a train of nervous and other symp- 
toms which constitutes the condition of "oxalic-acid di- 
athesis." This is, however, a disputed point. 

The occurrence of primary deposits of calcium oxalate, 
especially in masses of crystals and accompanied by blood 
or other evidences of irritation in the kidney, is often 
indicative of stone in the kidney or bladder. Caution 
should be used in applying the term oxaluria indiscrimi- 
nately when the deposit of oxalate is secondary — i. e., oc- 
curs on standing and decomposition. A large amount of 
calcium oxalate occurring in a fresh urine of high specific 
gravity justifies the term oxaluria. A clinical condition 
known by this name has been recognized, and gives the 
symptoms of neurasthenia and dyspepsia, hypochondriasis, 
and melancholia, with headaches, general malaise, and 
pains in the loins. In severe forms this condition has been 
incorrectly called "false Bright's disease,'' owing to the 
similarity of the symptoms to those of nephritis. 

Phosphates. — The earthy phosphates are the only 
varieties that appear in sediments of the urine. They 

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consist of — (a) Neutral magnesium phosphate; {b) triple 
phosphate (or ammoniomagnesium phosphate) ; (c) calcium 
phosphate. They occur in very feebly acid, neutral, or 
alkaline urine, especially after alkaline fermentation. We 
have already studied the gross appearance of these deposits 

(p. 30)- 

Neutral Magnesium Phosphate. — ^This is a very rare 

crystalline sediment, found in concentrated alkaline urines 
which have not yet undergone ammoniacal changes. 
When the latter occur, triple phosphate crystals (see above) 
appear. Neutral magnesium phosphate was found in 
cases of gastrectasia by Stein. It occurs in large, elongated, 
highly refractive rhomboid plates with one or both ends 
obliquely cut off, or in square plates, with or without needles 
at their ends. 

Ammoniomagnesiiun phosphate (MgNH4P04), or 
triple phosphate, occurs in two forms — the " coffin-lid " 
and the "feathery" or 
stellate crystals. The 
former is the most com- 
mon, and consists of a 
triangular prism with one 
of the three angles want- 
ing. These crystals are 
very typical and are quite 
large in size. At times 
they are shortened into 

squares Vjvhich may be 

Fig. 51. — Crystals of triple phosphate 
(ammoniomagnesium phosphate). 

mistaken for the Octahe- 
dral crystals of calcium oxalate (Fig. 51). The stellate 
or feathery crystals are not so common, but are found 
in the urine on addition of ammonia. Various stages 

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of their evolution into triangular prisms are often seen. 
The shorter, square, triangular prisms are distinguished 
from calcium oxalate by the fact that there are larger 
crystals of more typical shape about them, for these 
atypical triple phosphate crystals never occur alone. 
Besides, the phosphate crystals are dissolved by acetic 
acid, while those of the oxalate are insoluble in this acid. 

Fig. 52. — Acid calcium phosphate. 

Calcium phosphate is either amorphous or crystalline. 
The amorphous form is often present after meals as a 
whitish, flaky deposit, and is precipitated by heat, but 
readily dissolved by acetic acid. In very feebly acid urine 
it is seen in small, highly refractive granules, arranged in 
clumps or adhering to other elements of the sediment. It 
is often seen with triple phosphate in neutral or alkaline 

The crystalline form is often seen in urine, and may be 

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mistaken for crystals of sodium urate. Crystals of acid ^ 
calcium phosphate are found in urines about to undergo 
alkaline fermentation, and which are still weakly acid. 
They are prismatic and occur either singly or in star- 
shaped, often in fan-like groups. They are distinguished 
from sodium urate crystals by adding acetic acid, which 
rapidly dissolves the phosphate crystals, while the urate 
dissolves more slowly and often is replaced by crystals of 
uric acid. 

Clinical Significance. — By phosphaturia is meant, 
properly speaking, an excess of phosphates (phosphoric 
acid) in the urine, and not necessarily a precipitate of 
phosphates. The term has been applied incorrectly to 
cases where the urine was normal, but less acid than usual, 
owing to an excess of alkalis derived from the food, and in 
consequence showed a precipitate of phosphates. Normal 
urine two or three hours after a meal, especially under a 
vegetable diet, very often shows a deposit of amorphous or 
crystalline phosphates. These deposits, however, are not 
constant. Should the precipitate constantly be seen and 
be very abundant, phosphaturia may be suspected. In 
most cases phosphaturia shows a low state of nutrition and 
a condition of neurasthenia. The clinical diagnosis . of 
phosphaturia should be made only when the deposits occur 
immediately after the urine is voided, and when a change of 
diet will not rectify the trouble. (For further data con- 
cerning Phosphaturia, see p. 216.) 

Primary deposits of crystalline phosphates (deposited 
within the body) are often found in cases of inflammation 
and suppuration of the urinary tract, such as cystitis, 

^ This compound has long been erroneously called "neutral" calciuoi 

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pyelitis, etc., especially when there is a decomposition of the 
urine within the tract as the result of an obstruction some- 
where; for example, an enlarged prostate, a stricture of 
the urethra, etc. 

Infection of the kidney, pelvis, or bladder may be ac- 
companied by ammoniacal decomposition of the urine, 
which results in the deposit of triple phosphates. 

Calcium Carbonate. — This is a very rare deposit in 
human urine, but is found in large amounts in horses and 
other herbivora. It occurs in alkaline urine on standing 

Fig. 53. — Calcium sulphate (von Jaksch). 

for a long time, along with phosphatic deposit. It occurs 
either as an amorphous sediment or characteristically 
in small spherules, resembling ammonium urate, but 
smaller, colorless, usually in pairs (dumb-bells), often 
concentrically striated, and are distinguished by their 
effervescence (CO2) upon addition of acetic acid. 

Calcium Sulphate. — This is a very rare sediment 
and occurs in highly acid urine, of high specific gravity, 
in the form of needle-like prisms (Fig. 53), or in elongated 
plates with obliquely cut ends. They may be single or 
in sheaves or rosets. They are distinguished from cal- 

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cium phosphate by their insolubility in ammonia, acetic, 
and sulphuric acids, and their slight solubility in HCl 

Leucin and Tyrosin. — These two substances have 
already been described under the heading of Chemic 
Examination (p. 201). 

Leucin occurs in the shape of more or less yellow, highly 
refracting spheres which resemble oil-drops. By suitable 
illumination many of these spheres will be found marked 

Fig. 54. — ^Leucin (Jakob). 

with radiating and concentric stripes. They often are 
arranged in masses and chains, merging together at their 

The suspected urine should be evapora'ted slightly, 
and if leucin is present the crystals will usually be deposited. 
The spheres are, unlike oil-globules, insoluble in ether, but 
are soluble in alkalis and insoluble in cold mineral acid. 
They are distinguished from spheres of ammonium urate 
by the presence of spines on the latter and by the fact that 
the urate is soluble on being warmed. 

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Tyrosin. — Tyrosin crystallizes in the form of exceed- 
ingly fine needles arranged in sheaves or in rosets radiating 
from the center. These crystals are colorless, but when 
arranged in masses often look dark. They are tasteless, 
odorless, very sparingly soluble in cold water; more soluble 
in boiling water; almost insoluble in strong alcohol; in- 
soluble in ether; readily soluble in acids, alkalis, and alka- 
line salt solutions. Tyrosin is recognized after obtaining 

Fig. 55. — Tyrosin crystals (Jakob). 

the crystals by one of the tests described under Chemic 
Examination (p. 202). 

Cystin. — Cystin is a rare sediment in the urine. It 
occurs in crystals in the shape of hexagonal, colorless 
plates of moderate size and high refraction. They are 
often superimposed or may form more or less regular 
masses (Fig. 56). The sides of these plates are usually 
equal, but sometimes two sides are found shorter or longer 
than the others. Cystin also crystallizes in quadrilateral 
prisms or groups of prisms. The crystalline sediment 

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forms a whitish or yellowish-gray deposit, is met with in 
pale urine of acid reaction, and is gradually dissolved in 
alkaline urine, developing during decomposition the odor 
of sulphuretted hydrogen and of ammonia. 

Cystin sediment is soluble in ammonia, in mineral acids, 
and in alkaline hydrates and carbonates, except ammonium 
carbonate. It is insoluble in alcohol, ether, and water, and 
is precipitated from alkaline solutions by acetic acid. Its 
solutions rotate the plane of polarized light toward the 

Fig. 56. — Crystals of cystin (Jakob). 

left. Cystin is an amido-acid with the formula of CgHg- 
NSO2, and contains 26 per cent, of sulphur, which gives 
rise to the odor of sulphuretted hydrogen already spoken 
of. The crystals are not readily confounded with uric 
acid, but they may be treated with ammonia and the solu- 
tion evaporated. If the crystals are uric acid, ammonium 
urate will form and will remain as an amorphous residue. 
Hydrochloric acid also readily dissolves cystin, but leaves 
uric acid unchanged. Acetic acid redissolves triple phos- 

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phate crystals, but leaves cystin unaltered. The presence 
of cystin should be suspected in all urines in which an odor 
of sulphuretted hydrogen is detected. 

Clinical Significance. — Cystin is probably not present 
in normal urine. In disease the amount varies, and the 
daily quantity may reach as high as 1.5 gm., although ordi- 
narily it is very much smaller. The cause of cystinuria is 
not definitely known. Brieger and others have found that 
certain products of intestinal putrefaction — the diamins — 
are eliminated in the urine and feces of persons with 
cystinuria. These diamins are said to arise only as the 
result of putrefaction due to specific germs, and cystinuria 
may be regarded as the result of specific intestinal infection. 
As yet no definite relation has been found between the 
formation of cystin and of diamins, although both occur 
under the same conditions. Heredity seems to play some 
r61e in cystinuria, as many cases have occurred in several 
members of the same family. Both infants and adults may 
eliminate cystin, but it rarely occurs in old age. It may 
not be connected with any symptoms, although present for 
years; but usually there are symptoms of irritation in the 
urinary tract. It has been observed in some cases of liver 
disease and of acute articular rheumatism. 

Bilirubin and Hematoidin. — Bilirubin may be 
found in amorphous or crystallized form in the sediment 
of urine containing bile. The crystals occur as needles 
in stellate clusters, often adhering to cells, or in the form 
of minute rhombic plates varying in color from yellow to 
ruby red. They are soluble in sodium hydrate, and on the 
addition of nitric acid they show a green rim. 

Hematoidin is a derivative of hematin, and was first 
found by. Virchow in extravasated blood.. Its crystals are 

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identical in shape and all other respects to those of biliru- 
bin, and probably the two are identical. These crystals 
are found not uncommonly in urinary sediments after 
extensive hemorrhage, the evacuation of an abscess, or in 
pyonephrosis. They have been found in nephritis of preg- 
nant women, in acute yellow atrophy, cirrhosis of the liver, 
severe persistent jaundice, phosphorus-poisoning, and 
cancer of the bladder. 

Indigo. — ^Very small amounts may be present, except in 
intestinal obstruction, where larger quantities may be ex- 
pected. Indigo occurs as stellate needles or rhombic or 
lanceolate crystals of blue color, insoluble in water, readily 
in chloroform. (See Indican, p. 174.) 

Melanin. — ^This may be found in the sediment in the 
shape of black or dark-brown granules, free or within 
epithelia, casts, etc. 

Fat-globules. — Fat occurs quite frequently in the urine, 
but we must be careful not to confound it with that from 
outside sources contaminating the specimen, which, as a 
rule, occurs in larger, more irregular, and more yellowish 
globules. When enough fat is voided to be seen by the 
naked eye, and when little or no albumin is present, the 
term lipuria may be applied. When urine presents a 
milky appearance with a creamy layer on top on standing, 
the term chyluria is used. The latter has already been dis- 
cussed on page 203. Microscopically, fat globules and 
granules vary in size, and when the larger ones are found 
there may also be some slender needles of margaric acid 
lying between the globules or even within them. Fat 
globules are recognized by their dark contour and high 

Aside from the cases of chyluria and lipuria (the latter 

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has been observed in health temporarily after a fatty diet, 
in pregnant women, and in phosphorus- poisoning), a 
small number of fat-globules is seen in a great many cases 
of chronic inflammation in the genito-urinary tract. 
These globules are probably a product of protoplasmic 
degeneration, as they are found both free and in masses 
within epithelial and pus-cells. They are more numerous 
in the chronic cases, and often the cells may be completely 
changed into masses of fat-granules. These globules 
are found in chronic nephritis, pyelitis, cystitis, prostatitis, 
urethritis, and vaginitis. 

They are especially interesting in fatty casts (see p. 


Cholesterin is occasionally found in urinary sediments. 
It crystallizes in large, colorless, transparent plates whose 
angles and sides are often broken, and whose acute angles 
are often as small as 76 degrees. Larger masses of these 
crystals have a pearly lustre and a greasy feel. The occur- 
rence of cholesterin and its chemic characters have already 
been considered (p. 203). It is readily detected in the 
urinary sediment by means of the microscope. If a mix- 
ture of 5 parts of sulphuric acid and i part of water be 
allowed to act upon the crystals, a bright, carmin-red color 
appears, which changes to violet. Another method of 
testing under the microscope is by adding dilute sulphuric 
acid and then a solution of iodin. The crystals will show 
a play of colors, beginning with violet, then bluish-green, 
and finally blue (see Fig. 30). 


Name the principal forms of unorganized sediments. 
How does uric acid occur in the urinary deposits? 

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What does the presence of uric-acid crystals indicate ? What simple 
chemic tests may be used to distinguish these crystals? 

Describe the appearance of deposits of sodium urate; ammonium 
urate; potassium urate; calcium urate. 

How are urates eliminated from a urinary sediment? 

What is the clinical significance of urates? 

Describe the two forms of calcium-oxalate crystals. How are the 
dumb-bells distinguished from those of uric acid and of ammonium 
urate? From red blood-cells? 

What is meant by a primary deposit of calcium oxalate? 

What is the significance of calcium-oxalate crystals? What diet 
favors the appearance of these crystals in the urine ? 

In what conditions and diseases is oxalic acid increased? 

When should we apply the term "oxaluria"? 

What is meant by "oxalic-acid diathesis"? By "false Bright's 

What phosphates occur in the urinary sediments ? In what reactions 
of urine do they occur? 

In what forms do triple-phosphate crystals occur ? How are the square 
prisms distinguished from calcium oxalate? 

What two forms of calcium phosphate are found in sediments ? How 
is the crystalline form distinguished from sodium urate? 

What is meant by phosphaturia? What does phosphaturia indicate ? 

When are primary sediments of phosphates found? 

What carbonate compound is sometimes seen in sediments? How 
is it distinguished ? What sulphate^ and how does it occur ? 

Describe the appearance of deposits of leucin; of tyrosin; of cystin. 

What odor does cystin develop during decomposition ? How is this 
substance distinguished from uric acid ? What is the clinical sgnificance 
of cystin? 

Describe the crystals of bilirubin and hematoidin, and state their clin- 
ical significance. 

What mistake is often made in connecton with fat in the urine ? 

What is meant by lipuria ? By chyluria ? When does lipuria occur ? 

What does a small number of fat-globules indicate? In what con- 
ditions are they found? Describe their appearance. 

What is the appearance of cholesterin crystals? What reaction do 
cholesterin crystals give with HaSO^ and iodin? 

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The second group of sediments includes cells, fibers, 
and other formed elements of various parts of the urinary 
tract, some of which are normally present in the urine, while 
others indicate some disturbance or disease. The study 
of the organized sediments is the most important portion of 
the microscopic study of the urine, as upon the recognition 
of these elements very largely depend the localization of the 
diseases of the urinary tract and the determination of the 
nature and stage thereof. 


With the exception of the urine of women during men- 
struation, etc., in which the presence of blood is unimport- 
ant, the occurrence of red blood-cells in urinary sediments 
is always abnormal. Red cells vary in appearance accord- 
ing to the part of the tract from which they come, according 
to the freshness of the specimen, and according to the con- 
centration of the urine, the presence or absence of decom- 
position, etc. 

Normal blood-cells — i. e., cells so unaltered that they 
look very much like cells in fresh blood — are very charac- 
teristic in appearance. They are biconcave disks of a 
yellow color, considerably smaller than the white cells, 
about ^"5^ inch in diameter, without nuclei, granules, or 
other visible cell-contents. On careful focusing the rela- 

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BLOOD 27s 

tions of light and shadow at the center and periphery 
alternates as the objective is approached to the slide or 
removed from it. With the low power (objective § eye- 
piece No. I, B. and L.) the red blood-cells are visible 
as very minute faintly yellowish disks. They are best 
studied with the ^ or J objectives. 

The first change that blood-cells undergo in the urine 
is the alteration in outline known as "crenated," irregular 

Fig. 57. — Red blood-cells in the urine: Ay Normal; 5, abnormal. 

or "mulberry shaped." This may be found in urine with 
a high percentage of sodium chlorid. 

Abnormal Blood-cells, — Blood-cells which have entered 
the urine within three or four hours begin to lose their color 
and swell until they are mere rings or shadows. Instead 
of being biconcave, they become almost spheric, very pale 
or almost colorless, and ^tbout two-third§ of the normal 

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cells in diameter. Any blood-cell which has lost its yellow 
color and its characteristic outline is "abnormal." 

Normal blood, when present in large amounts, produces, 
in alkaline urine, a bright red color, and in highly acid 
urine, a brownish-red color. Abnormal blood, if present 
in sufficient amount, renders the urine brownish or smoky, 
and if in large amounts, almost black. Very commonly, 
however, the amount of blood is so small that it can be 
detected only microscopically. Urine containing blood 
always gives a reaction for albumin, even if the amount is 

Fig. 58. — Teichmann's hemin crystals (Jakob). 

Detection. — The chemic detection of blood by Teich- 
mann's method has already been described on page 178. 
The crystals of hemin which are thus obtained are brown, 
rhombic plates, the proper chemic name of which is hema- 
tin iodid or chlorid. The crystals are very small, and often 
crossed or arranged in groups (Fig. 58). This test is 
useful when there is any doubt as to the presence of blood 
in the urine. 

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BLOOD 577 

To Remove Blood from a Sediment.— The blood- 
cells may be so abundant in the sediment that they obscure 
everything else, and must be destroyed before examination. 
This is done as follows: The urine is allowed to settle 
slowly, the supernatant fluid is decanted, and a large 
amount of lukewarm water, with a few drops of dilute acetic 
acid, is added to the sediment. The mixture is stirred 
thoroughly, breaking up all clots, and allowed to settle 
again. The process is repeated until the water is free from 
color; the sediment is allowed to settle and examined. 
The blood-cells are washed out and almost invisible, while 
casts, etc., can be seen. 

Clinical Significance of Blood.— We have already 
considered this subject under the heading of Blood-pig- 
ments (Chapter XII, p. 193). The distinction between 
hematuria, in which blood-corpuscles are present together 
with blood-pigments, and hemoglobinuria, in which the 
pigment alone appears, can be made with the microscope. 
The first purpose of microscopic examination in connection 
with blood is to locate, if possible, the source of the hemor- 

Blood from the Kidney. — As blood from this organ is 
usually in contact with urine for a considerable time before 
it passes out, it is generally abnormal in character and more 
or less dark brown or smoky. In injuries to the kidney, 
in acute congestion, etc., however, the blood may be 
normal and bright red. The reaction of the urine contain- 
ing blood in the kidney is usually acid, although it may be 
alkaline if the amount of blood be large. A characteristic 
feature of blood from the kidney is that it is often accom- 
panied by casts to which red cells adhere. This is the only 
positive evidence that blood comes from the kidney. 

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Blood-clots may be found in such urines, but are usually 
smaller than those derived from hemorrhage lower down 
in the tract. 

{Ajter Oertely as quoted by Brooks) 




May occur in — 


Usually compar- 
atively small. 

Clots usually absent. 
Associated with 

and hyaline casts, 
renal epithelium. In- 
timately mixed with 
urine. Many swollen 
(loss of hemoglobin) 
phantom corpuscles. 
Sediment slight (or 

Acute and chronic neph- 
ritis. Malignant 
growths. Renal cal- 
culus, tuberculosis, 
embolism, abscess, 
acute febrile processes, 
hemophilia, and in 
filariasis (malaria) and 
distomiasis. Frequent- 
ly in poisoning from 
turpentine, etc. 

Pelvis of kidney 
and ureters. 


Absence of casts of 
any kind, or renal 
epithelium. Fibrin- 
ous molds of lureters 
may be present. Pus- 
cells in calculus. 

Diseases of pelvis, cal- 
culus, etc. 



Blood-cdls well pre- 
served unless urine is 
ammoniacal; clots fre- 
quent. Heavy sedi- 
ment (often scanty). 
Pus in cystitis. Shreds 
of tumor tissue in pa- 
pilloma or malignant 
growths. If neck of 
bladder is involved, 
blood appears at end 
of micturition. 

Stone, cystitis, tumors, 
varicose veins of vesi- 
cal neck. Distoma 
haematobium, etc' 



May be expressed; 
first part of micturi- 

Urethritis, trauma, etc. 

The causes of bleeding from the kidneys include acute 
congestion and acute nephritis, in each of which the amount 
of blood varies considerably, according to the severity 
of the condition. In chronic nephritis a small num- 
ber of red cells may be found, but during an exacerba- 
tion there may be an abundant bleeding, fresh blood-cells 

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BLOOD 279 

appearing suddenly, with a diminution in the daily quantity 
of urine. In chronic interstitial nephritis blood is not in- 
frequently found as the result of disturbances in circulation 
caused by heart disease or by diseased arteries. In amy- 
loid kidneys hemorrhage occurs sometimes, owing to the 
infiltration around the small blood-vessels. ' 

The three great causes of blood in the urine are tuber- 
culosis of the kidney, tumors of the kidney, and stone in the 
kidney. In tuberculosis the bleeding may be intermittent 
or continued for a long period, and is accompanied by pus 
in considerable amounts. The diagnosis is made by find- 
ing tubercle bacilli in the sediment. In tumors of the 
kidney blood appears in considerable amounts at times, 
usually in attacks. Here, also, there is usually pus in the 
urine, and the sediment contains at times a number of 
cells which resemble the characteristic elements of the 
tumor. Stones in the kidney or in the renal pelvis give 
rise to either constant or intermittent bleeding. The urine 
may contain pus and fragments of stone or masses of 
crystals which hint at the presence of calculus. It must 
be remembered that in the early stages of tuberculosis, of 
tumors of the kidney, and of stone there maybe no bleeding, 
but, as a rule, the appearance of blood in these conditions 
occurs sufficiently early to call attention to the possibility 
of one of these diseases, and unless their presence can be 
eliminated, the occurrence of attacks of hematuria is a 
sufficient basis for suspecting one of these three conditions. 
The study of the clinical symptoms, especially of the pres- 
ence of pain, colic, and tumor, and the study of the epi- 
thelial elements and of pus-cells and crystals, as well as 
the examination for tubercle bacilli, will usually lead to a 

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Certain drugs which irritate the kidney, such as can- 
tharides, turpentine, etc., may give rise to hematuria. 
Wounds, contusions, concussion of the kidney by indirect 
injury, and the invasion of the kidney by parasites (see 
p. 337) are also causes of bleeding. Other sources of 
hemorrhage in the kidney are cysts of that organ, purpura, 
and renal embolism. 

Hemorrhage from the Pelvis and Ureter. — ^There is 
nothing microscopically characteristic about bleeding 
from the ureter, but the passage of thin, cylindric clots 
may help in the diagnosis. The presence of a large number 
of epithelial cells from the ureter may assist in localizing 
the trouble, although these epithelia are often difficult to 
differentiate. The causes of these hemorrhages include 
acute pyelitis, stone, acute ureteritis, injuries, etc. 

Bleeding from the bladder is seen in moderate amounts 
in acute and chronic cystitis, but the most important causes 
of this bleeding are the same as in the case of the kidney — 
i. e,, stone, tuberculosis, or tumor of the bladder. Blood 
from the bladder is usually normal or comparatively 
unchanged; but if the urine is highly acid or alkaline, or if 
there is retention and the blood remains in the bladder for 
a long time, the blood-cells are abnormal. Bleeding from 
the bladder is characteristically associated with clots — ^at 
least more so than bleeding from the upper urinary organs. 
As a rule, pus is present in all conditions of the bladder 
accompanied by bleeding, with the exception of injuries, 
surgical operations, etc. In the diagnosis of the cause of 
the bleeding from the bladder the sediment must be ex- 
amined for characteristic cells or fragments of a tumor, 
for crystalline masses or fragments of a stone, for tubercle 
bacilli, or other bacteria. 

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PUS 281 


Pus-cells or leukocytes occur in the urine in. the form of 
small, round, granular bodies about twice the size of normal 
red blood-cells. They contain one or more nuclei, which 
may or may not be seen in the specimen, but appear very 
clearly on the addition of acetic acid. As a rule, they can 
be easily recognized, but if any doubt arises as to their 
nature it may be dispelled by the addition of a little solu- 
tion of iodin and potassium iodid. The leukocytes stain 
a deep mahogany-brown (glycogenic reaction), while epi- 
thelium, which may resemble them, assumes a light yellow 
color. In freshly passed urine leukocytes may exhibit 
active ameboid changes and assume irregular outlines. In 
dilute and highly alkaline urine they become swollen, 
globular, and hydropic, and the granulations in them be- 
come pale or disappear. In ammoniacal urines the pus- 
corpuscles may burst and coalesce into sticky masses. 

The amount of granulation varies widely in pus-cor- 
puscles, and the granules may be coarse or fine. In some 
cases minute fat-globules appear in the pus-cells, and the 
whole cell may be replaced by them. This is never found 
in acute inflammations, and the more fat-globules are 
found, the more chronic the process is, in all probability. 
Pus-cells may contain rust-brown crystals of hematoidin 
in the form of needles or flakes, especially in cases in which 
pyuria is accompanied by hemorrhage. Dark-brown 
pigment-granules may be found in these cells in chronic 
cystitis. Very rarely pus-cells may show delicate cilia, 
showing their origin from the epithelia of the uterus (endo- 

The pus-cells in the urine may be derived from the 
kidney or its pelvis, the ureters, the bladder, the urethra, 

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or from the rupture of an abscess into some portion of the 
urinary tract. Pus-corpuscles in the urine are also often 
formed from the connective tissue and from the epithelia 
of the various organs of the urinary tract. For this reason 
they bear at times characteristics of the epithelium whence 

rig- 59- — Pus-cells in the urine: A, Normal pus; By same after add- 
ing acetic acid; C, pus-cells showing ameboid movements; D, pus-cells 
in ammoniacal urine altered by ammonium carbonate. 

they come — as, for example, the pigmented pus-cells of 
chronic cystitis. 

Clinical Significance. — A few leukocytes may be 
seen in perfectly normal urine. When present in moderate 
numbers, the presence of an inflammation somewhere 
in the tract may at once be suspected. When they are 
very numerous, the diagnosis of suppuration may be made, 
provided the other features of the urine corroborate it. 

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PUS 283 

The presence of pus having been determined, the next 
step is to find its source, and the only way to do this is to 
study the other elements of the sediment, such as epithelia, 
casts, etc., which accompany the pus. 

Pus from the kidney may be found in any inflammatory 
or suppurative condition of this organ. A few cells will 
be found in simple irritation and in non-suppurative 
nephritis, showing that the pus-cells are the product of an 
inflammation. In chronic nephritis pus-corpuscles con- 
taining fat-globules and granules are frequently observed. 
In suppuration of the kidney and pelvis (pyelonephritis), 
due to ascending infection from the bladder or to a stone, 
a tumor or a tuberculous process, the presence of pus is a 
prominent feature. Pus from the kidney or pelvis is 
also seen in urine from abscess of the kidney, suppuration 
of the pelvis (pyelitis), and pyonephrosis. In cases of 
abscess of the kidney there may be no pus before the ab- 
scess ruptures into the pelvis or into a pocket communicat- 
ing with this part, when there will be a sudden appearance 
of pus. The same will be observed when there is a sudden 
removal of an obstruction in the pelvis or ureter. 

Pus from the bladder is seen in acute and chronic in- 
flammation and in stone, tumor, or tuberculosis of the 
bladder. Pus from the seminal vesicles is seen in sem- 
inal vesiculitis (spermatocystitis) . Pus from the prostate 
may be present in prostatitis, prostatic abscess, and pus 
from the urethra in urethritis, especially of gonorrheal 
origin. In all the above-named conditions the localization 
of the origin of the pus can be made usually by noting 
the presence of epithelia {q. t'.) from the corresponding 
organs. It is important to distinguish, in the urine of 
women, pus which comes from the uterus or vagina. 

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and if there is any doubt, the urine should be obtained by 
catheter or should be voided after a thorough vaginal 


These are found in the form of sinuous, highly refractive 
fibers, single, or more often in irregular bundles, and 
finely fibrillated or granular. Their thickness and length 
vary within wide limits. They are distinguished from 
mucus-threads by their high refraction, their fibrillated 
appearance, and wavy outlines. Linen fibers are coarser, 
not so wavy, and of higher refraction than connective- 
tissue shreds. 

Connective-tissue fibers in the sediment indicate a new 
growth or an ulcerative, suppurative, and to a lesser degree 
a severe inflammatory lesion of the genito-urinary tract. 

In chronic interstitial nephritis and in chronic diffuse 
nephritis connective- tissue shreds may be present in the 
urine along with other microscopic features. In tubercu- 
losis of the kidney, in tumors, or in stone of the kidney 
these shreds may also be present and indicate an intense 
destructive or inflammatory condition. Tumors of the 
bladder, especially cancer and papilloma, may also be 
accompanied by the appearance of these shreds, in con- 
junction with more typic tumor elements. Connective- 
tissue shreds may also occur in company with pus in ab- 
scesses from various portions of the genito-urinary tract 
and in hypertrophied prostate. 

Whenever these shreds appear in the urine they indicate 
a disintegration of connective tissue, consequently they 
are, as a rule, signs of deep-seated and serious lesions in the 
tract (Heitzmann). 

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Epithelial cells from various parts of the urinary tract 
occur in both normal and pathologic urines. In normal 
urine the epithelia are few or moderate in number, and 
represent the shedding of the surface layers from the ordi- 
nary wear and tear of the parts. In pathologic conditions 
not only is their number increased, but the cells are altered 
and the elements characteristic of the deeper layers appear 
together with those from the superficial strata. 

There is considerable divergence of opinion among 
modern authorities on urinary diagnosis as to whether it is 
possible accurately to recognize the sources of the various 
epithelia that may occur in the urine. The majority of 
authors take the negative side of this question. The 
reasons advanced for this view are twofold: First, that 
there is a great similarity between epithelia lining certain 
parts of the urogenital tract, and those derived from other 
quite distinct parts; and second, that even when there are 
marked differences between the epithelia belonging to dis- 
tinct portions of the tract, these differences are largely 
destroyed by the distortion (swelling, obliteration of con- 
tour) which all epithelia undergo in the urine. 

The writers who hold this view concede at most the pos- 
sibility of recognizing with certainty the origin of large flat 
epithelia (bladder, vagina), and the smaller rounded 
columnar or caudate cells which may come from the 
upper parts of the tract. A few of these authors go so far 
as to recognize the probability of caudate cells coming 
from the pelvis and the possibility of distinguishing renal 
epithelia by their small size and rounded outline. 

A more minute differentiation of epithelia from the 
various parts of the tract is regarded as feasible by a smaller 

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group of authors, who ding to the older views on this 
question which have been handed down to us by Ultzmann 
and his school. In Ultzmann's treatise on urinary diagnosis 
which appeared in 187 1, there are excellent, though slightly 
conventionalized, illustrations of the epithelia from each 
of the different parts of the urinary tract. These illustra- 
tions were drawn for Ultzmann by Carl Heitzmann, who 
afterward went a step further than his teacher and studied 
these epithelia still more minutely. The elder Heitzmann's 
views are ably supported by his son, Louis Heitzmann, 
who is perhaps the most radical exponent of these views 
among modern writers, and to whom urinary diagnosis 
owes the present development of this subject. 

An experience of ten years, covering the examination of 
many thousands of urines in private as well as in hospital 
work, has convinced the present writer that the recog- 
nition of the chief sources of epithelial desquamation is 
not only possible with practice, but is absolutely indispen- 
sable in urinary diagnosis. This conviction was reached 
after a study of a large number of cases of surgical affec- 
tions of the urinary organs in which the writer not only 
studied the urine, but personally examined the patients with 
the aid of the cystoscope, the ureteral catheter, etc., and 
in many instances controlled the diagnosis after operation. 
It is only those who have the opportunity of seeing the 
clinical as well as the microscopic side of these cases that 
can judge with certainty as to the real value of the methods 
of carefully studying the epithelia of the urine. Like 
all diagnostic methods, this one has many pitfalls and is 
at times misleading, but after a moderate amount of ex- 
perience one begins to realize its possibilities more and 
more, and soon learns to value it highly. 

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It may be said that every part of the urinary tract has 
theoretically its characteristic epithelium. In practice, 
however, it is not always possible to say of a given cell in a 
urinary sediment just where it came from. It is possible, 
however, to find enough cells bearing the characteristics 
of epithelia from a given part to form a judgment as to 
the portion of the tract which was the source of the des- 
quamation. The farther away we get from the bladder, 
the more difficult is it to distinguish the epithelia of one 
part of the tract from those of another. While it is true 
that the epithelium, as found in urinary sediments, usually 
has entirely different outlines from that found histologically 
in the portion of the tract whence it came, the change which 
is due to the influence of the urine affects all classes of epi- 
thelia more or less in the same way, so that the relative 
appearance remains distinctive in most cases. The whole 
basis of distinguishing certain epithelia, from the kidney, 
for example, from others derived from other parts, is 
the size of the cells as compared to a standard. As a rule, 
the standard cell of a urinary sediment is the leukocyte 
or pus-corpuscle, because it varies but little Fig. 60. 

Three general types of epithelia occur in the urine: 
The flat or squamous cells, the cuboid, and the columnar. 
These terms refer to the generic histologic types, and when- 
ever they are used in the following descriptions, table, etc., 
it is understood that the terms "cuboid" and " cylindric " 
refer to cells which were originally of these shapes. Cuboid 
cells usually appear in the urine as round or slightly ovoid. 
Cylindric cells appear often as caudate, pear-shaped bodies, 
the angular outlines having been rounded off under the 
influence of the urine. 

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The cell bodies of the urinary epithelia are more or less 
markedly granular. The amount of granulation varies 
in different regions of the genito-urinary tract, and with 
the reaction of the urine. Particles of pigment and fat- 
droplets are sometimes found in the cell bodies. The latter 
usually indicate chronicity of an inflammatory process. In 
urine containing bile the granulations appear yellow. 

The epithelia always possess one or more nuclei, but at 
times the nucleus drops out, leaving a vacuole. The 
prominence of the nucleus varies with the amount of granu- 
lation and the density of nuclear substance. It also 
depends on the reaction of the urine. On. addition of 
acetic acid to the drop of sediment on the slide, the nuclei 
stand out and the granulations become indistinct. Urinary 
epithelia should be studied with a J or J objective and a 
I -inch eye-piece. A compensating eye-piece is of advan- 
tage, but not essential. 

In distinguishing epithelia the average size and average 
shape of a number found should be considered. Usually 
one or two types predominate in a specimen. Transitional 
types and sizes cannot be taken as criteria. 

The table on p. 289 will prove useful to the student 
inexperienced in differentiating epithelia in the urine. 
The cells are classified here according to general shape 
in three columns. When cells are encountered of a given 
shape they may belong to one of a number of parts of the 
genito-urinary tract. By glancing at the proper column, 
the student at once will be able to know between what 
group of cells he must differentiate. He must next seek 
to determine the size of cells seen, by comparing them 
to the standard- — the pus-cell. In the table the pus-cell 
from the urine under consideration in each case is taken as a 

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(U . 

> B 
o «J 



.S 8 

O rt 






w ti « 

J ?: 5 

w o 2 

+ + 




> M 
C ^— ' 

C ^s 














(U C ^ 

« >< c S 

^ Pi 




K -r- H- 

C S 

+ -f 

+ + 
t^ 00 
I I 

O ^_^ 

> > 


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unit. The size of pus-cells varies in different urines, 
but the relative size of the epithelia varies to a smaller 
extent. The numbers on the left side of the table show the 
order of sizes, while on the right side of each column ap- 
pears the diameter of each group of cells com.pared to the 
standard. The figures stand for an average size. Practice 
alone can enable a student to differentiate between cells 
with close ratio. In some instances the distinction is im- 
possible — e. g,, between cells from the prostate and those 
from the ureter, between those from the cervix and the 

The table and Plates 9 and 10 show, perhaps, better 
than any description the possibilities and the limitations of 
the method of differentiating epithelia in the urine. 

In the following each of the groups of epithelia belong- 
ing to the different organs of the genito-urinary tract will 
receive separate consideration. 

Epithelia from the Bladder. — The upper layers are 
flat, the middle layers cuboid or round, the deepest 
layers columnar or caudate. A small number of the flat 
epithelia appear in every normal urine and have no signifi- 
cance. If they appear accompanied by pus and with 
round vesical epithelia, they show disease in the bladder. 
The flat epithelia are found free or in pavement clusters 
of irregular size and shape. They are smaller than the 
cells from the upper layers of the vagina, but near the neck 
of the bladder they become quite large and may be con- 
founded with vaginal epithelia. They do not contain 
bacteria, however, as the latter frequently do, and the 
nuclei of bladder epithelia are almost always larger in pro- 
portion to the cells than those of vaginal epithelia. Cu- 
boid or round epithelia from the bladder, when present 

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^ " ® ^ ^© ^ <s 


f ^>?f^ ^^^4^ 

Epithelia in the Urine from the Bladder, Ureter, Renal Pel- 
vis, AND Kidney. X about 500. 
I. Bladder: (a) Superficial, (6) middle, and {c) deep layer. 2. Renal 
pelvis. 3. Ureter: (a) Cuboidal, (6) columnar. 4. i^ewa/ tubules: (a) 
Convoluted tubules, (6) straight collecting tubules. 

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in moderate or large numbers with the flat epithelia from 
the upper layers, indicate an acute cystitis. Cuboid 
or round epithelia alone, without the flat cells, indicate a 
chronic cystitis, and the presence of columnar or caudate 
epithelia from the deepest layer of the bladder indicates 
deep ulceration, tumors, or an intense inflammation. 
Cuboid and columnar epithelia may contan fat-granules, 
which indicate a chronic process. In the epithelia from the 
middle layers the formation of so-called endogenous pus- 
corpuscles may be observed — that is, pus-corpuscles are 
formed within the epithelia, especially in cases of hypertro- 
phied prostate, of uterine tumors pressing on the bladder, 
or any other condition which keeps up irritation or pressure 
from the outside. 

Epithelia from the Ureters. — These are especially 
seen in specimens obtained by the ureteral catheter, but 
may occur in urine mixed with pelvic epithelium. Two 
forms of epithelial cells from the ureter are seen: (i) 
Cuboid or round cells identical in size with those from 
the acini of the prostate and twice the diameter of a pus- 
cell. They are rarely numerous, and when present with 
renal and pelvic cells, the diagnosis between them and 
prostatic cells can be safely made. (2) Small caudate 
cells, smaller than the corresponding cells of the pelvis, 
from the deepest layers of the ureteral lining. These cells 
are distinguished from columnar cells in the bladder by 
the fact that they are much smaller. The ureter is rarely 
affected alone, except by irritation from stone, etc., and 
the presence of cells from the ureter is almost always ac- 
companied by the signs of pyelitis or cystitis. 

Epithelia from the Pelvis of the Kidney.— The 
epithelia in this part are very irregular in shape. The 

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characteristic form is the caudate, pear-shaped, or len- 
ticular, but round and cuboid shapes, smaller than 
bladder epithelia, also occur. The pelvic cells are smaller 
than those from the bladder and larger than those from 
the ureter and often have curved or bifurcated tails. 
Their transverse diameter is a little larger than that of a 
pus-cell. Their long diameter is three to four times this 
diameter. They have distinct nuclei and well-marked 
granules. Their presence indicates irritation or inflam- 
mation in the renal pelvis, and they occur in large numbers, 
with pus, in pyelonephritis. The round-cells, which are 
• less frequently found, closely resemble the renal cells, but 
are larger, being three to four times the diameter of a pus- 

Renal Epithelium.— The characteristic epithelial cell 
from the tubules of the kidney is small, round, more or less 
granular, with a single nucleus. These epithelia are the 
most important of all the cells found in the urine, and at the 
same time are the most difficult to recognize and the most 
frequently overlooked. Two forms are distinguished — 
the cuboidal (round), from the convoluted tubules, and the 
columnar, from the straight collecting tubules. Renal 
epithelia are much smaller than those of the pelvis of the 
kidney or of the ureter in the same person. They are 
quite constantly one-third larger than the pus-cells. 

The following description from Heitzmann sets forth 
clearly the method of looking for renal cells: 

"In every case examined, the first step is to look for 
pus-corpuscles, which are known to be small in some people 
and are usually the smallest granular corpuscle seen. 
As soon as these are decided upon, the next step is tb de- 
termine whether bodies distinctly larger than these are 

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present. If such bodies, one-third larger than pus-cof- 
puscles, are found in at least moderate numbers, we can be 
certain that they are epithelia from the convoluted narrow 
tubules of the kidney. The presence or absence of nuclei 
has no significance whatever, although such a nucleus is 
usually found in the kidney epithelia, but may be invisible 
in the pus-corpuscles. The relation between the size of 
the pus-corpuscles and that of the epithelia from the 
convoluted tubule is always the same — that is, the latter 
are one-third larger than the former. If the pus-corpuscle 
happens to be small in the case examined, the kidney epi- 
thelia will be small, but if large, the epithelia will be larger. 
The comparative sizes of the different smaller formations 


Fig. 60. — Corpuscles and epithelia, showing their comparative sizes. 

found in the urine are illustated in Fig. 60. The smallest 
corpuscles with double contour, and which are not granular, 
are the red corpuscles; the next in size, being the smallest 
granular corpuscles, are the pus-corpuscles; then follow 
the smallest epithelia found in urine, one-third larger than 
the pus-corpuscles — the epithelia from the convoluted 
tubules of the kidney. Finally, the next larger epithelia 
are shown, always twice the size of the pus-corpuscles, 
which are those from the ureter or from the prostate gland, 
between which no difference can be noted. If this relation- 
ship is kept in mind, no mistake can be made, though it 
must be remembered that when an individual small epi- 
thelial cell is found, the diagnosis cannot be positively 
made until they are compared with the pus-corpuscles." 

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The epithelia from the straight collecting tubules are 
less frequently seen, and occur in larger numbers only in 
the severe forms of nephritis. They are about the same 
size as the cuboidal, but narrower. Kidney epithelia 
may occur in clusters or in cast-like groups (epithelial 
casts, q. v.). 

The clinical significance of the presence of renal epithelia 
is not always appreciated. They are indicative of renal 
inflammation, and when casts are absent, as is often the 
case, they assist in making the diagnosis of nephritis. 
Renal epithelia are also present in suppurative conditions of 
the kidney, and, in combination with pus and cells from the 
pelvis, assist in making the diagnosis of pyelonephritis. It 
is very important, therefore, to look for renal epithelia 
whenever a renal affection is suspected. 

Epithelia from the Urethra. — The male urethra is 
lined with stratified epithelia which vary in different 
portions of the canal. In the fossa navicularis there 
is a stratified squamous lining. Cells from this portion 
are seen in the early stages of acute urethral inflamma- 
tion, after instrumentation, etc. They are flat, smaller 
than bladder cells, averaging five pus-cell diameters, with 
large nuclei (Fig. 6i). The anterior urethra is lined with 
columnar stratified epithelium. The most common ureth- 
ral cells come from this portion, and the majority of ureth- 
ral cells in urethritis (both in urine, shreds, and discharges) 
are of this type. They are oval, irregular, elongated, but 
maintain a fairly wide transverse diameter. Occasionally 
they are caudate and narrower (deeper cells). Their long- 
est diameter is about four times that of a pus-cell (see 
Plate ID and Fig. 80, A). 

In the membranous urethra the cells are practically 

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Plate io 

6 b 

m i< 

Epithelia in the Urine from the Urethra and Genital Organs. 
X about 500. 
I. Urethra. 2. Prostate: (a) Acini, {b) ducts. 3. Vesicles, 4. Ejac- 
ulatory ducts. 5. Vagina: (a) Superficial, {b) middle, (c) deep layer. 
6. Cervix: (a) Cuboidal, (fe) columnar. 7. Uterine mucosa. 

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• Digitized by VjOOQIC 



identical with those of the anterior urethra. In the pros- 
tatic portion there is a gradual transition toward the flat 
stratified epithelium of the bladder. The cuboid and 
columnar epithelia from this por,tion come from the numer- 
ous glands opening into the prostatic cavity. 

Fig. 61. — Epithelia from the fossa navicularis. 

In chronic urethritis, large flat, horny epithelia, looking 
like vaginal, and practically of the same size as the latter, 
but with very small, round nuclei, appear in the urine, as a 
result of the keratification of the urethral mucosa, which 
is transformed in places frankly into the stratified squa- 
mous type. These cells, when numerous and when occur- 
ring in shred-like masses with pus, indicate the probability 
of stricture formation (see Fig. 80, B). 

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In the female the urethra is lined with a very variable 
type of cells. In some women the squamous, in others the 
columnar, type predominates. The squamous cells are 
most numerous toward both ends of the canal. As a 
rule, squamous cells are most commonly found in the 
female urethra, while in the male, cylindric cells predomi- 
nate. The siise of urethral cells in both male and female is 
about three to five "pus-cell diameters" (in the longest 
direction), though the squamous cells may reach much 
larger sizes. 

Epithelia from the Prostate. — ^These are cuboid or 
columnar, the latter derived from the duct of the gland. 
The cuboid epithelia are twice the si^e of pus-cells, and 
identical in appearance with those from the ureter, but 
larger than those from the kidney. If these epithelia are 
present in large number, while renal and pelvic epithelia 
are absent or few in number, the cells of ambiguous si^e are 
undoubtedly prostatic and not ureteral. The accompany- 
ing presence of other prostatic elements (mucus-plugs, 
spermatozoa, etc.) also assists in the diagnosis. Prostatic 
epithelia may be found in the urine after coitus, after mas- 
sage of the prostate, and in the sediment of urine in cases 
of prostatic inflammation and prostatic abscess. 

Epithelia from the ejaculatory ducts and seminal 
vesicles may also be found in the urine, and are of 
the columnar ciliated variety. The cilia may become 
broken, but the character of the cell can be made out 
from the delicate striation of rods along the upper surface. 
These cells are very narrow and long, about five pus-cell 
diameters in length. Cells from the vesicles are of medium 
size, elongated or irregular, highly granular, about two 
and one-half pus-cell diameters in size, and often adherent 

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to spermatozoa. These epithelia may be found in the 
urine in cases of vesiculitis, tuberculosis of the vesicles, etc., 
and after massage of the vesicles. 

Epithelia from the Vagina. — ^These are the largest 
epithelia found in urine. Those from the upper layers are 
flat; from the middle layers, cuboid; from the deepest 
layers, columnar. The flat variety is present in most 
urines in women in health. They are increased in leukor- 
rhea, and may be present in masses, accompanied by 
bacteria, mucus, and granular matter. They may be 
shrunken and folded, and may contain fat-globules, which 
have no significance. They have very pale, fine granula- 
tions. The cuboid epithelia in the middle layer are seen 
in vaginitis in considerable numbers, and in chronic 
cases contain fat-granules. The columnar epithelia are 
seen in ulcerations and deep-seated inflammations. All 
these vaginal cells are larger than those of the corresponding 
layers in the bladder. They average seven or eight pus- 
cell diameters in size (the columnar, in their longest di- 
mension), but may reach even larger sizes. 

Epithelia from the Uterus. — These are not so fre- 
quently found in the urine, but should be remembered, 
as they may give rise to confusion. Epithelia from the 
cervix are flat, cuboid, or columnar, usually irregular 
in shape, and smaller than those in the vagina. They 
are practically identical with the irregular epithelia from 
the urethra, and can hardly be differentiated. Epithelia 
from the mucosa oj the uterus are tall, columnar, ciliated, of 
delicate structure. They are about one-fourth to one-fifth 
shorter than those of the ejaculatory duct, and less irreg- 
ular, but if the patient^s sex is known there is no need for 
this differentiation. Their presence indicates endometritis. 

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Extraneous Epithelia. — In both normal and pathologic 
urines scales of epidermis in the form of flat, horny cells 
from the genitals (prepuce, clitoris, and labia) are often 
present. They are recognised by their zigzag contours, 
by the absence of nuclei, the presence of fat-globules 
and dust particles, their pallor, and their shrivelled con- 


True casts of the kidney were first described by Henle 
in 1842, but they had been seen by Vigla, Quevenne, and 
Rayer in the years 1837 to 1840 in France, and by Simon 
and Nasse in 1842 in Germany. The first detailed de- 
scription was given in 1867 by Rovida. Casts may be 
defined as cylindric bodies which represent the molds of 
the uriniferous tubules of the kidney. The origin of 
renal casts is still unsettled. At one time they were 
considered as the product of secretion of the epithelia of 
the tubules, or as masses of transformed or disintegrated 
epithelia (Rovida). Later on their production was 
ascribed (Ribbert) to the transudation of coagular ele- 
ments of the blood, which pass into the tubules as a result 
of lesions in the walls of the latter, solidify in the lumen, 
and are voided with the urine. This last view is probably 
more close to the correct solution of this question than the 
others, and casts are probably the products of an exudation 
from the blood-vessels with the admixture of fragments 
of epithelia. 

One serious defect in this theory which has not yet been 
remedied or explained is the fact that undoubtedly there 
are cases in which casts are present in the urine without 
any albumin being detected by chemic means. The oc- 
currence of casts without any renal disease is now a well- 
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CASTS 299 

established fact (see below), and recent experimental and 
clinical research seems to point to the probability that casts 
may be regarded as evidences of an effort of nature to keep 
the renal tubules open and free from accumulations of dead 
epithelia. The epithelium shed is transformed into a 
plastic permeable mass and the latter is driven out witH 
the stream of urine as soon as it becomes sufi&ciently 

Clinical Significance. — In speaking of albuminuria 
we have tried to emphasize the fact that the presence of al- 
bumin does not necessarily mean the presence of nephritis. 
The same is true of casts. At least some varieties of casts 
occur without any renal lesions, indeed, may occur under 
certain conditions in health. That casts may occur with- 
out renal disease is now well established by the researches 
of Nothnagel, Senator, and others. The occurrence of 
casts in the urine after muscular exercise (Penzoldt, 1893, 
von Noorden, 1904), after drinking alcoholic beverages 
(Luthje), and after taking large doses of irritating sub- 
stances (Filosofofl, 1905), such as pepper, mustard, onions, 
alcohol, turpentine, have also been well demonstrated. 

Filosofoflf^ examined 50 healthy young men whose 
history was free from alcoholism and acute nephritis, and 
whom he had watched for a long period on a known diet. 
These men were kept constantly at rest during the observa- 
tion. In 17 of these men he found hyaline casts; in 12 
granular casts; and in 13 cylindroids. In other words, 52 
per cent, of these young men showed some form of cylindric 
elements in the urine. 

It seems settled that casts may occur without the pres- 
ence of albumin. In the writer's experience, which em- 

^ Roussky, Vratch, 1905, No. 50, p. 1561. 

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braces an examination, up to the time of writing, of over 
10,000 specimens of urine, at least 10 per cent, of all speci- 
mens in which casts were found contained no albumin that 
was apparent upon clinical tests. Actual figures are not 
available, but this is a conservative estimate. The casts 
found in these cases were usually hyaline, and sometimes 
faintly granular. Hyaline casts are found much more 
frequently in healthy urines than is generally supposed, 
provided the examiner uses proper care in his work. 

Although the presence of a feW casts without albumin 
in an otherwise normal urine is still looked upon as evi- 
dence of an impaired risk by insurance companies, and 
although unfortunately some physicians continue to make 
the diagnosis of Bright^s disease upon this basis, the writer 
is convinced from his experience that the clinical signifi- 
cance of casts in these circumstances has been very greatly 
exaggerated. In order to make a diagnosis of renal disease 
it is always important to weigh separately each micro- 
scopic and each chemic finding as a part of the evidence, 
and to base our judgment upon the particular combina- 
tion found in each case. When thus considered the pres- 
ence of casts is a very useful factor in localizing and differ- 
entiating renal disease. 

In the following pages a detailed description of the 
various casts will be given. Pure hyaline and faintly gran- 
ular casts are the most common forms, and are not neces- 
sarily nephritic in origin. Coarse granular, epithelial, fatty, 
and other forms are always pathologic. 

Classification of Casts. — The following table (Og- 
den) shows a useful classification of tube-casts: 

'(i) Pure hyaline. 
I. Hyaline (transparent) casts. . . . -j (2) Fibrinous. 

,(3) Waxy. 

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CASTS 301 

({i) Fine. 

/ II. Granular casts "{ (2) Coarse. 

1(3) Pigmented. 

III. Epithelial casts. 

IV. Fatty casts. 
V. Blood-casts. 

VI. Pus-casts. 

C(i) Urate. 

VII. Crystalline casts -^ (2) Oxalate. 

((3) Cystin. 
VIII. Bacterial casts. 

Hyaline Casts. — There are three varieties of hyaline 
casts: (i) Pure hyaline; (2) fibrinous; (3) waxy. 

Pure Hyaline Casts, — These are pale, delicate, trans- 
parent, homogeneous cylinders, varying in diameter and in 
length, usually with rounded ends and parallel and straight 
sides, but sometimes indented, twisted, serpentine in shape, 
with ragged ends. It is very dijfficult to detect pure hyaline 
casts, except by constant focusing with the fine adjustment 
of the microscope and by diminishing the amount of light 
in the field. Pure hyaline casts occasionally contain 
some very fine pale granules, or here and there show 
upon their outlines a blood-cell, a leukocyte, a droplet of 
oil, etc. Such casts are still in the hyaline class. The 
source of the hyaline casts may be to a certain extent de- 
duced from their diameter. The smaller, narrower casts 
arise from the convoluted tubules, while the larger ones 
come from the straight or collecting tubules. 

The mode of origin of hyaline casts is still unsettled. 
According to Rovida, they are the products of secretion 
by the tubular epithelium, but experiments on animals 
made by Ribbert show that they are probably due to the 
exudation of albumin within the tubules. Whatever may 
be their origin, the mere presence of pure hyaline casts 
must not lead to the hasty conclusion of the existence of 
renal disease. 

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Hyaline casts are commonly found, however, in a great 
many diseases and disturbances of the kidney, especially 
in chronic interstitial nephritis, in amyloid kidney, and in 
passive congestion. In acute nephritis and in active 
congestion they are most numerous. They may be the 
only indications of a severe nephritis, and, on the other 
hand, these casts are met with in the urine of persons with 

Fig. 62. — Hyaline casts viewed in a darkened field of the microscope. 

healthy kidneys in whom no albuminuria or any other 
sign of renal inflammation had ever been observed. They 
may be evidences of a renal irritation caused by a strain upon 
elimination due to overabundant food, excess of meat in 
the diet, or intestinal intoxication. In such cases albumin 
is often absent, and the casts disappear after the cause is 
removed. To find hyaline casts we use, in preference, 
fresh urine, and sediment it, instead of centrifuging. 

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Plate u 

Fibrinous Casts [Ogden), 

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CASTS 303 

Fibrinous casts are dense, highly refractive, transparent, 
and of a yellowish color, which ranges between pale yellow 
and deep brown. Like pure hyaline casts, they vary in 
shape and si^e, but are, as a rule, larger than the average 
hyaline cast. They should not be confounded with waxy 
casts, which are always perfectly colorless. The term 
fibrinous casts is inappropriate, as they have nothing to do 
with fibrin and are suggestive only by their yellow color. 
Like pure hyaline casts, they may be studded with fine 
granules and may have adhering blood or fat-droplets. 
Their presence indicates an acute disease or disturbance 
in the kidneys, and fibrinous casts are, as a rule, seen only 
temporarily during the acute stage of these conditions. 
They are not unfavorable signs in prognosis. , 

Waxy Casts.— Thtse casts are very highly refractive 
and always perfectly colorless and transparent. They 
are usually large in diameter, and vary in shape like the 
pure hyaline. They may be studded with coarse granules, 
and may have adhering the same elements as the pure 
hyaline casts. They are so dense that they may look 
cracked or broken into segments, with irregular ends. 
They are never present in active congestion and in acute 
nephritis, but are found in advanced stages of chronic 
nephritis, both interstitial and parenchymatous. They 
are, as a rule, of bad prognostic significance. They are 
often seen in amyloid infiltration of the kidneys, and in 
this condition are of some diagnostic value, although not 
pathognomonic, as they occur in other chronic diseases of 
the kidney. It must be remembered, however, that the 
term "waxy ^' is misapplied to these casts, as they show the 
"amyloid reaction" with methyl- violet and potassium 
iodid and iodin solution, in the absence of amyloid de- 

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generation, and, on the other hand, this reaction is absent 
in some cases when this degeneration exists. 

All the other casts to be described are practically modi- 
fications of the hyaline cast, which forms the groundwork 
upon which various elements adhere or into which they 
become imbedded. A hyaline cast covered with granules 
is a granular cast; one covered with epithelia is an epi~ 
thelial cast, etc. 

Granular casts consist of a hyaline basis in which fine, 
coarse, or pigmented granules are imbedded. These 

Fig. 63. — fl, Hyaline and finely granular cast; ft, finely granular 
cast; c, coarsely granular cast; d, brown granular cast; ^, granular cast 
with normal and abnormal blood adherent; /, granular cast with renal 
cells adherent; gy granular cast with fat and a fatty renal cell adherent 

granules probably come from the disintegration of renal 
epithelia, or partly from the destruction of blood-cells. 
The pigmented granules, also called "brown granules," 
probably derive their color from blood-pigment. Granu- 
lar casts may be stained yellow or brown by bile. 

These casts vary considerably in dimension, and are 
often broken, the end often being concave or zigag. Some- 

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CASTS 305 

times they show fragments of epithelial cells and transition 
forms which prove that the granules are derived from the' 
epithelia, and that granular casts are degenerated forms of 
epithelial casts. They may be found in any inflammatory 
condition of the kidney, and do not indicate any particular 
disease of this organ. Their presence is about equally 
significant with that of renal epithelia as evidence of neph- 

Fig. 64. — I, Epithelial cast; 2, blood-cast; 3, pus-cast; 4, fatty cast; 
5, fatty cast with a compound granule and fatty renal cell adherent 
(crystals of the fatty acids protruding) (Ogden). 

Epithelial Casts. — ^When a cast is entirely covered 
with renal epithelium, it is called an epithelial cast. The 
basis of this formation may be either hyaline or granular, 
and the cells may be imbedded or only adherent. When 
only one or two cells adhere to a hyaline cast, the term "hy- 
aline with adherent epithelium" should be used. The 
outlines of the cells are not always distinguishable, but 
their nuclei usually stand out prominently. The cells 
may contain fat-globules, and leukocytes may adhere to 
these casts along with the epithelium. 

Perfectly formed epithelial casts appear in urine under 
such conditions only as cause the separation of renal epi- 

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thelium in the entire circumference of a renal tubule. 
They always indicate an active inflammatory process in 
the parenchyma of the kidney, and "their presence alone 
sufiices to establish the existence of acute nephritis or the 
supervention of a fresh paroxysm in that disease" (von 
Jaksch). The intensity of the inflammatory process is in 
proportion to the number of these casts. They are rarely 
found in chronic and interstitial nephritis and in amyloid 
kidney. Epithelial cylinders with a lumen may be seen in 

Fig. 65. — Blood -casts, composed wholly of red or white corpuscles, or 
hyaline substance covered with blood-corpuscle. 

cases of great congestion in which the lining of the tubules 
is thrown off unchanged. 

Blood-casts. — These casts consist of a hyaline or granu- 
lar base, covered with red blood-cells or of cylinders of 
coagulated blood (fibers) with imbedded blood-cells. 
The occurrence of blood-casts indicates a hemorrhage 
into the tubules. According to the length of time which 
these casts have remained in the tubules, the blood-cells 
on them may be normal or abnormal (see p. 275). 

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CASTS 307 

Blood-casts are found in the renal hematuria due to 
tuberculosis, stone, tumor, etc.; in acute nephritis, acute 
congestion, and hemorrhagic infarcts of the kidney. 
Their presence simply shows the existence of renal hemor- 
rhage, and not necessarily of renal disease. 

Fatty casts are cylinders which are thickly studded 
with fat-droplets and granules. The term does not apply 

Fig. 66. — Fatty casts (after Peyer). 

to hyaline or granular casts which show one or two oil- 
globules. They occur in short, highly refracting cylinders, 
and may show bristling, needle-like hair or crystals of fatty 
acids. The minute fat-drops are highly glistening, and 
should not be confounded with granules, which have a 
duller luster. 

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These casts were first discovered by Knoll, and are 
usual in protracted cases of chronic nephritis with a 
tendency to fatty degeneration of the kidney. Fatty de- 
generation, it must be remembered, shows an advanced 
stage of alteration in the renal cell. Fatty casts are also 
found in the fatty stage of acute nephritis, and occasion- 
ally in severe renal congestions. 

Pus-casts are hyaline or granular cylinders covered 
with pus-cells or leukocytes. They are often confounded 
with epithelial casts because the pus-cells are often so 

Fig. 67. — Casts formed of leu- Fig. 68. — Casts of urates from a 
kocytes from a case of acute neph- case of emphysema (von Jaksch). 

ritis (von Jaksch). 

granular that the nuclei are obscured. The addition of 
dilute acetic acid dissolves the granular matter and shows 
the nuclei of the leukocytes. 

Pus-casts are not met with, except in a chronic suppura- 
tive process in the kidney, such as an abscess, tuberculosis, 
and chronic pyelonephritis. In cases of chronic pyelitis 
or pyelonephritis there may be casts from the pelvis, calices, 
or from the straight tubules, consisting of large and ir- 
regularly shaped plugs of coagulated material covered with 
pus-cells. In acute non-suppurative nephritis and in acute 

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exacerbations of chronic nephritis there may be hyaline 
or granular casts, with a few adherent pus-cells, but these 
do not constitute true pus-casts. 

Crystalline Casts. — These are simply hyaline or 
granular casts to which crystals or amorphous granules 
of a chemic sediment are adherent or in which these are 
imbedded. A urate cast is one covered with crystals of 
ammonium urate, usually of the characteristic spheric 
shape. The cystin cast is rarely seen in cystinuria, and 
is covered with cystin crystals. The calcium oocalate casts 
are covered with the crystals of this substance. Amor- 
phous urates, when present in large amounts, may coat 
hyaline or other casts and obscure their true morphology. 
In such cases it is important to dissolve the urates in warm 
water, as has been described on page 258. 

Bacterial casts are cylinders covered with bacteria, 
but masses of germs that resemble these casts, and that 
sometimes are seen in urine undergoing decomposition, 
do not constitute bacterial casts. The latter are some- 
times confounded with the pigmented or brown granular 
casts, but resist the action of acetic acid and strong alkalis. 
Bacterial casts are rare, and usually indicate renal suppu- 
ration or renal embolism. 


False casts, mucous casts, or cylindroids are occasionally 
found in urine, and seem to be pure mucous molds of 
tubules. Their true chemic nature is not exactly known, 
but they have little clinical significance and are frequently 
present without any albumin. They are smooth, long, 
flat, transparent, finely fibrillated, with indistinct, wavy, 
longitudinal striations, and have tapering ends. They are 

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characterized especially by their great length, and are 
often twisted or folded. The chief interest in false casts 
is their resemblance to true casts, and they must be care- 
fully distinguished by means of the peculiarities just de- 
scribed. Occasionally, epithelia or other elements may 
adhere to them and increa,se their resemblance to true 

False casts are found usually wherever there is irritation 
of the bladder and lower urinary passages which has ex- 
tended up to the kidneys. They are also found in urine of 
very high specific gravity, but it must be remembered 
that they are not identical with mucus threads, although 
chemically false casts and mucous threads are probably 
the same. Mucus in the urine may often be found 
moulded into false casts upon prolonged and rapid centri- 


Mucous threads appear in normal urine in the form of 
more or less opaque, ropy masses of irregular shape, 
but sometimes in the form of long and transparent shreds, 
the ends of which taper or split in fine divisions, which 
fade away imperceptibly. They are often covered with 
amorphous urates, and may be mistaken for casts. They 
are, however, flat and not cylindric; generally very much 
narrower than casts, and their granules can be dissolved 
with a little heat on the addition of acids or alkalis. The 
presence of these threads has no very marked clinical 
significance unless there is an excessive amount of mucus, 
which indicates irritation or inflammation in some part of 
the genito-urinary tract. Mucin threads may be demon- 
strated by the addition of a little acetic acid and a little 
solution of iodin, potassium iodid, tartaric acid, or dilute 

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mineral acids, but an excess of the latter will redissolve 
the mucin. Mucin threads may be found in urine without 
addition of acids, being probably precipitated by the action 
of acids formed in acid fermentation. The greater the 

Fig. 69. — False casts (after Peyer). 

irritation in the genito-urinary tract, the more opaque, 
the thicker, and the more ropy becomes the mucus, and 
appears then in the form of clouds mixed with epithelial 
cells from the seat of the trouble. 


Prostatic plugs are large, colorless, or yellow molds 
of the prostatic ducts (Fig. 70), cylindric, with rounded 
ends, or of irregular shape. Their outlines are not sharply 

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defined, as they generally are found in clouds of mucus, 
but their chief characteristic is the fact that they have im- 
bedded in them or adherent to them spermatozoa and 
epithelial cells from the prostatic ducts. Their presence 
indicates an inflammation of the prostate involving the 
ducts, and they are said to occur in urines after massage 

Fig. 70. — Spermatozoa: At a are so-called Bottcher crystals; at b, amy- 
loid bodies; at c, a prostatic plug (Jakob). 

of the prostate, but the examination of a very large number 
of such specimens by the writer showed that they are very 
rare in massage-urine. They are interesting because they 
are apt to be mistaken for casts. Their occurrence is, in 
fact, a matter of some doubt. 

Amyloid bodies, or corpora amylaceay are minute bodies 
which are found in the acini of the prostate, and occa- 
sionally occur in the urine, ^ especially after massage of a 

^ Amyloid bodies are also found in urethral shreds, and are said 
to be present normally in the urine in very small numbers. 

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prostate in the state of chronic follicular prostatitis. The 
word "amyloid" is a misnomer, as these bodies have noth- 
ing to do with starch chemically. They are more or less 
opaque, rounded bodies, of either homogeneous or lamel- 
lated structure. Their central portions consist of a darker 
or more densely lamellated core. They are not affected by 
hot water nor dissolved by strong nitric acid; they are 
colored red with methyl-violet, while starch takes a blue 
color. Amyloid bodies, when treated with iodin, often 
show a violet color which becomes blue on the addition of 
sulphuric acid. Their clinical significance is doubtful. In 
old men larger masses of these bodies may occur, visible to 
the naked eye, and surrounded with a mixture of phos- 
phates to form the so-called prostatic concretions which 
form in the follicles of the prostate. 


Spermatozoa are bodies about 50 [i in length, consisting 
of an oval head, a minute body, and a long, delicate, 
whip-like tail (Fig. 70). In fresh semen they show active 
eel-like movements, but in urine they usually become 
motionless in a short time. They require the high power for 
their detection and fine focusing for their demonstration. 
In the urine they may be accompanied by mucus, pros- 
tatic plugs, amyloid bodies, and by epithelia from the pros- 
tate, the vesicles, and the neck of the bladder. The so- 
called spermin crystals (Bottcher^s crystals) which are 
present in prostatic secretion never occur in the urine, as 
they do not form in acid media. 

Clinical Significance. — Spermatozoa are found fre- 
quently in the urine of healthy men, and of both sexes after 
coitus. They are found also in men after nocturnal 

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emissions, and sometimes in the urine in acute fevers, 
sepsis, and convulsions. Their most important clinical 
bearing is in cases of spermatorrhea, when they are con- 
stantly found in the urine, and also in cases of acute and 
chronic prostatitis and seminal vesiculitis, or of congestion 
or irritation of the prostatic region. The presence of an 
inflammatory condition in cases in which spermatozoa are 
found may be inferred from the coexistence of mucus, 
pus, epithelia from the region concerned, and from the 
broken tails and immovable condition of the spermatozoa. 

Dead spermatozoa frequently are found curled up into 
various grotesque shapes. 

The detection of spermatozoa is important from the 
medicolegal aspect in cases of suspected rape. It is easy 
to show their presence in vaginal secretion, and stained 
linen may be soaked in either water or salt solution and 
the sediment examined. A chemic reaction which may 
aid in their recognition was described in 1897 by Florence, 
of Lyons. A few drops of the suspected fluid are treated 
with a drop of Florence's reagent, which consists of: 

Potassium iodid 1.65 gm. 

lodin 2.64 " 

Distilled water 30.00 " 

This reaction is probably dependent on the presence of 
cholin. If semen is present, small, dark, rhombic crystals 
appear, resembling closely the hemin crystals described in 
Teichmann's test for blood. 


By massage-urine is meant the urine voided by the 
patient after the contents of the prostate and seminal 

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vesicles have been expressed into the prostatic urethra 
by kneading and stripping these organs through the rectum. 
In such urines a variety of semisolid elements occur; the 
microscopic structure and clinical significance of which 
were made a subject of research by the writer.^ 

Fig. 71. — Stained smear taken from a sago body ( X 257. Eosin meth- 

One or more of the following classes of elements may 
be found present in these urines: (i) "sago bodies"; 
(2) "sugar granules"; (3) vesicular "skins"; (4) vesicular 
casts and vesicular shreds. 

^ Saxe, A Study of Sago Bodies and other Vesicular Elements in 
Massage-urine, etc., New York Med. Jour., Nov. 23, 1907. 

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Sago bodies were originally described by Lallemand and Trousseau 
in the urines of patients with spermatorrhea. They consist of sago-like 
masses of colloid material of the size of a small pea or lentil in which are 
embedded numerous motionless spermatozoa. The latter are often packed 

Fig. 72. — Casts from the vesicles and the ampulla of the vasa deferentia 
in a case of atonic vesiculitis. ( X 5- In dish with salt solution.) 

closely at the edges, in several layers. These bodies contain epithelia from 
the vesicles and occasionally a leukocyte (Fig. 71). The sago bodies are 
derived from the recesses of the seminal vesicles which offer molds for 
their formation. 

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Sugar granules are much smaller, of the size of a pinhead or a little 
larger, and are glassy, translucent, having the appearance of melting 
sugar. They settle at the bottom of the vessel and dissolve rapidly. 
Their structure is practically the same as that of the sago bodies, save that 
they contain fewer spermatozoa. They may consist merely of a translu- 
cent colloid matrix, highly refractive. The writer found them to be 

Fig. 73. — Vesicular cast, showing the characteristic concentric arrange- 
ment of the spermatozoa and the lobulation. (§ obj. Eosin-methylene- 

fragmented masses of secretion from parts of the vesicle where there were 
few or no spermatozoa — i. e., probably from the fundus of the organ. 

The vesicular skins are fine, translucent or slightly opaque, whitish 
pellicles, often presenting an appearance of hollow shells, like the thin 
shells of lemon seeds, grouped in masses. When removed from the urine 
they collapse into viscid shreds. The skins are probably composed of 
inspissated or thickened vesicular secretions which have lain for a consid- 

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erable time in the vesicles, and which have been stripped by massage. 
Microscopically they contain the same elements as the sago bodies, but 
densely packed and mixed with ropy mucoid material. 

Vesicular casts are moulded forms of vesicular contents (see Figs. 
72-74) which may be grouped in grape-like masses or may occur 

Fig. 74. — Gonococci and streptococci, epithelia and pus-cells, in stained 
smear from a vesicular cast (Gram's stain: X960). 

in elongated, sausage-likfe forms. They are semi-opaque, whitish, and 
are easily seen with the naked eye. Microscopically, they present a 
lobulated border, with concentric layers of spermatozoa in dense masses 
at the edges and numerous spermatozoa in the central portions (Fig. 73). 
They may contain gonococci, staphylococci, streptococci, etc., in vesiculi- 
tis due to these germs (Fig. 74). 

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Vesicular shreds are often of large size and look like pieces of egg- 
membrane. They consist of a mucoid matrix in which are imbedded 
many spermatozoa, vesicular epithelia, and pus-cells. They often contain 

Clinical Significance. — A careful study of the clinical 
significance of these bodies showed that the sago bodies, 
the sugar granules, and the "skins" may occur without 
any vesicular inflammation. They may be present in 
normal individuals who are relatively sexually continent, 
but they are increased as the result of a stagnation of 
secretion in the vesicles in that type of vesicular atony 
which the writer has termed "spermatostasis." Vesicu- 
lar casts and vesicular shreds, on the other hand, especially 
when they contain pus-cells and bacteria, are evidences of 

Smears from any of these structures may be made by 
washing the bodies in normal salt solution, spreading thinly 
on a slide, fixing with equal parts of alcohol and ether for 
fifteen minutes, and staining with eosin and methylene- 
blue according to the method described for urine sediments 
on p. 244. Gram's stain may be used to show gonococci, 
which, however, are rarely found. An examination of 
stained smears of the massaged material is essential before 
making a diagnosis of vesiculitis, as the mere presence of 
even large amounts of semisolid massaged bodies is not 
conclusive evidence of vesicular inflammation. The find- 
ing of pus and of bacteria is necessary before the diagnosis 
of vesiculitis can be made. 


Urethral shreds occur in the urine in chronic inflamma- 
tions of the urethra, particularly in chronic gonorrhea and 

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Stricture. Very little information concerning shreds 
appears in the text-books and the writer herewith presents 
a summary of his own studies on these elements, based on 
extensive clinical material.^ 

The Author's Technic. — Shreds may be obtained di- 
rectly from the urine or by washing the different portions 
of the urethra, as described in text-books on urology. 
They should be fished out with sterile platinum wires and 
spread on slides. They should then be fixed with equal 
parts of alcohol and ether for ten minutes, stained for 
from one to two minutes in Unna's polychrome methylene- 
blue, washed thoroughly in distilled water, and dried. 
They may then be immediately examined after mounting 
in balsam, or if still better pictures are desired, the dried 
film should be dehydrated for a few seconds in alcohol, 
dried with filter-paper, and cleared in xylol or oil of cloves. 
On drying, the film may be mounted in balsam and ex- 
amined. For the detection of gonococci in shreds, Gram's 
stain (see p. 331) may be used instead of the polychrome 
blue, the other steps in the technic being the same. 

Urethral shreds proper may be divided into four varie- 
ties: pus shreds, mucopus shreds, mucous shreds, and epi- 
thelial shreds, each of which have special naked-eye and 
microscopic characteristics. 

Pus Shreds (Fig. 75). — These are dense, heavy opaque, yellowish- 
white, often thick and shaggy, usually short and friable. They tend to 
sink readily to the bottom of the vessel. Microscopically, they consist of 
innumerable pus-cells, closely packed in a scarcely visible matrix of 
homogeneous character, and contain singly or in small groups epithelia 
from the urethra. The latter may be normal or they may be in a state of 

* See Saxe, A Study of Shreds in the Urine in their Relation to 
Diagnosis and Prognosis, New York Med. Jour., March 2, 1907. 

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hyalin degeneration. In this case, the writer has found them to ♦stain 
quite dififerently from normal epithelia, with polychrome blue (Fig. 76). 
They stain dififusely without chromatic distinction between nucleus and 
cell body, and are markedly mor6 reddish than normally staining urethral 
cells, which show deep purple nuclei and pale bluish-violet cell bodies. 
For a fuller description of urethral epithelia, see page 294. 

Yig, 75. — Pus shred, showing pus, epithelia, and strands of matrix 

Mucopus Shreds. — These are longer, more wavy or twisted, very ir- 
regular in shape, thinner, more translucent, grayish white, and show 
faint whitish longitudinal streaks and occasional large opaque nodes. 
One of their ends may curl up into a knob, causing them to resemble com- 
mas. Microscopically (Fig. 76), they consist of the same elements as the 
pus shreds, save that the homogeneous mucoid matrix is much more abun- 
dant, while the pus-cells are fewer in number and appear in scattered 
groups. Some of the pus-cells are fragmented, showing the beginning of 
disintegration. The epithelia vary in number and may be so numerous 

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as to justify the name epitheliomucous shreds. They show the same 
changes as those found in pus shreds. 

Mucous Shreds. — These are the lightest of all urinary shreds and 
persistently float at or near the surface of the fluid. They are long, thin, 
almost transparent, with faint gray striations. When removed from 
the urine they appear as translucent, viscid streaks of mucus. Micro- 
scopically (Fig. 77), they consist of a mucoid matrix arranged in fibrillated 
layers and staining a deep purple with polychrome blue in contrast to the 

-f^ " 

— ^C 

Fig. 76. — ^Mucopus shred, showing amyloid body (A) and contrast be- 
tween normal (B) and chromatically degenerated epithelia (C) ( X 249)- 

lighter shade seen in the matrix of pus shreds and mucopus shreds. 
Within the strands of mucus there are usually a few epithelia which show 
distinctly by contrast, and occasionally there are the remains of a few 

Epithelial Shreds. — Of these there are two varieties: The first 
consist of large masses of epithelia with a moderate proportion of pus-cells, 
and without any distinctly visible matrix. These shreds are found in 
the urine as short, flaky, or scaly masses, usually rather loosely knit and 

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shaggy. Their microscopic appearance is shown in Fig. 78. They 
are characteristic of very chronic urethral inflammations, specially of 
stricture formation. 

The second variety of epithelial shreds are purely epithelial and are 
comparatively rare. They are very thin, semitransparent, sink quite 
rapidly, wrinkle, and look like bits of desquamated epidermis. They 
are composed simply of a pavement of large pale, flat cells, which cling 

Fig- 77* — ^Mucous shred in a case of chronic urethritis with glandular 
lesions, showing stratification of matrix and remains of pus-cells 
(X 147-5). 

to one another, occasionally overlapping (Fig. 79). The squamous cells 
found in the epithelial shreds of both varieties are altered urethral cells 
which are characteristic of chronic urethritis with hard infiltration (Fig. 
80). In this condition the cells of the superficial layers of the urethral 
mucosa are transformed into squamous cells, contrasting with normal 
urethral epithelia, which are commonly of the stratified cylindric type. 
The pure epithelial shreds are seen sometimes after the passage of in- 
struments or after applying solutions of silver nitrate through the ureth- 

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roscope. They may appear, however, spontaneously in patients with 
hard infiltrates in the urethra. 

Comma Shreds. — These are of two varieties in the writer's experience: 
The false comma shreds (already mentioned), which may come from 
any part of the urethra and which are nothing but mucopus shreds curled 
up at one end. They may come from any part of the urethra and appear 
in the urine as short comma-like structures which have been erroneously 
supposed to come from the prostatic ducts. The true comma shreds are 

Fig. 78. — Epithelial shred from a case of stricture 12 F. at P. S. junction, 
showing flat epithelia and pus-cells (X 167.4). 

rarely found in the urine, except in the last glass in a test involving a 
sequence of glasses into which the patient is asked to urinate. (The 
Kollmann five-glass test.) They are sometimes found in urine after 
prostatic massage. These true comma shreds come from the prostatic 
ducts and outwardly resemble the false comma shreds, but microscop- 
ically they consist of epithelial masses from the prostatic ducts, usually 
arranged in two layers, one of which is composed of cylindric, the other 
of smaller rounded, cells. 

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Urethral shreds 325 

Clinical Significance of Shreds.— The examination 
of shreds in the urine is of great importance in diagnosticat- 
ing the stage of a chronic urethritis and in determining the 
character of the lesions in the urethra, and is of value to 
some extent in the prognosis of chronic urethritis. 

I^ig' 79- — Pure epithelial shred in a case of chronic urethritis with 
hard infiltration in the bulbous urethra, showing pavement of cells and no 
pus (XI47-5)- 

The examination of shreds is not of much value in local- 
izing the affection in the anterior or posterior urethra. 
The presence of prostatic or vesicular epithelia and of 
spermatozoa in the shreds may point to the involvement of 
the prostatic urethra, but the localization of a urethritis 
must be carried out by other methods which do not belong 
to urine analysis. 

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Urethral shreds appear with a fair degree of regularity 
with each stage of urethritis, the order usually observed 
beginning with a subacute case and ending with a pro- 
nouncedly chronic condition with induration and stricture 
formation: (i) Pus shreds; (2) mucopus shreds; (3) 

Fig. 80. — Epithelia found in shreds: A, Normal urethral epithelia; 
B, modified flat cells from the superficial layers in the stage of hard in- 

mucous shreds, and (4), epithelial shreds. While this is 
the typic evolution of shreds in chronic urethritis, this 
rule is subject to many exceptions. For example, if an 
acute exacerbation occurs in the course of a chronic case, 
some of the types of shreds which had been present earlier 
will reappear. Moreover, the same urine may contain 

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several varieties of shreds, as different parts of the urethra 
may not keep equal pace in the progress of the disease. 

Each of the varieties of shreds described, however, has 
a distinct significance as regards the pathologic process in 
the urethra which each type represents. Pus shreds indi- 
cate a subacute or chronic exudative process. They are 
the first signals of chronicity and appear in the chronic stage 
whenever an active inflammatory process is going on. As 
the urethritis becomes more chronic the pus-cells gradually 
disappear and the epithelia and mucoid matrix increase, 
bringing the shreds closer to the mucopus variety. The 
latter are first found when the chronic process begins to 
assume the catarrhal type and when the glandular in- 
volvement first comes to the fore. The mucopus shreds are 
the most frequent and the most persistent type of shred in 
the urine. As the exudative inflammation gradually dis- 
appears and the catarrhal phase frankly sets in, the next 
variety, the mucous shreds, appear. The mucous shreds 
signalize chronic soft infiltration with predominant glandu- 
lar involvement. There may be single mucous shreds per- 
sisting for a long time. If the process now heals, this last 
shred disappears. But if hard infiltration develops, as is 
usually the case, shreds of flat epithelia, with or without 
pus, are seen. The epithelial shreds with pus are evi- 
dences of ulcerative conditions or of strictured areas around 
which there are ulcerating or granulating lesions. 


The urine may contain bacteria, molds, or yeasts. 
Fresh urine is said to be sterile in « normal persons if 
obtained directly from the bladder, but is contaminated 
in transit by the bacteria always present in the urethra. 

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If urine is allowed to stand in the air for some time, 
it becomes turbid from masses of bacteria of the non- 
pathogenic variety. The conversion of urea into am- 
monium carbonate is probably 
produced by several bacteria, 
of which the Micrococcus 
ureae (Fig. 8i) is the most im- 
portant. This germ is found 
very frequently on the surface 
of decomposing urine, and 
occurs in chains of round, 
highly refracting dots. It is contantly present in the air. 
Large varieties of other bacteria which take part in the 
decomposition of the urine have been described. 

Molds are not seen normally in decomposing urine, 
but often occur in diabetic urines floating on the surface. 


8 1 . — Micrococcus 
(after von Jaksch). 

Fig. 82. — Sediment from fermenting diabetic urine with casts of 
micrococci: a, 6, c, Various forms of uric acid; </, micrococci in form of 
casts; e, molds; /, yeast fungi; gy bacilli and micrococci (after von 

A variety of molds may be found in urines which have 
been allowed to stand in uncovered vessels. 

Yeasts. — The beer-yeast fungus is found in diabetic 
urine or in urine contaminated accidentally with sugar. 
It occurs in oval, transparent cells, free or in groups of 

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three or more, and multiplies rapidly in acid urine, but 
ceases to grow when it becomes alkaline. They should not 
be mistaken for red blood-cells, and are distinguished by 
their oval shape and the presence of a cell body without 
a focal point. 

The Sarcina urinae is found occasionally in urine, 
resembles the sarcina of the lung, and occurs in cubes of 
eight cells, each arranged like a bale of goods. In some 
cases very many sarcinae are present. Their clinical sig- 
nificance, if any, is not established. 

Pathogenic Bacteria.— Of these, a large number 
have been found in urine. In a great variety of the 
suppurative conditions of the urinary tract the bacteria 
of pus-formation are found — Streptococcus pyogenes; 
Staphylococcus pyogenes albus, citreuSy and aureus. 
In many specific diseases, as in typhoid fever, anthrax, 
glanders, erysipelas, and tuberculosis, the germs of these 
affections are found in the urine. 

Technic of Preparing Bacterial Smears from Urine. — Much diffi- 
culty is often encountered in making good stained smears from urine for 
bacterial study, and this is especially the case when the urine is clear, 
contains no pus, and little epithelial or mucoid material. The urinary 
salts, especially urea, interfere materially with staining (see Methods of 
Staining Urinary Sediments, p. 244). 

The best results are obtained by thoroughly centrifuging the sediments. 
If any visible sediment can be obtained the centrifuge tube should be 
quickly drained and the sediment adhering to the bottom scraped off 
with a platinum loop, the tube being held bottom up during this pro- 
cedure. In this way smears with a minimum of urinary salts will be ob- 
tained. If very scanty sediments are present, especially if there is no pus, 
the urine should be diluted with from one to two volumes of alcohol, 
allowed to settle, and the sediment centrifuged thoroughly. Smears 
made from such sediments are quite free from urinary salts. 

If the smear thus obtained will not adhere to the slide, which is the 
case when there are no pus-cells and few epithelia, the addition of a little 

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egg-albumen and glycerin to the sediment on the slide will often help to 
secure better films. The mixture is thinly spread upon the slide with the 
platinum loop. 

After the film is spread the slide is fixed by being passed thrice through 
the flame of a Bunsen burner. A better way is to cover the film with 
equal parts of absolute alcohol and ether and allow the fluid to evaporate 
slowly till the film is dry. The film is then ready to be stained. The 
methods of staining will be described in dealing with the different germs. 

The most important pathogenic germs in the urine are 
the Bacillus coliy the gonococcus, and the tubercle bacillus. 

The Bacillus coli (colon bacillus) is not a single germ, 
but is a name for a large group of germs. It varies in 
length, but usually is a short, thick bacillus with rounded 
ends (i to 2.5 ^ long and 0.5 ^ thick), sometimes occurring 
in pairs and sometimes so short as to look like a coccus. 
It is very common in urinary infections, and is derived 
usually from the intestinal tract, where it is constantly 
met with. It is feebly motile in the urine and decolorizes 
by Gram's stain (see below). It can be stained with any 
of the ordinary anilin dyes. When a bacillus of the type 
described is found in urine the practitioner must content 
himself with the statement that a bacillus resembling 
morphologically the colon bacillus is present, unless he 
wishes to make further studies with the aid of cultures. 
As these are not ordinarily used in practice, the methods 
of cultivating the Bacillus coli are here omitted. (Compare 
text-books on Bacteriology.) As it is very important often 
to determine the exact germ contained in a urinary infec- 
tion, the urine, drawn by a sterile catheter into a sterile 
bottle, should be sent promptly to a competent bacteriol- 
ogist for such examinations. A pure culture of the germ 
in question can serve for the preparation of a vaccine for 
the treatment of the infection by Wright's method. 

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The Bacillus coli is one of the most frequent causes of 
cystitis. Melchior found it in 37 out of 72 cases of cystitis — 
29 times in pure culture. He found that the Bacillus coli 
is not pathogenic when injected into normal bladders, but 
when there is obstruction to the flow of urine, or an injury, 
or a previous irritation this germ may produce cystitis, 
pyelitis, pyelonephritis, etc. 

Gonococcus. — The gonococcus of Neisser is the specific 
agent of gonorrhea, and is a diplococcus, consisting of 
groups of kidney-shaped cocci with flattened surfaces 
facing each other. They are found in the discharge from 
the urethra in gonorrheal urethritis, and it is characteristic 
of them that they occur within the bodies of the pus-cells. 
It is often very difficult to demonstrate gonococci in urine. 
For this purpose the specimen must be chosen from the 
portion of urine which contains most pus and threads, 
preferably after massage of the prostate and vesicles, and 
must then be centrifuged, the thickest part of the sediment 
spread on several slides, and allowed to dry in the air. 
It is then fixed by heat or, better, with alcohol and 
ether (see p. 330), and is then stained as hereafter 
described. A thin part of the specimen where there 
are pus-cells must be sought, and the slides carefully 
gone over to find the characteristic diplococcus within 
the pus-cells. Inasmuch as there are germs in the 
urine which resemble the gonococcus very closely, the true 
germ of gonorrhea may be distinguished by Gramas method 
as follows: 

This method is of no value unless correctly applied, and, 
unfortunately, its proper application is not always taught 
in text-books. Its principle is as follows: All germs stain 
readily with a solution of gentian violet. Some of them 

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33^ sxaminatiOn of the urine 

form a purple compound of gentian violet and iodin 
when an iodin solution (Gram's solution) is added to the 
first stain. This compound is insoluble in alcohol, and 
the germs forming this compound are Gram-positive — i, e.y 
they stain purple with this method. On the other hand, 
other germs do not form the iodin-gentian-violet com- 
pound. When alcohol is added to the film after the iodin 
is poured off, the former reagent does not alter the Gram- 
positive bacteria, but removes all the violet color from 
the others. The latter are known as Gram-negative germs. 
When a fainter contrast stain is added which does not in- 
terfere with the purple color of the Gram-positive germs, 
the bacteria which had been decolorized by the addition 
of alcohol take up the contrast stain and are readily dis- 
tinguished from the purple-colored Gram-positives. 

The gonococcus is Gram-negative — i,e., it does not stain 
purple with Gram's method. The pseudogonococcus is, 
on the other hand, Gram-positive, and takes the purple 
color with this method. Other germs in the Gram-negative 
class are the Bacillus coli and Proteus vulgaris. On the 
other hand, the Streptococcus pyogenes and the Staphylo- 
coccus aureus are Gram-positive. 

In using Gram's stain the writer- has found that the 
original Gram's method is far more satisfactory and more 
trustworthy than any of the modifications more recently 
introduced. Students are warned to adhere to it strictly 
and not to use the shorter but less reliable methods, such 
as that of NicoUe (decolorization with acetone-alcohol). 
The best results are obtained with absolute alcohol, as 
was pointed out by Weinrich, and as the writer has been 
able to prove in a study of many hundreds of specimens. 
The directions given should be followed minutely. The 

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following technk oj Gram's stain is, therefore, recom- 
mended to the student and practitioner: 

I. The fixed film is stained for one and one-half minutes in carbol- 
gentian violet (the original method prescribes anilin-gentian violet, but 
the carbolic solution keeps well, while the anilin solution must be made 
freshly) : 

H, Saturated alcoholic solution gentian-violet., .i part 
Carbolic acid in water (5 per cent.) 9 parts 

II. Without washingj but after simply pouring off the violet, the slide 
is covered with Gram's iodin solution: 

H, Iodin I part 

Potassium iodid 2 parts 

Water 300 " 

This is poured off after a few seconds, and some fresh Gram's solution is 
poured upon the film. After repeating this application of the iodin solu- 
tion two or three times the solution is allowed to remain on the slide for 
two minutes. It is then poured ofiF. 

III. Without washing in water, the film is washed with absolute alcohol^ 
gently rocking the slide to and fro, and adding fresh alcohol. Not more 
than thirty seconds must be used for this decolor ization. If the alcohol 
is used longer, there is danger of decolorizing the Gram-positive germs. 
The alcohol is drained off and the slide quickly washed for a few 
seconds in distilled water. 

IV. The slide may then be dried by waving through the air a few 
times and the counter-stain should be applied. Bismark brown makes 
the best contrast stain. It is prepared as follows: 

Bismark brown 3.0 

Alcohol (90 per cent.) 30.0 

Mix and add 

Hot distilled water 70.0 

Mix and cool. Stain, when cold, for thirty seconds. Great care should 
be taken not to overstain with the brown color, as the purple bacteria 
may take on a brownish hue if too much brown is used. The gonococci 
appear brown, likewise the pus-cells and the epithelia. The pseudo- 
gonocpcci and other Gram-positive germs appear purple. 

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Instead of the Bismark brown a weak aqueous solution of fuchsin or of 
eosin may be used, staining the gonococci red, while the Gram-positive 
germs stain purple. With the red stains there is rather more danger of 
overstaining the contrast color than with the brown, but in either case 
great care should be taken to guard against this error. 

V. The film is now washed for a few seconds in water and is dried 
and mounted in balsam. An oil -immersion lens -j^-inch focus is neces- 
sary for the accurate study of gonococci. 

There is a diplococcus closely resembling the gonococcus, 
and decolorizing with Gram's method, which can only be 

Fig. 83. — Pus from gonorrhea, showing gonococci (Jakob). 

distinguished by cultural methods. In men this diplo- 
coccus oocurs in but 4 to 5 per cent, of chronic urethral 
infections. Hence in 96 per cent, of cases Gram's stain 
is accurate in revealing the gonococcus in the male. 

When diplococci of the characteristic kidney shape occur 
within the bodies of pus-cells and do not stain purple with 
this method, one may be quite satisfied, if the patient is 
of the male sex, that the gonococcus of Neisser is present. 
In women, however, no method short of a culture gives 

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positive assurance that we are dealing with the true gono- 
coccus, as the female genitals often harbor diplococci nega- 
tive to Gram and resembling gonococci in other respects, 
which prove to be non-gonorrheal germs on culture. 

It is in chronic gonorrhea, with scarcely any discharge 
excepting a morning drop and a few shreds, that gonococci 
are looked for in the urine. Wherever there is a sufl5cient 
discharge the germs should be looked for in the pus. The 
absence of the gonococcus from the urine is of no conclusive 
negative value, as the germ may be deeply lodged in the 
follicles of the prostate or the urethra. 

The Tubercle Bacillus. — It is still more diflScult to 
discover the tubercle bacillus in the urine. For this pur- 
pose it is important that the urine should be fresh and, 
preferably, it should be obtained by catheter after thor- 
oughly cleansing the external genitals, and examined at 
once. In this manner we prevent its destruction by de- 
composition, and also avoid the admixture of the smegma 
bacillus, which is found on the prepuce and glans, and 
which resembles the tubercle bacillus very closely. 

Technic of Staining. — The sediment obtained by the method de- 
cribed on p. 329 is smeared on several clean slides. The smears are fixed 
with heat in the usual way. The slides should be immersed in carbol- 
fuchsin solution in a tray or dish and the latter kept over a Bunsen flame 
till the dye begins to steam. The writer uses an aluminum box provided 
with a rack for six slides, which is filled with carbol fuchsin and placed on 
a piece of asbestos over a tripod under which is a burner. The films are 
well stained in five minutes or even less. They are removed from the tray; 
the excess of dye is allowed to drip off and the decolorizing solution is at 
once applied. The best decolorizer is a 3 per cent, solution of pure HCl 
in 95 per cent, alcohol. This is poured on the slide repeatedly until no 
more red color comes off, and the film appears grajdsh. After washing 
off the acid with water the films are counter-stained with aqueous methyl- 
ene-blue for about two minutes, thoroughly washed in water, dried, and 
mounted in balsam. They are examined with a -j^ oil-immersion lens. 

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The acid and alcohol decolorize smegma bacilli, but do 
not affect the tubercle bacilli, which remain stained by the 
fuchsin, while the other germs, pus-cells, etc., are stained 
blue. The tubercle bacillus is recognized by its charac- 
teristic form and grouping. It occurs in long, thin rods, 
slightly curved or bent, and often crossed and arranged 
in parallel formation. Its ends are slightly clubbed and 
it presents a series of unstained vacuoles. 

Finally, injections of portions of the sediment of a 
urine suspected of containing tubercle bacilli into guinea- 
pigs offer a useful means of diagnosis. The lesions ob- 
tained in these animals, however, take some time to develop, 
and a negative result, even in these animal experiments, 
is not always conclusive- 

Technic of Animal Inoculation. — The sediment is thoroughly cen- 
trifuged in a sterile tube and the urine is decanted. Sterile normal salt 
solution is substituted for the urine and the sediment is again centrifuged. 
This is repeated several times until a suspension of the sediment in salt 
solution is obtained fairly clear of urinary salts. The suspension should 
measure i or 2 cc. in bulk, and should be drawn into a sterile h)rpodermic 
syringe. The guinea-pig is held belly-side up by an assistant. The 
groin is rendered aseptic and shaved as for a surgical operation. The 
glands in the groin are felt as very minutie prominences, or if they are not 
felt, their site is easily guessed at. The suspension is injected slowly into 
the subcutaneous tissue of the groin of the animal as nearly as possible 
into the region of the glands. The region is then massaged and the glands, 
if felt, are squeezed for a minute or two. The guinea-pig should be kept 
under observation (with good air, food, and shelter) for at least six weeks. 
The animal is then killed by means of chloroform and an autopsy is per- 
formed. The presence of tuberculosis in the lungs, peritoneum, glands, 
and other organs should be looked for. 

During the period of observation the animal's inguinal glands may be 
examined from time to time. If they swell, the autopsy should be per- 
formed sooner, within twenty-one days. Bloch has recently excised the 
smaller inguinal glands after from nine to eleven days and found tuber- 
culosis in microscopic sections of the lymph-nodes of guinea-pigs. 

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)i \ 

Tubercle Bacilli in Urinary Sediment; X ^^o- {Ogden.) 

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The absence of tubercle bacilli in an ordinary micro- 
scopic examination of the sediment is by no means decisive 
in diagnosis, and tuberculous lesions may exist in the kid- 
neys or elsewhere in the genito-urinary tract without any 
discharge of tubercle bacilli into the urine. (See Tuber- 
culosis of the Kidneys, etc., Part IV, p. 358.) 


It is very rare to find parasites in the urine, and a detailed 
description of these must be sought in works on pathology. 
The following parasites have been found in urine on rare 

Filaria sanguinis hominis, 
the parasite of chyluria, dis- 
covered by Lewis, of Calcutta, 
and found in the blood and urine 
of persons passing a milky urine. 

Fig. 84. — Embryos of Filaria 
sanguinis: Length, 0.0075 to 0.21 
mm.; thickness, 0.004 to 0.36 mm. 
(after Scheube). 

Fig. 85. — Eggs of Distomum 
haematobium (Bilharzia haemato- 
bia): Length, 0.12 mm.; breadth, 
0.05 mm. (after Bilharz). 

Distoma hasmatobium, a form found in eastern South 
Africa, whose eggs may infect the urinary passages, the 
veins, etc. They produce a sharp pain when they are 
passed along the urethra, and the urine contains blood, pus, 
fat, and the eggs of distoma. 

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Echinococcus. — ^The booklets of Tcmia echinococcus 
are found in urine in cases of parasitic cysts in the kid- 
ney, or in cases of rupture of such cysts into the urinary 
tract from some neighboring organ. 

Fig. 86. — Echinococcus elements: i, Free scolices; a, rostellum 
projected; b, rostellum withdrawn; 2, hooklets; 3, membrane (X cross- 
section) (after Heller). 

Ascarides. — ^The presence of these worms in the urine 
may be due to the accidental washing away of one of these 
parasites from the region of the anus, or to an abnormal 
communication between the intestine and the urinary 


What does the term organized sediments include ? What is the rela- 
tive importance of organized and unorganized sediments? 

Blood, — What influences the appearances of red cells in urine ? 

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What are "normal" blood-cells? Describe them. . 

What is the first change blood undergoes when it enters the urine ? 

What are "abnormal blood-cells"? 

How is normal blood distinguished from abnormal on gross inspec- 
tion ? 

Describe hemin crystals. 

How may blood be removed from a sediment? 

What is the clinical significance of blood in the urine? 

What are the characteristics of blood from the kidney ? What are the 
causes of blood from the kidney? 

What are the characteristics of bleeding from the bladder ? 

Piis. — Describe a typic pus-cell. What occurs on the addition of 
acetic acid? lodin? 

What occurs in the pus-cells in ammoniacal urine? 

What do fat-globulins in the pus-cells show ? 

What is the significance of pus in the urine ? 

In what conditions of the kidney are pus-cells found in the urine? 
Pus from the bladder? The prostate? The urethra? 

What precaution should be taken in women in regard to pus in the 
urine ? 

EpUhelia. — What epithelia occur in normal urines? 

What difficulties present themselves in distinguishing epithelia from 
one part of the tract from those derived from another part? 

What are the three great classes of epithelia ? Which of these is 
sometimes ciliated ? 

What is the appearance of epidermal scales? 

Describe epithelia from the vagina; from the uterus; from the bladder. 

What does the presence of bladder epithelia indicate? 

How can the intensity of a cystitis be judged by the character of these 
cells? What is meant by an endogenous pus-corpuscle? 

Describe epithelia lining the pelvis. What does their presence indi- 

Describe the two types of cells from the ureter. When are they present 
in sediments? 

Describe a typic renal epithelial cell. What does their presence 
indicate? What two forms are distinguished and where do they come 

How are renal epithelia distinguished from other cells of similar ap- 
pearance ? 

^ha|: do epithelia from the straight collecting tubules indicate? 

^yjia^ i§ the clinical significance oi renal epithelia? 

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What is the appearance of urethral epithelia? Of those from the 
deeper layers ? From the prostatic portion ? From the proskUe ? The 
ejaculatory duct? The vesicles? 

Casts. — Define casts. What are the theories of their origin ? 

What is the relation of casts to albumin ? 

What is the clinical significance of casts and when have they been 
seen without renal disease? 

Name the principal classes of casts. 

Describe a pure hyaline cast. What may be concluded from the size 
of these casts ? What is their mode of origin ? What do they indicate ? 

Describe fibrinous casts. What do they indicate and what is their 
prognostic value? 

Describe a wctxy cast. In what conditions are they found? What 
is their prognostic meaning? 

Define a granular cast. Where do the granules come from? What 
do they indicate ? 

Define an epUhtifhl cast. 

What term is used when only a few epithelia adhere to a cast? 

What does the presence of epithelial casts show? 

What are epithelial cylinders with a lumen? 

Define a blood-cast. What does their presence indicate? When 
are they found in the urine? 

Define fatty casts. 

What variety of casts may be mistaken for fatty casts? When are 
these casts found ? 

Define pus-casts. What do they indicate ? 

What varieties are found in pyelitis? 

Define crystalline casts. 

Define bacterial casts. What do they indicate? How are they dis- 
tinguished from brown granular casts? 

Describe false casts. What are they made of? Why are they in- 
teresting? Where are they found? 

Describe mucous threads. How do they differ from casts? 

What does an excess of mucus show? 

How are mucin threads demonstrated? 

Descibe connective-tissue shreds. What do they indicate and in what 
diseases are they found in urinary sediments? 

What are prostatic plugs ? Describe them. What does their presence 
indicate ? 

Describe amyloid bodies. What is their significance? 

Describe spermatozoa and their appearance in the urine, What does 

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their presence indicate ? How are they shown in medicolegal investiga- 
tions? Describe Florence's reaction. 

What elements occur in the urine after the vesicles have been massaged ? 
How may these be examined microscopically? What is their clinical 
significance ? 

Give the classes of urethral shreds, their clinical significance, and the 
method of staining them. 

Describe micrococcus urecs. Describe yeast fungi. 

What impedes the growth of yeast in urine? 

Describe sarcina urincB. 

What pathogenic bacteria may occur in urine? What three germs 
are important diagnostically ? 

Describe the gonococcus. May they be isolated in urine ? 

What is Gram's method and what is its value ? 

How do the gonococci stain by this method? 

Describe the method of staining for tubercle bacilli in the urine. 
What methods may be used to facilitate the precipitation and isolation of 
tubercle bacilli in the urine ? What method may be used when the urine 
sediment shows no tubercle bacilli? 

Describe the appearance of the bacillus in stained specimens. 

What parasites are sometimes found in the urine ? 

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In the foregoing pages we have discussed the methods of 
examination and the clinical significance of the various nor- 
mal and abnormal constituents of the urine. In applying 
this knowledge to diagnosis the student's chief concern will 
be the recognition and differentiation of the various diseases 
of the kidney. In doing so he will meet the difficulty of 
deciding as to the particular lesion which is present in the 
kidney, and as to what stage the process has reached. 
Unfortunately, each renal disease, though clearly defined 
pathologically, does not present a separate and distinct 
type of urine. Not only this, but two or more types of 
lesions may be present in the same kidney at the same time, 
and may obscure each other to a certain extent, so that only 
repeated examinations, the careful elimination of all ex- 
ternal factors influencing the constitution of the urine, and 
the scrupulous weighing of each element in the findings, 
will lead to a correct diagnosis. In the following summary, 
which is necessarily brief, are given the characteristics of 

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the urine in the various diseases of the kidney, and with 
restrictions and limitations just mentioned borne in mind, 
these data may be used in the diagnosis of renal disease. 


Acute or active congestion of the kidney is always a 
secondary condition, due to disturbances of circulation 
or to the action of toxic or irritant substances. The 
most frequent cause is exposure to cold and wet, which 
chills the surface of the body and induces a congestion of 
the internal organs. In some diseases, such as delirium 
tremens and acute mania, sudden changes in the circula- 
tion may also cause renal congestion. Local irritation 
through the presence of gravel or calculi (oxalic, uric acid, 
phosphatic, etc.), and general irritation, induced by drugs 
or by the poisons of infectious diseases, may also cause 
acute congestion in the kidney. Of the drugs, we may 
mention arsenic, lead, mercury, cantharides, turpentine, 
cubebs, carbolic acid, salicylic acid, and the essential oils. 
Of the toxins concerned in renal congestion, we may 
mention those of pneumonia, typhoid, erysipelas, measles, 
scarlet fever, diphtheria, acute rheumatism, acute tuber- 
culosis, cerebrospinal meningitis, malaria, intestinal in- 
toxication, and enterocolitis in children. In chronic 
disases, such as tuberculosis and rheumatism, there may 
be transient congestions due to the temporary accumulation 
of toxins. In local suppuration in any part of the body 
there may also be absorption of toxin and renal conges- 
tion. Large amounts of bile irritate the kidney in their 
transit and considerable amounts of sugar often cause con- 
gestion. This condition is also observed in strictures, en- 
larged prostate, and other obstructive diseases of the uri- 

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nary tract; after operations on the urethra, bladder, etc. 
In itself acute congestion is a transient condition, but is 
chiefly interesting because it often precedes acute nephritis. 

The urine varies according to the degree and duration 
of the congestion. In mild cases it may be normal, except 
a few red cells, a few hyaline casts, a few renal epithelia, 
and a small amount of albumin. The quantity is usually 
increased at first; the acidity may be normal; the specific 
gravity may be somewhat lowered, and the total solids 
somewhat reduced. 

In severe cases the urine changes completely. It is 
usually high colored, reddish or smoky, and contains visi- 
ble amounts of blood. The quantity is small — sometimes 
less than 300 cc. The acidity is increased; the specific 
gravity is usually higher than normal. The total solids 
are increased. Albumin is always present — sometimes in 
considerable amounts for a day or two. A few hyaline 
and finely granular casts, blood-casts, red cells, renal 
epithelia, and crystals (these causing irritation) are found 
in the sediment. In acute congestion that has lasted some 
time we find fatty renal epithelia; occasionally small fatty 
casts and fat-globules; some pus-cells, pelvic epithelia, etc., 
showing the extent and severity of the process. Acute 
congestion is differentiated from nephritis chiefly by the 
transitory nature of the signs in the urine. Albimiin is 
usually present in small amounts, and the casts are few 
in number, appear suddenly, and diminish rapidly. The 
urine just before death in chronic interstitial nephritis re- 
sembles that of acute congestion, except that its specific 
gravity is low and the solids reduced. 

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Chronic or passive congestion is always secondary to a 
disturbance of circulation due to disease of the heart, 
arteries, or the liver, to tumors of the abdomen, or to 

The urine is diminished in quantity in uncomplicated 
cases. Its color is usually high, brownish red, but if diu- 
retics have been given, or if the patient is in a bad state 
of nutrition, it may be pale. It is generally somewhat 
cloudy, owing to increase of urates and mucus, and, as a 
rule, strongly acid in reaction. The specific gravity is typ- 
ically high, but may be normal or low in pale urines. The 
absolute amount of solids is diminished, especially if there 
is dropsy. The relative amount of solids is increased, ex- 
cept in extreme cases of dropsy. There is usually a slight 
trace or a trace of albumin; occasionally albumin is absent 
and the degree of congestion does not correspond with 
albuminuria. The sediment contains a few small hyaline 
casts, with occasional adherent red and white blood-cells, 
and a few free red cells, although blood is often absent. In 
pregnancy the urine is lighter, of a lower specific gravity, 
and occasionally contains much albumin, without any com- 
plication in the shape of nephritis. In such cases we must 
look out for convulsions. The urine of chronic congestion 
is diagnosed from that of chronic interstitial nephritis by 
the low specific gravity, the small amount of urea, and the 
predominance of urine passed at night in interstitial neph- 
ritis. The two urines are difficult to distinguish from each 
other in interstitial nephritis near death, when the quantity 
is practically normal. This is particularly true when blood 
is absent in chronic congestion, as is the case in patients 
with compensation which is beginning to fail. 

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Acute nephritis, acute diffuse nephritis, and acute 
Bright's disease are the names applied to an acute de- 
generative or inflammatory process in the kidneys. The 
causes of this condition include those mentioned as pro- 
ducing acute congestion, and acute nephritis may be the 
sequel of an acute hyperemia. The most frequent cause is 
some acute infectious fever, such as scarlatina, diphtheria, 
pneumonia, typhoid fever, and influenza. Sudden and 
violent exposure to cold sometimes operates as a cause, and 
occasionally the acute inflammation follows extensive 
burns, erysipelas, and other local affections of the skin. 
Acute nephritis may also occur in women during pregnancy. 

According to Councilman, acute diffuse nephritis in- 
cludes a nimiber of pathologic processes, any one of which 
may predominate, or be exclusively present, or be com- 
bined with other lesions in the list: (i) Acute degenera- 
tion of the kidney; (2) acute glomerular inflammation; 
(3) acute hemorrhagic inflammation; (4) acute interstitial 

Characters of the Urine.— The quantity is diminished 
at times to an extreme degree, and at the height of the 
disease it may be reduced to a few ounces. If the disease 
loses its acute character, the quantity increases, but dur- 
ing the acme of the disease there may even be suppression, 
which, if it lasts long, may be considered fatal. 

The specific gravity varies with the quantity and in- 
creases to 1025, 1030, or even higher during the acute stage 
of the disease, while during convalescence it becomes 
lower as the volume increases. 

The color also varies with the quantity voided and with 
the amount of blood, but the typic urine of this disease 

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is dark brown, approaching chocolate in color, smoky, 
opaque, and dull in lustre. During convalescence the 
urine gradually clears up and becomes lighter. The 
reaction is always highly acid, except when large amounts 
of alkaline salts are given in the treatment. Of the normal 
constituents, the urea and the chlorids are diminished in 
quantity, and the total solids (actual) are correspondingly 
reduced. The relative amount of solids, however, varies 
with the volume excreted, and in the early stage, when the 
urine is very scanty and concentrated, this amount may 
be normal or high. During convalescence the amount of 
urea and chlorids increases, but during the acme of the 
disease the urea is often reduced to 100 grains (6.0 gm.), or 
even less, for twenty-four hours (Purdy). 

There is always a large amount of albumin, usually 
from 0.5 to I per cent, by Esbach's method. It is in these 
cases that the urine coagulates on heating, so that it appears 
almost solid, whence the erroneous expression of " 100 per 
cent, of albumin" has arisen. In rare cases albumin is 
absent throughout the disease. In a few cases it is present 
intermittently, and in some cases it appears suddenly 
toward the acme of the disease. The amount of albumin 
decreases toward convalescence. 

• The amount of blood in the urine in acute diffuse neph- 
ritis varies considerably, both in different individuals and 
in different periods of the disease. Usually it appears 
early and disappears before the albuminuria vanishes. 
The amount of blood and the amount of albumin are 
valuable prognostic indications, and the sudden increase of 
albuminuria and hematuria shows a relapse of the disease. 

The sediment is usually copious and brownish or reddish, 
owing to the presence of blood, urates, and a large amount 

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of coloring-matter. The predominant element imder 
the microscope is the red blood-cell, which is usually 
present in considerable numbers, and appears in the ab- 
normal form (see p. 275), unless the hemorrhage is very 
marked. There are always some pus-corpuscles in moder- 
ate numbers; epithelium from the renal tubules is always 
in evidence, and may be present in large numbers. There 
may be a few caudate cells from the pelvis or some cells 
from the calices. 

Hyaline and finely granular casts, coarsely granular, 
epithelial blood, and fibrinous casts are usually present 
in considerable numbers, together with masses of granular 
debris from broken-down cells. 

If the disease goes on after the acute stage subsides, it 
enters the so-called fatty stage, which is characterized 
by fatty renal cells and fatty casts, the number of which 
depends upon the severity of the preceding acute stage. 
During the convalescent stage the character of the urine 
becomes gradually normal, the sediments show fewer 
casts, fewer renal cells, arid fewer blood-cells, until there 
may be only a trace of albumin, a few hyaline and granular 
casts, and an occasional blood-cell or renal cell. This 
urine is identical in microscopic features with that of 
acute congestion. Acute nephritis very often becomes- 
chronic, and during the convalescence there may be re- 
lapses or exacerbations in which the urine again shows 
the features of the acute stage. 

Differentiation. — In mild acute nephritis it is not 
always easy to differentiate from severe acute congestion 
by examining the urine alone. We must rely chiefly on 
the persistence of marked albuminuria, of a considerable 
amount of blood, and of many casts. 

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The second stage (fatty stage of acute nephritis) may 
be mistaken for subacute parenchymatous nephritis com- 
plicated by an acute process. In the latter the acute 
complication will gradually subside, leaving the disease in 
its original form. In the subacute condition the amount 
of albumin is usually larger, and the total amount of urea 
is much lower than in the acute cases. 

(Chronic Nephritis with Exudation; Chronic Glomerular Nephritis; 
Chronic Arteriosclerotic Nephritis; Chronic Parenchymatous 
and Interstitial Nephritis.) 

This disease either follows acute nephritis or develops 
as a chronic condition from the start. In this condition 
the lesions are both parenchymatous and interstitial. It 
is well for the student, therefore, to understand the changes 
in the urine which are supposed to characterize each of 
these distinct sets of lesions. As has already been said 
in the introductory paragraphs of this section (p. 342) the 
urine does not always show the precise lesion existing in 
the kidney, and a diagnosis of the exact lesion is not always 
possible intra vitam. 

Interstitial lesions give rise to an increased quantity, a 
pale color with a low specific gravity, and a diminution of 
the relative and absolute solids, especially of urea. The 
parenchymatous lesions are represented by a comparatively 
large amount of albumin and the presence of renal casts 
and of renal cells in various stages of fatty degeneration. 
The rule is that in chronic diffuse nephritis the interstitial 
changes predominate, but this is by no means always so. 

The causes of chronic diffuse nephritis are the same as 
those of the acute form, and the chronic type is often the 
sequel of ^cute nephritis; but it is well to remember that 

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chronic diffuse nephritis is more apt to develop from acute 
nephritis due to scarlet fever, diphtheria, pneumonia, or 
other infectious diseases. 

Characters of the Urine.— The qtumlity is dimin- 
ished, as a rule, but not so markedly as in acute nephritis, 
and the daily amount fluctuates much more markedly 
than in the acute form. In the late stages, when the in- 
terstitial changes gain the ascendency, the volume increases. 
The specific gravity varies with the quantity, but is usually 
low — ^at least below 1020, and in the later stages it is often 
below loio. The color is variable, but generally light, the 
urine being often cloudy, owing to the presence of a large 
amount of sediment. 

There is always some albumin — sometimes a large 
amount, up to i per cent.; but the average is between 
J and \ per cent. The amount of albumin fluctuates, and 
seems to be in fairly constant relation to the specific gravity. 
It generally increases for a time, but in the later stages, 
tending toward the interstital type, the amount of albumin 
often becomes reduced. The total solids are more or less 
diminished, although there may be a temporary increase of 
solids when dropsy subsides under diaphoretics. Urea 
and chlorids are below the normal, and indican is either 
normal or increased. The most important features of the 
urine are found in the sediment. The latter is abundant, 
and contains numerous casts, of practically all types. 
The characteristic casts are, however, the so-called fatty 
casts, which indicate an advanced chronic parenchymatous 
lesion. In the earlier stages these fatty casts are few, and 
the hyaline, faintly granular, and epithelial casts predomi- 
nate. In the more advanced cases the fatty casts become 
more numerous, and they are accompanied by casts with 

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dark and prominent granules and by broad casts from the 
large straight tubules. In addition to casts, the sediment 
contains many renal cells, some of which are fatty, but 
usually no blood is seen unless there is an acute exacerba- 
tion. A few pus-cells are usually seen. Connective-tissue 
shreds are always present, and a fair number of large shreds 
may be seen in the sediment. Pelvic epithelia, ureteral 
and bladder epithelia may also be present, but are not 
characteristic. In advanced cases waxy casts may be found, 
sometimes in large numbers, and as the interstitial lesions 
increase the sediment becomes more and more scanty, 
the casts and renal epithelia fewer, and the fatty elements 
less numerous. 

(Subacute or Chronic Glomerular Nephritis; Fatty Degeneration of 
the Kidneys; Chronic Diffuse Nephritis of the Parenchymatous 
Type; Chronic Degeneration of the Kidneys*) 

This is a chronic disease of the parenchyma of the kid- 
ney, characterized by marked changes in the glomeruli 
and the epithelial lining of the renal tubules. The vascular 
tufts of the glomeruli are swollen, the number of cell nuclei 
in them is increased, and the glomerular blood-vessels are 
degenerated and become obliterated. The capsule of 
the glomerulus shows proliferation of epithelium and new 
connective-tissue growth. The tubular epithelium is 
extensively diseased, necrosed, and becomes detached. 
There are edema and proliferation of connective tissue to a 
minor extent in the intertubular tissue. 

This condition often accompanies chronic diseases — 
^- S-y syphilis, tuberculosis, malaria, etc. — ^but it may be a 
sequel of acute nephritis — e, g,, after scarlet fever. In 
such cases it is at first subacute and later becomes chronic. 

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Chronic parenchymatous nephritis may occur in old per- 
sons, and in some cases without discoverable cause. It 
is one of the possible sequels of heart disease and of other 
disturbances of circulation (emphysema, pleuritic effusions, 
etc.) such as cause chronic congestion. 

Characters of the Urine.— The urine varies at differ- 
ent stages of the disease. During the active stage^ or during 
acute exacerbations, when there is marked dropsy, the 
amount of urine is scanty, the color high or bloody, the 
reaction markedly acid, the specific gravity high — up to 
1035. The solids, especially urea and chlorids, are low, 
on account of dropsy, but relatively there is an increase of 
urea unless there are interstitial changes setting in strongly. 
A very large amount of albumin is present — up to 3, 4, 
or even 5 per cent. — but the average is 0.75 per cent. The 
reddish or dark sediment is abundant, contains urates, 
hyaline, granular, and fatty casts, and fatty epithelia from 
the kidney. In advanced cases one finds waxy casts. 
Blood-cells and leukocytes are also usually present. 

During the inactive, chronic stage the dropsy and edema 
are diminished or disappear, and the amount of urine in- 
creases, being about normal. The specific gravity is 
slightly lowered, the solids are diminished, though the 
chlorids may be higher than in the active stage (absorption 
of dropsy). Less albumin is present, but there is still a 
considerable amount. An abundant sediment is found to 
contain the same elements, but fewer casts and fewer renal 
epithelia and blood-cells are found. 

During the final stage the kidneys become atrophic, and 
the urine, while about normal in amount, is very low in 
specific gravity, contains little albumin, and a scanty sedi- 
ment consisting largely of fatty elements and waxy casts. 

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Differentiation. — Subacute cases (subacute glomeru- 
lar nephritis) are noteworthy for the great frequency 
with which acute exacerbations occur in the inactive stage. 
In these exacerbations the urine resembles that of acute 
diffuse nephritis, with the fatty elements in prominence and 
with a marked proportion of blood-cells and blood-casts. 
Such cases cannot be distinguished from the second 
(fatty) stage of acute nephritis except by the clinical 
history. The symptoms and urinary changes of an acute 
diffuse nephritis are transient, those of a subacute or 
chronic parenchymatous nephritis, more or less permanent. 

From chronic diffuse nephritis subacute and chronic 
glomerular nephritis may be distinguished not only by 
the clinical history, but by watching the quantity of urine 
voided. If this be permanently increased, the condition 
is chronic diffuse nephritis. The two exceptions to this 
rule are: (i) Cases of chronic diffuse nephritis during 
acute exacerbations, when the amount is often reduced. 
(2) Cases of chronic diffuse nephritis near death, in which 
the amount is normal or low. In both these cases there is 
no way of distinguishing the two conditions under discus- 


(Chronic Bright's Disease; Renal Grrhosis; Sclerotic Kidney^ 
Chronic Nephritis without Exudation; Chronic Nephritis; 
Chronic Diffuse Nephritis of the Interstitial Type; Chronic 
Catarrhal Nephritis,) 

This disease may be interstitial from the beginning, or 
it may be an outgrowth of chronic diffuse nephritis.^ The 

^ Delafield and Prudden ("Handbook of Pathological Anatomy and 
Histology," New York, 1896) do not use the classification of chronic 
renal inflammation which is currently employed — i. e., the distinction 
between chronic parenchymatous and chronic interstitial nephritis and 


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causes of this condition are probably toxic in their ultimate 
analysis. Chronic poisoning with lead, arsenic, and alco- 
hol are prominent causes. Persons with gout are subject 
to chronic interstitial nephritis, although just how gout 
produces this disease is not exactly known. Syphilis 
and chronic malaria are known to be accompanied often 
by chronic interstitial nephritis. Arterial disease (arterio- 
sclerosis) produces changes in the arteries of the whole 
body which are identical with those found in the arteries 
of the kidney, and there is a distinct causal relation be- 
tween arteriosclerosis and interstitial nephritis. In con- 
nection with urinalysis, the chief thing to be remembered 
about the lesions of chronic interstitial nephritis is that they 
are often insidious and take years to develop, and that in the 
early stages a diagnosis is often impossible unless the urine 
be carefully watched from day to day and repeatedly ex- 
amined. The lesions of interstitial nephritis consist chiefly 
in the growth and increase of connective tissue in the stroma 
of the kidney, and secondarily in changes in the glonieruli 
and tubules. The study of the urine must be pursued 
bearing these facts in mind. 

the designation of a combined parenchymatous and interstitial inflamma- 
tion as "diffuse." These Authors believe that both parenchymatous and 
interstitial changes are present in all chronic nephritides almost from the 
first, and divide chronic nephritis into two classes — chronic nephritis 
without exudation (corresponding to the interstitial type of other authors) 
and chronic nephritis with exudation (corresponding to the parenchyma- 
tous and diffuse types of other observers). In this book I have followed 
the classification usually employed, as it is the most convenient for urine 
analysis and is still adhered to by most physicians. Those who wish to 
use Delafield's classification will find that the urine which I describe as 
typic of chronic diffuse nephritis may be fairly said to be that found in 
"chronic nephritis with exudation, " as described by Delafield. The urine 
herein described for interstitial nephritis practically corresponds to that 
found in "chronic nephritis without exudation." 

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Characters of the Urine. — The typic urine of 
chronic interstitial nephritis is increased in quantity, usu- 
ally perfectly transparent, and paler than normal in color, 
with a markedly acid reaction and a rather low specific 
gravity. Albumin is present in small quantities, or it 
may be absent. Very few casts are seen in the sediment, 
chiefly of the small hyaline variety. The chlorids are not 
markedly changed in amount, the phosphates are reduced, 
and the urea is more or less diminished. 

The qtcantity is usually increased until the last stage, 
when heart-failure sets in, and the urine is secreted in 
smaller amounts. A diminution of the quantity is, there- 
fore, a bad sign in chronic interstitial nephritis. The 
specific gravity is lowered in proportion to the extent of the 
interstitial changes, but it is never so low as in chronic 
diffuse nephritis or in amyloid kidney. Usually it ranges 
between loio and 1015. In the last stage, after heart- 
failure, the specific gravity rises somewhat. There is 
some difference of opinion as to the frequency of albumi- 
nuria in this condition. According to Purdy, the reason 
why albumin is so often found absent in this disease is 
that the albuminuria is intermittent. It is probable that 
very slight traces are always present, even in the early stage. 
The amount of albumin is always small, unless the inter- 
stitial nephritis becomes complicated by transient acute 
conditions. In the last stages — in heart-failure — the al- 
bumin increases, but it never reaches the extreme limit 
which is seen in chronic diffuse and chronic parenchy- 
matous nephritis. 

The amount of urea diminishes from the first, and this 
reduction is proportionate to the extent of the interstitial 
lesions. The phosphates are also very constantly reduced, 

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but the chlorids do not suffer reduction to any extent. The 
total solids are greatly diminished, both absolutely and 

The sediment contains few or no red blood-cells, but a 
moderate number of pus-cells, some containing fat-globules 
and granules; epithelia from the renal tubules, some of 
which are fatty; and, in severe cases, columnar epithelia 
from the straight collecting tubules are present in small 
numbers (Heitzmann). Crystals of hematoidin in the form 
of rust-brown needles and plates, either free or within the 
pus-cells or epithelia, may be found, indicating the chronic 
nature of the disease and denoting a previously existing 
hemorrhage. Connective-tissiie shreds of various sizes are 
often noted. Casts from the renal tubules in this disease 
are rarely found in large numbers, and often they are diffi- 
cult to detect. They are of the hyaline or of the finely 
granular type, and come usually from the narrow tubules. 
Crystals of uric acid and of calcium oxalate may be seen, 
especially in the early stages. The sediment, as a whole, 
is quite scanty, and even after centrifuging, very little is 

When acute exacerbations of nephritis occur, the urine 
presents the altered characters which would be expected 
in an acute process. The quantity of albumin becomes 
increased and the sediment resembles that of acute neph- 


(Waxy Degeneration; Lardaceotis Kidney*) 

This is a chronic condition of the kidney which is usually 

the expression of amyloid degeneration in various organs 

of the body. It may be met with in syphilis, tuberculosis, 

chronic bone disease, and chronic wasting diseases. It is 

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frequently mistaken for chronic diffuse nephritis, although 
it is very important to distinguish these conditions, as the 
emaciated and cachectic persons who have amyloid de- 
generation require treatment entirely different from that 
applicable in chronic diffuse inflammation of the kidney. 

Characters of the Urine. — The amount is increased, 
the color lighter than normal, but the transparency re- 
mains unaltered. The specific gravity is low, and there is 
a well-marked reaction for albumin in the typic cases. 
Besides serum-albumin there is usually a considerable 
amount of globulin. The sediment is usually scanty, 
and contains but few cells and a moderate number of casts, 
of the hyaline, granular, or, occasionally, the waxy variety. 

It is still a matter of discussion whether waxy casts 
are characteristic of amyloid disease and consist of amyloid 
material. Amyloid material in tissues is distinguished 
by its reactions to certain stains, but it is very difficult to 
stain casts with these dyes. The sediment is washed 
repeatedly by decantation with diluted glycerin and a little 
methyl-violet solution is added. Both waxy and hyaline 
casts will assume a light reddish tint (see Waxy Casts, 

Amyloid degeneration may be complicated by paren- 
chymatous degeneration as the result of interference with 
the renal nutrition. When this takes place, the urine will 
resemble that of diffuse nephritis so closely that it cannot 
be differentiated. The above description applies to typic 
urine of amyloid. There are certain variations, according 
to the stage of the process and the severity of the lesions. 
The amount of urine continues increased, as a rule, but 
there are often periods of temporary reduction in volume, 
accompanied by attacks of diarrhea. When the specific 

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gravity is comparatively high (1016 to 11 18), the prognosis 
is more favorable, but in the average case it is low, and 
may even reach 1004 in the late stages. In the early stage 
of the disease the amount of albumin is usually small, then it 
increases, and toward the end it may again decrease, with 
a marked polyuria. The solids, especially the urea, de- 
crease in proportion to the lesions and to the low state of 
nutrition. In the late stages the casts are very few, hyaline, 
and usually of comparatively large size. 

Differentiation. — It is almost impossible to differen- 
tiate amyloid kidney from chronic interstitial nephritis,' 
unless we admit that waxy casts are characteristic of the 
former, and this has not yet been settled. An unusually 
large proportion of globulin may lead to the suspicion of 
amyloid kidney. 


This may be primary, but more frequently it is an 
accompaniment of tuberculosis in other organs. The 
kidney is often the first organ of the urinary tract to be 
affected (blood infection). In other cases the infection 
apparently results from the extension of tuberculosis from 
the lower part of the urinary tract. 

In order to understand the various features that are 
found in the urine of tuberculous kidneys it must be re- 
membered that, in addition to the formation of tubercles, 
there is usually a certain amount of chronic interstitial 
nephritis, and that in the later stages there is also a break- 
ing down or caseation of the tuberculous nodules in differ- 
ent portions of the kidneys. Besides, there are often 
secondary infections with pus-germs, producing suppurative 
pyelonephritis. All these factors play a r6le in the appear- 

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ances of the urine. The latter also shows marked varia- 
tions, according to the position of the lesions and the extent 
of the process. If the lesions are mainly cortical, and so 
long as they are productive in character, as is the case in 
the early stages, there will be but slight changes in the urine. 
When the lesions affect the central portions of the kidney, 
and when caseation and ulceration occur, when small ab- 
scesses form, and when the pelvis is involved, the features 
of the urine are very characteristic. 

Characters of the Urine. — In the early stages the 
urine becomes increased in quantity, and the desire to 
pass urine is more frequent than normally. The color of 
the urine is pale; it is cloudy, with a slightly lowered specific 
gravity and an acid reaction, and contains traces of albu- 
min, a few pus-cells, and a few renal epithelia. Tubercle 
bacilli are not usually found in the urine in this stage. 

In the ulcerative stage the urine is pale, cloudy, with 
a lower specific gravity, and ordinarily an alkaline reaction. 
On standing, it slowly deposits a thick sediment of pus, 
and from time to time there is found an appreciable amount 
of blood or a very marked hemorrhage. In the advanced 
cases the urine becomes very offensive, of ammoniacal odor, 
and contains small cheesy lumps. Microscopically, the 
chief features are pus, with usually smaller amounts of 
blood; numerous renal cells in various stages of degenera- 
tion and fatty change, occasionally large hyaline and 
granular casts, which may be covered with blood-cells 
when there is an acute exacerbation of the process, or an 
intermittent hematuria. If the pelvis and calices are in- 
volved, there appear large clumps of pus, mucus, and 
debris, which may be recognized as casts of the calices. 

The chief diagnostic feature of the urine in these cases is 

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the presence of the tubercle bacillus in the sediment. The 
detection of this germ has already been considered on 
page 335. When the tubercle bacillus is absent, we cannot 
exclude tuberculosis of the kidney because this germ 
may not appear in the urine until late in th& disease. In 
cases of doubt we must look for some other focus of tuber- 
culosis, and we may use tuberculin injections for diagnostic 
purposes or inject portions of the sediment into the peri- 
toneal cavity of a guinea-pig. 


The effect of stone in the kidney upon the urine is three- 
fold: (i) In cases of stone uncomplicated by inflamma- 
tory conditions there is an increase in the chemic elements 
which constitute the stone — e. g., uric acid, calcium oxalate, 
etc., both in the urine itself and in the sediment. (2) 
When inflammation ensues due to the irritation produced 
by the stone or to secondary infection, either ascending 
or hematogenous, thenr there are, in addition, the signs 
of suppurative nephritis, and, if the pelvis is involved, of 
suppurative pyelonephritis. (3) When the process is 
complicated by chronic interstitial changes or by paren- 
chymatous nephritis, the features of these also appear in 
the urine. 

Characters of the Urine. — The urine is usually 
highly colored, concentrated, of high specific gravity, and 
of markedly acid reaction. It may be dark and smoky, 
owing to the presence of altered blood-pigment. Blood 
is present during and just after the attacks of colic, and 
appears fresh and of considerable quantity during these 
paroxysms. In the intervals between the paroxysms the 
blood may be found intimately mingled with the urine, 

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profoundly changed, and brownish in color. The solids 
are usually increased relatively, but normal absolutely. 
There is always some albumin when there is any blood or 
when there is an irritation of the kidney, but albumin 
may be absent in the earlier stages. 

In the sediment we find the signs of acute congestion 
(which see), and very often an abundance of crystals, 
singly or in masses (small concretions; gravel; sand), 
of the same substance as the stone. In the earlier stages 
it is usual to find a few blood-cells and some scattered 
leukocytes, some renal epithelia, and some epithelial cells 
from the pelvis and the ureter, as well as some bladder- 
cells, showing irritation all along the tract, due to the pas- 
sage of small concretions. 

When inflaimnatory and suppurative changes are 
established, the urine shows the features of pyelonephritis. 
There is an abundant sediment of pus, more or less blood, 
and crystalline elements or concretions, but the latter may 
not be present. The urine is very turbid, and is either 
faintly acid or alkaline. Its specific gravity is low; the 
normal solids are diminished, owing to the presence of pus 
and of a complicating nephritis. The sediment contains 
chiefly pus-cells, often in clumps; shreds of connective 
tissue; renal epithelia, also in clumps, mixed with pus and 
mucus, and red blood-cells in moderate numbers. Casts 
may be present, but may be obscured by pus. 

Differentiation. — It will be seen that the urine in 
the earlier stages is rather characteristic, and whenever 
we find the signs of congestion, hemorrhage, and an imu- 
sually abundant sediment of crystals in urine immediately 
on voiding, the presence of stone in the kidney may be 
thought of seriously. In the later stages, with suppura- 

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tion setting in, the dififerentiation of stone from tuberculosis, 
from tumor of the kidney, or from pyelonephritis presents 
serious difficulties. The finding of tubercle bacilli, on 
the one hand, and of tumor elements, on the other, differ- 
entiates from tuberculosis and from tumor. The passage 
of small concretions of masses of crystals, when seen soon 
after voiding, are significant of stone also in this stage, but 
there are undoubtedly cases in which the examiner must 
content himself in the suppurative stage of stone with a 
diagnosis of pyelonephritis "possibly due to stone." 

It must be remembered that in very many cases stones 
may exist in the kidney, in the pelvis, or even in the ureter, 
without giving rise to any clinical symptoms and without 
showing any changes in the urine. In such cases the 
^v-ray alone can help the diagnostician. 


Of these, the malignant growths, h)rpernephroma, sar- 
comata, and carcinomata, are interesting in their relations 
to urine. Sarcoma is met with in young persons. Hyper- 
nephroma, a tumor developing from inclusions of supra- 
renal tissue remaining in the kidney since fetal life, has 
come to be more and more frequently found on operation 
and at autopsy. There is no way of differentiating this 
new growth by means of urinary analysis. Malignant 
tumors of the kidney are usually slow to develop, but when 
they have reached a certain stage they grow rapidly and 
lead to death in a year or two. The disease may be uni- 
lateral, especially in primary cases. 

The Urine. — In malignant tumors of the kidney more 
or less blood is always found — occasionally large amounts 
of fresh blood, when there is a paroxysm of hematuria. 

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Albumin is present in the urine in large or smaller quanti- 
ties, according to the amount of blood and the state of the 
renal parench)ana. Acetone is frequently found in the 
urine in cancer of the kidney. The amount of urine is 
usually increased unless the ureter is blocked. The 
specific gravity and the solids are altered, according to the 
extent of the renal destruction, the involvement of the op- 
posite organ, and the presence of congestion or inflamma- 
tion of the kidneys. As in stone of the kidney, the urine 
is changed, not only owing to the presence of the disease 
itself, but also owing to the accompaniment of nephritis, 
and, in the later stages, the breaking down of the tumor, 
the ulceration and the suppuration which ensue, especially 
when there is secondary infection and when the malignant 
disease invades the renal pelvis. The sediment of a case 
of malignant tumor presents the features, in the early 
stages, of simple acute congestion of the kidney. Later, 
when the ulcerative changes take place, the urine shows 
the features of chronic pyelitis already mentioned under the 
heading of Stone. 

Differentiation. — It is very diflScult to make a diag- 
nosis of renal malignant tumor from the urine alone, as 
the only real characteristic features of such urines is the 
presence of portions of the tumor with their distinct al- 
veolar structure. These are found very rarely. The pres- 
ence of single tumor cells, even in considerable quantities, 
is not of much value, as they may not appear till the pelvis 
is involved, and as the cells themselves do not present 
any definite diagnostic features. 

Whenever grotesquely shaped or pigmented epithelioid 
cells are found, especially in groups or nests, the suspicion 
of malignant tumor is reasonable. 

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Cystic degeneration of the kidney is a congenital 
condition characterized by a conglomeration of cysts of 
various sizes occupying the renal tissue. The entire kidney 
may be destroyed. The affection is almost always bilateral. 

Solitary cysts of various sizes may occur in the kidney 
as the result of the blocking of a tubule or of the capsule 
of Bowman. In chronic interstitial nephritis it is common 
to see small single cysts of this kind. 

The diagnosis of congenital cystic disease is rarely made 
during life. Greatly enlarged kidneys; a hypertrophy of 
the left cardiac ventricle, and increased arterial tension 
are the chief diagnostic guides. Large single cysts may 
give rise to palpable tumors. 

The urine is not changed in any way in some cases, when 
the renal tissue is comparatively unaffected. When much 
of this tissue is destroyed, the urine shows the signs of 
chronic interstitial nephritis. 


This is a circumscribed suppuration found in the kidney 
as the result of secondary infection in cases of injuries, 
stone, tuberculosis, etc. When such an abscess ruptures 
into the pelvis, the urine will of a sudden become markedly 

The urine of renal abscess, aside from this sudden 
pyuria, shows nothing absolutely characteristic. There 
may be a considerable number of connective-tissue shreds 
from the breaking down of renal tissue. While the ab- 
scess is developing the urine is that of an acute congestion. 
When the abscess ruptures, there is often an abundant 
hematuria due to the breaking of blood-vessels. 

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The diagnosis is made from the history of the case and 
the appearances following rupture. 


Renal embolism occurs when a formed in 
some blood-vessel or in the heart is carried into the renal 
vessels. The condition is rarely diagnosticated during 
life, and but little help may be obtained from the urine for 
its diagnosis. 

The urine suddenly gives the characters of acute con- 
gestion — i. e,, it is greatly diminished in amount, with a 
high specific gravity, increased solids, albumins, and the 
characteristic bloody sediment of acute hyperemia. 


Pyelitis is an inflammation of the pelvis of the kidney. 
Pyelonephritis is a combined inflammation of the kidney 
and the renal pelvis. Acute pyelitis often complicates 
acute nephritis. It may be due to an extension of the dis- 
ease from the kidney; to infection from below, from the 
bladder, or to irritation due to stones or concretions. 
Pyelitis alone, without nephritis, is usually due to the last- 
named cause. 

The urine in acute pyelitis resembles that of acute 
nephritis in all respects, save that it contains more pus-cells 
and a large number of epithelia from the pelvic lining. 
When acute nephritis is associated with pyelitis, renal 
epithelia and casts are prominent in the sediment, and the 
relative importance of the coincident nephritis may be 
judged from this. When pus is present in considerable 
amounts, the term "acute suppurative pyelitis" may be 

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The same remarks apply to the relation of chronic 
pyelitis and chronic nephritis. In chronic (non-suppura- 
tive) nephritis there may be a certain amount of chronic 
pyelitis, shown by a few pelvic cells in the sediment, but 
it is the suppurative forms of chronic pyelitis and pyeloneph- 
ritis that are clinically interesting. Chronic suppurative 
pyelitis may be due to the irritation of stones, to tubercu- 
losis, or to tumors of the kidney or pelvis, or both; to in- 
fection through the blood in fevers; to obstruction of the 
ureter due to stones, stricture, etc. ; to ascending infection 
from below (bladder); to strictures of the urethra; tumors 
of the bladder; movable kidney, or enlarged prostate. 

The urine of chronic pyelitis is characterized by a di- 
minished quantity; a foul odor, sometimes both of sulphur 
and of ammonia; a pale, turbid appearance, due to pus; 
an acid reaction on voiding, and a low specific gravity 
(1012 to 1015). The normal solids, especially the urea, 
are diminished. There is albumin present, according to 
the amount of blood and pus. The sediment consists 
of pus, in clumps or free, of blood-cells, and of numerous 
pelvic epithelia. If the kidney is involved, there are, in 
addition, renal epithelia, casts, and shreds of connective 
tissue. Pus-casts may be present, and large clumps of 
hyaline matter coated with pus from pelvic calices are seen. 
Crystals of various kinds may be found and may indicate 
the presence of stone (see Differentiation from Cystitis, 

P- 370). 


Hydronephrosis is an accumulation of non-purulent 
urine in the renal pelvis and in a sac produced by the grad- 
ual dilatation of the renal cavity, due to an obstruction 

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of the ureter by a stone, by pressure from without (tumors, 
etc.), by kinking of the ureter, etc. The kidney gradually 
is destroyed, and may be dilated into a thin sac forming 
a single cavity with the pelvis. 

In cases of movable kidney the kinking of the ureter 
may produce hydronephrosis, which disappears when the 
kidney is replaced (intermittent hydronephrosis). 

The urine presents at first signs of acute congestion, 
as the opposite kidney takes up the work of both. The 
quantity is markedly diminished, the solids somewhat 
lowered, and there may be some albumin. Hyaline casts, 
a few blood-cells, and a few renal epithelia may be seen in 
the sediment. 

When hydronephrosis intermits — i, e,, is relieved — 

there is a sudden polyuria, with sometimes an increase in 

the amount of albumin and blood. The contents of the 

hydronephrotic sac are practically water with a slight 

amount of urinary salts, a trace of albumin, and a few red 

and white blood-cells and epithelia from the kidney and 



Pyonephrosis is an accumulation of purulent urine in the 
renal pelvis and renal cavity, due to an obstruction of the 
ureter, together with infection. It may follow a hydro- 
nephrosis when infection supervenes, or it may develop 
from an acute or chronic pyelitis when the ureter becomes 
obstructed. The causes of ureteral obstruction are the 
same as in hydronephrosis. The kidney is gradually 
destroyed and atrophies, forming finally a large abscess 

The urine shows the signs of an acute or active conges- 
tion, due to the overwork of the opposite kidney when the 

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obstruction is absolute. In such a case there is no pus, 
and the diagnosis cannot be made from the urine alone. 

When the obstruction is relative, or if it is removed 
suddenly, there is a considerable flow of pus, and the urine 
assumes the characters described under Chronic Pyeloneph- 
ritis. It is turbid, with an abundant greenish-white sedi- 
ment, consisting of pus, epithelia from the kidney and pel- 
vis, connective-tissue shreds, and blood (slight amounts 
usually), together with fragments of stone (when stone is 
present) and larger debris of kidney tissue. There is 
usually a considerable amount of albumin and a marked 
proportion of globulin. 


Inflammation of the ureter alone is rare, and is scarcely 
ever diagnosticated from the urine alone. Catheteriza- 
tion of the ureter may, however, reveal ureteritis, stric- 
ture of the ureter, calculi impacted in this canal, etc. 

Ureteritis may form part of pyelitis or cystitis by ex- 
tension, or may result from the irritation due to the pas- 
sage of a calculus with sharp points. It may follow com- 
pression of the ureter by tumors from without, strictures, 
or kinks of the ureter. Tuberculous ureteritis may occur 
when the kidney or the bladder is similarly diseased. 

The urine in a simple ureteritis is that of acute renal 
congestion, with high color, high specific gravity, and 
small amount of albumin and blood. The sediment 
shows blood, pus (few cells), and the characteristic cells 
of the ureteral lining. 

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Acute Cystitis. — ^This is an acute inflammation of 
the bladder, caused by infection with the gonococcus 
or with some pus-producing germ, usually by an extension 
of infection from elsewhere in the tract or by the use of 
dirty instruments. Acute cystitis also results from ex- 
posure to cold and wet; sexual excesses; acute urinary 
retention; the use of irritant drugs (copaiba, cantharides), 
or injury to the bladder. It may also occur as a complica- 
tion of infectious diseases. 

The urine, as a rule, is diminished in amount. It is 
bloody or smoky, strongly acid, with a high specific 
gravity and relatively high solids. The amount of albu- 
min varies with that of blood and pus. The sediment 
contains fresh blood, pus, mucus, mucous threads, and 
many epithelia from the superficial layers of the bladder. 

Chronic Cystitis. — This may follow an acute cystitis 
and be due to the same causes. A common cause of 
chronic cystitis is an enlarged prostate or some other form 
of urethral obstruction. In these cases the urine cannot 
be voided completely, and stagnates in the bladder, 
inducing cystitis. The same takes place in paralysis 
of the bladder. In tumors, stone, or tuberculosis of this 
24 369 

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organ there is usually a chronic cystitis. Between the 
vagina and the bladder there may be fistulas communicat- 
ing which complicate the cystitis. 

The urine is not markedly affected in quantity; usually 
pale and cloudy or bloody, with an ammoniacal or putrid 
odor, and thickened in consistence (mucus). In the early 
stages it may be highly acid, but later becomes alkaline. 
The albumin depends on pus and blood. An abundant 
thick and heavy sediment is present, chiefly of pus; of cells 
from all the layers of the bladder epithelium; of mucus, 
amorphous phosphates, triple phosphates, and ammonium 
urate. A number of bacteria may be found in the urine 
in acute, and especially in chronic cystitis. Besides the 
gonococcus there may be staphylococci, various bacilli, 
especially of the "colon group," the proteus vulgaris, 
various diplococci, etc. Cystitis may be due to one or 
more varieties of these germs. 

Differentiation of Pyelitis and Cystitis.— The de- 
tection of numerous epithelia from the pelvis, on the one 
hand, and from the bladder, on the other, does not always 
sufl5ce to make a distinction between pyelitis and cystitis. 
In fact, very well-trained observers have been misled 
into regarding a specimen of urine in a case of pyelitis 
for one due to cystitis alone. In view of the great import- 
ance of this differentiation the recent researches of Rosen- 
feld, extending through a number of years, are of interest. 
Rosenfeld found that the urine of a pyelitis differs from 
that of a cystitis in several important respects, which may 
be briefly summed up as follows: 

I. The reaction of the urine in pyelitis is almost always 
acid. An alkaline reaction is never found in uncomplicated 
pyelitis. An alkaline reaction, therefore, speaks for 

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cystitis, while an acid reaction does not exclude cystitis. 
The reaction must be observed in freshly voided urine. 

2. In pyelitis the pus-cells are characteristically ragged 
and distorted in contour. In cystitis they are characteris- 
tically round and uniform in shape. The distinction 
should be drawn only when large numbers of pus-cells 
show either of these types. The finding of round forms 
does not exclude pyelitis necessarily, but testifies to the 
presence of cystitis. 

3. The red blood-cells from a pyelitis are "abnormal," 
i. e,, washed out, altered in form, while in cystitis, except 
when due to tumors, they are fresh and "normal." This 
does not apply to hemorrhages other than microscopic. 

4. The ratio of albumin to the amount of pus is the most 
important point. In cystitis there may be great amounts 
of pus, but the albumin never exceeds from o.i to 1.5 per 
cent. In pyelitis, however, the amount of pus may be very 
small, yet from o.i to 0.15 per cent, of albumin and 
over will be found, and when the pus is abundant, the al- 
bumin reaches higher amounts — ^up to 0.3 per cent. 


Tuberculosis of the bladder is usually secondary to that 
of other organs of the genito-urinary tract. The first 
stage — of productive lesions (tubercles) in the bladder — 
does not give marked changes in the urine, while the second, 
marked by ulceration and by complicating chronic cystitis, 
gives a rather characteristic urine. 

The urine is diminished in amount, pale or bloody, and 
turbid, varies in reaction, with a low specific gravity 
and diminished normal solids. The albumin varies 
with the amount of blood and pus present, and may be 

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abundant during attacks of hematuria. The sediments 
consist of large amounts of pus, bladder epithelia, and 
blood-cells. The presence of tubercle bacilli with a 
large number of bladder epithelia, especially from the 



^ -jr. 



L. ■■ __J 

Fig. 87. — Portions of a villous growth of the bladder: o, Magnified 190 
diameters; 6, magnified 370 diameters (Ogden). 

middle and deep layers are conclusive evidences of tuber- 
culous cystitis. The absence of tubercle bacilli from the 
urine does not, however, necessarily exclude the presence 
of this disease. 

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Of the benign -tumors in the bladder the most common 
are papillomata, but fibromata and fibromyxomata also 
occur. Papillomata are diagnosticated in the urine from 
the presence of masses of villous growths of microscopic 
size in the sediment. In malignant growths of the bladder 
the urine presents the same features as in chronic cystitis, 
but there is apt to be more blood and even large blood- 
clots. Shreds of tissue and portions of the tumor may 
be found in it. Cells resembling those of the new growths 
are also sometimes seen in the sediments, but no positive 
diagnosis can be made from their presence. The cystoscope 
and exploratory operations are often required for diagno- 
sis, but the urine alone often points to the presence of 
bladder growths. 


The diagnosis of stone in the bladder is not usually 
made from the urine alone. Sounds, and the stone- 
searcher are used as aids, as well as the :x:-rays and the 

The urine presents the characters of acute or chronic 
cystitis, according to the length of time the stone has been 
in the bladder and the shape and size of the stone. Small 
concretions and an unusually abundant sediment of a 
crystalline or amorphous deposit, such as uric acid, cal- 
cium oxalate, etc., are sometimes clues to the diagnosis. 

Acute prostatitis is an acute parenchymatous in- 
flammation of the prostate gland. It is caused by infection 
aided by congestion (exposure to cold and wet, sexual 

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excitement, urethral stricture, traumatism, passage of 
calculi). The chief infectious agent is the gonococcus, 
which enters the prostatic ducts from the posterior urethra 
in cases of gonorrheal, urethritis. During an attack of 
gonorrhea acute prostatitis may be excited by a variety of 
causes, chiefly by sexual intercourse, alcoholic indulgence, 
instrumentation, etc. 

Characters of the Urine. — Acute prostatitis is often 
accompanied by a congestion of the kidneys, and in such 
cases the urine gives the signs of renal hyperemia, with a 
high or bloody color, high specific gravity, scanty amount, 
and a trace of albumin. The urine may, however, show 
none of these signs except a diminished amount and a 
little blood. Microscopic examination reveals many 
red blood-cells, pus-cells, epithelia from the prostate and 
its ducts and from the seminal vesicles; spermatozoa, 
most of which are dead and have broken tails; and plugs 
from the prostatic ducts. 'The pus-cells are not greatly 
altered, as a rule, and the epithelium is fairly fresh. 

Chronic prostatitis may follow the acute form or 
may be chronic from the start, due to gonorrheal infec- 
tion, or sexual overindulgence, masturbation, or coitus 
interruptus. It may also result from chronic urethral 
obstruction — e. g., by strictures, narrow meatus, phimo- 
sis, etc. — or from irritation or injury to the prostate by 
passing stones. 

Characters of the Urine. — ^Unless kidney lesions be 
present at the same time, the urine is not very markedly 
changed in chronic prostatitis. It is usually pale, acid, 
turbid, with slightly lowered specific gravity, and an amount 
of albumin varying with the amount of pus. In the sedi- 
ment we find large numbers of pus-cells, chiefly in masses. 

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mixed with a mucous substance; many epithelia in various 
states of disintegration and fatty change from seminal 
vesicles, the prostate, its ducts, and the neck of the bladder. 
There are rarely many blood-cells, but spermatozoa are 
in evidence, free and embedded in masses of pus, epithelia, 
and mucus. These masses often assume the shape of 
casts and plugs, already described under Acute Prostatitis. 
Shreds of connective tissue, niucus, and round cells, massed 
together with adherent spermatozoa and pus-cells, are also 
often found in this condition. Amyloid bodies (see p. 
312) are sometimes found in considerable numbers, but 
usually only a few are present. They assist in the localiza- 
tion of the trouble in the prostate. The presence of an 
accompanying cystitis will give its signs already described. 
Chronic prostatitis occurred in 60 per cent, of cases of 
gonorrheal infection in a series of 180 cases observed by 
the writer. In the sediment from the Jnassage-urine in 
these cases the gonococcus may frequentiy be found after 
centrifuging and staining the deposit (thinly spread on a 
slide). The method of staining these sediments is the same 
as that used for smears from sago bodies, etc. (see p. 244). 
Very frequently other bacteria, e, g,, especially the staphy- 
lococcus, the streptococcus, and bacilli resembling the 
colon bacillus, or sometimes the pseudodiphtheria bacillus 
are found in these massage-urines. 

Tuberculous prostatitis is almost always a part of 
a tuberculous process in some other genito-urinary organ. 
The urine does not differ essentially from that which char- 
acterizes chronic prostatitis, except that its sediment on 
centrifuging (or after massage, on standing) contains 

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tubercle bacilli. Several examinations are often needed 
to find these germs (see Tubercle Bacillus, p. 335). 

Cancer of the prostate is rare, especially the pri- 
mary form. The urine is practically that of chronic 
prostatitis, with an occasional hemorrhage. The pres- 
ence of cells with large round nuclei from the tumor cannot 
serve for a positive diagnosis, but in conjunction with 
clinical signs may hint at cancer. 


Inflammation of the seminal vesicles occurs as the result 
of the same causes as prostatitis. Acute seminal vesiculitis 
is a complication of gonorrheal urethritis. The chronic 
variety occurs with or without prostatitis as a sequel to 
gonorrhea, stricture, etc., and from such causes as con- 
gestion, overindulgence in sexual intercourse, masturba- 
tion, etc. 

The diagnosis of seminal vesiculitis is usually made 
by palpating the vesicles. The urine in the acute form 
shows pus-cells, blood, epithelia from the vesicles, numer- 
ous spermatozoa, shreds of vesicular lining, and plugs of 
coagulated matter from the vesicles. The signs of renal 
congestion may also be present. In the chronic form the 
urine shows, in addition to the signs of chronic prostatitis 
and chronic urethritis, masses of epithelia from the vesicles 
in a state of fatty change; spermatozoa more or less broken 
and distorted; plugs of coagulum and shreds consisting of 
connective tissue; numerous round cells, masses of mucus, 
and pus-cells. 

Smears prepared with material from massage-urine and 
properly stained as described, show pus, epithelia, and 
bacteria from the vesicles (see p. 314). 

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In the functional disturbance known as spermatorrhea 
semen is found in the urine, especially after defecation. 
The discharge of thin, mucoid matter which follows or 
accompanies defecation contains many spermatozoa, 
some of which are alive. The structures may be stained 
with anilin dyes or may be tested with Florence's reaction 
(see p. 314). In addition, spermin crystals, fat-droplets, 
prostatic and vesicular cells, granular matter, and mucus 
are found in this discharge. 


In acute gonorrheal urethritis the urine is cloudy, acid, 
and deposits a sediment of mucopus, epithelia, and shreds 
from the urethra. With ensuing posterior urethritis there 
comes blood, in addition to these elements, in the shape of 
a moderate number of red cells. The amount of albumin 
depends upon the pus, and in other respects the urine is 
unchanged unless the kidney is afifected. 

In chronic urethritis the urine shows a much more 
scanty deposit of mucus and pus and usually a number of 
shreds from the urethra. The latter have been fully 
dealt with on p. 319. 

The diagnosis of specific urethritis is based upon the 
finding of the gonococcus (see p. 331). It is always best 
to seek this germ in the pus pressed out of the urethra or 
in the "morning drop'' of chronic cases. In the urine the 
gonococcus must be looked for in the centrifuged pus or 
in shreds picked out with a pipet or a platinum loop. 
The urine voided after prostatic (or vesicular) massage 
may contain gonococci. In these cases the centrifuged 

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sediment or the solid elements (p. 314) should be smeared 
on slides and stained according to the methods already 

I. Acuie Congestion of the Kidneys. — ^What are its causes? What 
is the most frequent cause ? Why is it chiefly interesting ? What is 
the character of the urine ? How is it distinguished from acute nephritis ? 
From chronic interstitial nephritis just before death? 

2. Chronic Congestion of the Kidneys. — What are its causes ? Describe 
the urine. How is it distinguished from that of chronic interstitial 
nephritis ? 

3. Acute Diffuse Nephritis. — ^What are its causes? What pathologic 
processes may be present ? Describe the characters of the urine. What 
do the amounts of blood and of urine indicate ? What is the fatty stage ? 
What other renal disease does it resemble? 

4. Chronic Parenchymatous Nephritis. — ^What are its causes? Its 
lesions? Describe the characters of the urine in this disease. How is 
it differentiated from other forms of chronic nephritis? 

5. Chronic Diffuse Nephritis. — ^What are its causes and lesions? 
Describe the urine of this disease. What are the characteristic casts 
in this form of nephritis ? What changes in the urine indicate interstitial 
lesions, and what changes stand for parenchymatous lesions? 

6. Chronic Interstitial Nephritis. — ^What are its causes ? Its lesions ? 
Describe the characters of the urine in this condition. 

7. Amyloid Kidney. — ^What are its causes? Describe the chief 
characters of the urine. What is noteworthy of the quantity, the specific 
gravity, the solids, and the varieties of casts found ? 

8. Tuberculosis of the Kidney. — What elements in the lesions influence 
the characters of the urine in this disease ? What is noted in the urine in 
early stages? In advanced stages? 

9. Storte in the Kidney. — ^What three elements are at work in this 
disease in determining the characters of the urine? Describe the urine 
in the early stages; in the late stages, accompanied by infection. 

10. Tumors of the Kidney. — ^What malignant growths occur in the 
kidney ? Which is more common in children ? What are the characters 
of the urine? On what should the diagnosis be based? What is the 
value of "cancer cells" in the sediment? 

1 1 . Cysts of the Kidney. — In what forms may cysts occur in the kidney ? 

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What symptoms lead to a diagnosis of congenital cystic degeneration? 
What does the urine show in cysts of the kidney ? 

12. Abscess of the Kidney. — Define renal abscess. What are its 
causes ? What does the urine show before rupture ? After rupture ? 

13. Embolism of the Kidney. — Define it. When does it occur ? What 
changes in the urine are found in such cases? 

14. Acute Pyelitis and Pyelonephritis. — Define each. What are the 
causes of acute pyelitis ? What are the characters of the urine ? How 
is acute pyelitis distinguished from acute pyelonephritis? What is sup- 
purative pyelitis? 

15. Chronic Pyelitis and Pyelonephritis. — Define each. To what 
is chronic supptirative pyelitis due ? What are the characteristics of the 
urine ? 

16. Cystitis. — (a) Acute. — ^What are the causes and the characters of 
the urine? 

{b) Chronic. — What are its causes? What are the features of the 
urine? How is pyelitis differentiated from cystitis? What is peculiar 
of the ratio of albumin to pus in cystitis? In pyelitis? 

17. Tuberculous Cystitis. — ^What are the two stages of this disease 
and how do they show themselves in the urine ? What does the absence 
of tubercle bacilli show? 

18. Tumors of the Bladder. — ^What benign tumors occur in the bladder ? 
Which is the most common ? How are the papillomata diagnosticated 
from the urine ? What is the character of the urine in malignant growths 
of the bladder? 

19. Stone in the Bladder. — How is it diagnosticated? What, in 
general, are the characters of the urine? 

20. Describe the characters of the urine in acute prostatitis; in chronic 
prostatitis; in tuberculosis of the prostate; in cancer of the prostate. 

21. What characteristics are observed in the urine of seminal vesicu- 
litis ? Of spermatorrhea ? 

22. Describe the sediment in the urine of urethritis — (o) acute, (6) 

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The amount of urine excreted is usually increased in 
diabetes mellitus. If there is over 3 per cent, of sugar, 
the increase becomes more and more marked as the amount 
of sugar rises. Very large amounts, even 10 liters daily, 
have been seen. From 2000 to 3000 cc. are commonly ex- 
creted. In moderately severe cases the amount of urine 
frequently reaches 5 or 6 liters daily, but diminishes when 
the diet is regulated. The proportion of sugar is ordinarily 
increased with the increase of quantity, and, what is most 
important, the specific gravity is not decreased in diabetes 
with an increased excretion of urine. Von Noorden gives 
the following table which demonstrates this: 


Specific Gravity. 


1500- 2,500 cc. 


2-3 per cent. 

2500- 4,000 " 

1030- 1036 

3-S " " 

4000- 6,000 " 


4-7 " " 

6000-10,000 " 


6-9 " " 

The diet has a great deal to do with the quantity of 
urine as well as of sugar. When carbohydrates are ex- 
cluded, the amount of urine diminishes, as well as the 
amount of glucose, and when the sugar disappears under 
the influence of diet, the quantity becomes almost normal, 
although the specific gravity remains high. 

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The specific gravity of diabetic urine, as has been hinted, 
is characteristically high, usually from 1030 to 1040. 
The color of the urine is usually pale yellow, sometimes 
greenish yellow. Sometimes the urine will ferment in the 
bladder with a development of gases (pneumaturia). 
The fermentation may give rise to cystitis. 

The form oj sugar almost invariably present in the urine 
of diabetes is glucose; sometimes levulose is present, but 
only in small quantities, not exceeding i per cent. When 
levulose is taken by mouth by diabetics, it is usually ex- 
creted as dextrose. Inosite and pentose have been found 
associated with glucose. 

In testing jor sugar ^ especially in the mild cases, the urine 
voided from four to six hours after a breakfast at which 
starch and sugar had been taken is to be preferred for exam- 
ination. The largest amount is said to be excreted in the 
late forenoon, and another considerable rise in the sugar 
excretion takes place toward the evening, about 6 p. m. 
The morning urine and the urine passed during the night 
contains the smallest amount of sugar. In order to deter- 
mine the amount of sugar excreted the total twenty-four- 
hour quantity should be collected, thoroughly mixed, 
accurately measured, and a sample examined. If a dis- 
tinction is desired between the day and the night urine, one 
portion should be taken, beginning after breakfast and 
ending late in the evening (day urine), and a second 
portion, beginning at night until before breakfast of the 
following morning. 

The severity of diabetes cannot be measured by the 
quantity oj sugar excreted in twenty-four hours. This is a 
common practice, but very often leads to errors in progno- 
sis. The percentage of glucose excreted rarely exceeds 

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8 per cent., although cases have been reported in which as 
much as 20 per cent, has been excreted. Von Noorden 
divides these cases into three groups: The mild cases, the 
severe cases, and the moderately severe cases. A mild 
case is one in which the urine becomes free of sugar a few 
days after the exclusion of carbohydrates from the diet. 
This does not mean that the patient no longer manufactures 
sugar in his tissues, but that the process goes on so grad- 
ually when no carbohydrates are taken in, that the organ- 
ism is able to cope with the glucose manufactured, and 
none is excreted in the urine. 

The severe cases are those in which in spite of the re- 
moval of carbohydrates from the food for days or even 
weeks, there is no complete disappearance of glucose from 
the urine. A case of moderate severity, according to 
Naunyn, is one in which the sugar cannot be removed 
from the urine by simply excluding carbohydrates from the 
diet, but in which the glycosuria can be checked by 
regulating the amount of proteids ingested. There are 
many gradations between the types just defined. A 
diabetes of moderate severity is usually a transition form 
between the mild and the severe types. The only way to 
test the severity of a case of diabetes is by a carefully 
regulated diet, the rules for which will be found in von 
Noorden's and other text-books. 

The amount of sugar is increased by carbohydrates in 
the diet, but some carbohydrates, as potato and oatmeal, 
have less influence than others. Lactose, levulose, and 
compounds derived from these sugars have less influence 
than dextrose. An increased amount of proteids may also 
increase the sugar output, but fats do not have any in- 
fluence on the glycosuria. Sugar excretion is markedly 

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influenced by mental strain, excitement, worry, and other 
psychical influences. Glycosuria is decreased by muscular 

During fevers and acute infectious diseases there is 
said to be a marked diminution in the sugar excretion ; 
although von Noorden has not found this diminution to 
occur as was supposed. The sugar output is diminished 
in certain chronic wasting diseases, as in tuberculosis and 

Albumin is frequently found in diabetic urines, and may 
be present apparently without a complicating nephritis. 
On the other hand, when chronic nephritis develops in 
the course of diabetes, the glycosuria may disappear 
(Frerichs, von Noorden, etc.). It appears that the kidneys 
are unable to excrete sugar when they are affected by 
chronic nephritis, and in such cases enormous amounts 
of sugar have been found in the blood. Diabetes is closely 
allied to gout, and glycosuria may alternate with gouty 
paroxysms, the sugar disappearing during the attacks. 

An increased excretion of creatinin is often noted in 
diabetes as the result of a predominating meat diet. 
Uric acid is usually present in normal or slightly increased 

Acetonuria is an important symptom in diabetes. It has 
already been discussed on page 165, but a few additional 
clinical points may be mentioned here. 

It should be remembered that the acetone bodies occur in 
other conditions than diabetes. Thus, acetone occurs in 
starvation and in other conditions in which the same factors 
obtain as in starvation, for example, in high fever, in acute 
gastro-intestinal diseases, in obstruction of the intestine, 
in puerperal toxemia, etc. Von Noorden found acetone 

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in the urine of patients with acute pneumonia who were fed 
exclusively on meat broths and eggs. The acetone bodies 
come from the fatty acids of the organism and appear in 
the urine when the body is unable to burn up carbohy- 
drates (von Noorden). 

Acetonuria is absent in mild cases of diabetes and the 
excretion of acetone bodies is more accurately proportion- 
ate to the severity of the disease than the excretion of glu- 
cose. Von Noorden distinguishes several degrees of ace- 
tonuria. In the first degree there is only acetone in the 
urine. In the second degree diacetic acid is also present, 
while in the third degree oxybutyric acid is present. 

When large amounts of acetone or diacetic acid or, in 
the severest cases, oxybutyric acid appear, the system 
of the diabetic is said to be in a condition of "acidosis." 
The abnormally manufactured acids are said to produce 
an intoxication which may be counteracted by an in- 
creased supply of alkalis. Diabetic acidosis is said to lead 
to the coma which characterizes the most dangerous phase 
of this disease. While the presence of the acids men- 
tioned, especally in large amounts, indicates a severe 
type of diabetes, their occurrence does not necessarily 
mean impending coma. Acidosis may exist for years 
without coma. When the acid bodies reach a certain 
amount, however, coma seems to be impending. According 
to Herter, when there are 25 gm. of oxybutyric acid daily 
coma is probably approaching. As it is difficult to esti- 
mate the oxybutyric acid, a better way is to measure the 
amount of ammonia, which is in proportion to oxybutyric 
acid usually. When over 3 gm. of ammonia per day are 
excreted there is danger of coma (Naunyn). Alkaline 
treatment is indicated in such cases and the urine should 

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be watched for the appearance of casts of the granular 
type in large numbers, which precede the appearance of 
coma, according to Kiilz, 


This is a rare condition (variously called hydruria, 
polydipsia, persistent polyuria, insipid diabetes, etc.), 
characterized by the excretion of large amounts of urine of 
a low specific gravity, containing no sugar nor any other 
abnormal constituent. 

The etiology of true (or "idiopathic") diabetes insipidus 
is obscure. Lancereaux found that heredity, syphilis, 
gout, and Jithemia were concerned in 74 cases which he 
collected. No cause can be discovered in most cases, 
and we can only say that diabetes insipidus is a "mani- 
festation of disturbed metabolism," the mechanism of 
which is not known. 

True diabetes insipidus must be distinguished from 
symptomatic polyuria, due to hysteria or other nervous 
affections, renal disease, injuries to the skull, etc. 

The urine in diabetes insipidus varies in quantity, as 
much as 20 and even 40 liters daily having been recorded. 
The specific gravity varies from looi to 1009. The color 
is very pale, the reaction faintly acid. No sugar is present 
nor any albumin or casts (distinction from interstitial 
nephritis). The total urea excreted may be increased 
owing to the ravenous appetite shown by some patients. 
The patients complain of great thirst, dry skin, and fre- 
quent necessity to void the bladder. The disease is 
of long duration and is not directly fatal, but may last a 
lifetime and materially weaken the patient. 


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Nitrogen Partition.— During the past few years a 
considerable amount of experimental work has been pub- 
lished by a few observers ^ which demonstrates the clinical 
value of determining in pregnant women suspected of 
toxemic conditions leading to eclampsia or to toxic per- 
nicious vomiting (a) the total nitrogen and (b) the sepa- 
rate quantities of nitrogen derived from urea, uric acid, 
ammonia, creatinin, and the residual or "undetermined 

While the subject is as yet comparatively new, enough 
evidence is at hand now to make it necessary to acquaint 
students and practitioners with the great importance of an 
accurate study of nitrogen elimination in the diagnosis and 
prognosis of toxemias of pregnancy. Students are referred 
to the original papers for details, but a brief summary of 
the practical aspects of this subject is as follows: 

The normal relations of urea, uric acid, ammonia, etc., to the total 
N. output in the urine have already been given (p. 131). In pregnancy 
there is normally in most cases a disturbance of metabolism lowering the 
urea and increasing the "undetermined nitrogen" and to a less extent 
(Ewing and Wolf) or to a marked extent (Williams) the ammonia. After 
delivery the normal relations are restored. 

When a toxemia develops in the course of pregnancy it is usually 
characterized by one of the following groups of symptoms: (i) Persist- 
ent vomiting; (2) the clinical condition known as the pre-eclamptic state, 
or threatened eclampsia, in which the symptoms are practically those of 
impending uremia: dizziness, weakness, headache, transient visual dis- 
turbances, vomiting, increased blood-pressure, and marked edema 
and albuminuria; (3) eclampsia, with or without the previous existence of 
the condition described under (2). 

^ Zweifel, ArcK f. Gynak., 1904, Ixxii, i ; 1906, Ixxvi, 536 ; Wil- 
liams, Johns Hopkins Hosp. Bull., 1906, xvii, 71 ; and Ewing and 
Wolf, Am. Journ. Obst, 1905, li, p. I4S» and 1907, Iv, No. 3. 

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The work of the authors mentioned above seems to show that these 
three groups of conditions arise from similar causes — a, general intoxica- 
tion of the system in which there may or may not be (opinions differ as yet) 
a predominance of acidosis. The behavior of the nitrogen elimination in 
these conditions, according to Ewing and Wolf, is as follows: 





I. Toxemia charac- 


Usually high. 


terized chiefly by 


II. Pre-eclamptic 





in. Eclampsia. 

Low in pro- 


High, but not so 

portion to 

accurately pro- 


portionate to 
severity as urea. 

The term "undetermined nitrogen" is used to designate that amount 
of nitrogen which cannot be accounted for in the form of urea, uric 
acid, ammonia, or creatinin — i. e.y the nitrogen remaining unaccounted 
for after subtracting from the total nitrogen the nitrogen determined as 
existing in the form of the substances mentioned (each separately tested). 
Detailed studies showed that this "undetermined nitrogen" was due in a 
large measure to amino-acids, which are decomposition products of pro- 
teids that normally are further split up into ammonia, and then into urea. 
The undetermined nitrogen, therefore, is also called "the amino-acid 
nitrogen." The failure to split up amino-acids into ammonia and urea is 
called by some authors (Zweifel, Ewing, and Wolf) "desamidation." 
It is possible, though not completely proved as yet, that the toxemias of 
pregnancy are dependent upon this failure to split up amino-acids. 

Clinical Value of Nitrogen Partition. — From the above facts one 
feels now that a physician does not do his full duty to his patient (as E. 
B. Cragin puts it) unless the nitrogen excretion is determined in all cases 
of pernicious vomiting in pregnancy and in the cases of threatened eclamp- 
sia in which the symptoms are vague and the other findings in the urine 

It must be remembered, however, (i) that in normal women (without 
toxemia) there may be a disturbed state of metabolism during pregnancy, 
with a lowered urea and an increased "undetermined nitrogen," and to 
a less marked extent an increased NHg nitrogen (Ewing). This may be 

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due to nitrogen retention in pregnancy. (2) That urea may be distinctly 
low and undetermined nitrogen high withotU any symptoms in some cases. 
Such women should be watched for a possible predisposition to eclampsia. 

When vomiting is persistent or when the toxic symptoms of im- 
pending eclampsia are present, however, with a low urea ratio and a high 
ratio of "amino-acid" or "undetermined" nitrogen, especially when in- 
dicanuria, acetonuria, and albuminuria exist at the same time (the last 
three are not constant, as will be seen by reference to the appropriate 
sections), the patient is in a state of toxemia and should be treated ac- 

The quantitative determinations of nitrogen necessary for this work 
cannot be done save in a completely equipped laboratory and should be 
entrusted only to experts in these analyses. The twenty-four-hour 
quantity of urine should be very carefully collected and the specimens 
sent as quickly as possible to the laboratory. The bottle in which the 
urine is collected should contain half an ounce of chloroform, and should 
be well shaken after each addition. 

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Within the past ten years there have arisen certain 
new methods of urinary diagnosis which aim to deter- 
mine the functional efficiency of the kidneys, or of one 
of these organs as compared to the other. The terms 
"sufficiency" and "insufficiency," as applied to the func- 
tions of an organ of the body, were first used in relation to 
the stomach by O. Rosenbach in the expression "gastric 
insufficiency." The same idea had been suggested in the 
writings of Stokes concerning the functions of the heart. 

The "sufficiency" — i. e,, capacity for work or functional 
efficiency of an organ — depends upon the condition of that 
organ and the demands Therefore, sufficiency 
is a relative term only, and hence, if we find that an organ 
at a given examination shows insufficiency, we mean that 
it is incapable of doing the work it needs to do in the body. 


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The study of the functional value of the kidney is an 
important supplement to the study of the anatomic features 
of this organ in health and disease. If we can find and 
exactly measure the amount of work that the kidneys are 
doing, and if we can compare this amount of work with 
that of normal kidneys in a man of the same size, weight, 
and age, we gain a means of determining the actual value 
of a diseased kidney from a functional viewpoint. It is, 
of course, important to know what lesions are present in the 
kidneys; whether they are acute or chronic, parenchyma- 
tous or interstitial, but it is even of greater value to know, 
both for prognosis and for the choice of treatment, the 
amount of functional efficiency left in a diseased kidney — 
i, e,, whether it is sufficient for the present needs of the 
body. The functional study of an organ, as Virchow 
pointed out long ago, broadens our knowledge of pathology 
and is just as important as the anatomic study of its 

But, in addition to its general value in pathology, diag- 
nosis, and prognosis, the functional state of the kidneys, or 
usually of one kidney as compared with the other, has 
become highly important of late in surgical affections of 
these organs. Just as one ventricle of the heart may com- 
pensate for the functional inefficiency of the other, so one 
kidney may compensate for the functional insufficiency of 
its fellow. When one kidney is perfectly healthy, the 
removal of the other functionally useless kidney, which 
may be the seat of a suppurative condition, a malignant 
tumor, tuberculosis, etc., is not fraught with much danger 
to the patient's life, as the healthy kidney will take care 
of the work of both. On the other hand, should the op- 
posite kidney be the seat of chronic lesions, producing 

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a more or less marked state of insufficiency, then neph- 
rectomy is contraindicated. Modern surgery regards as 
unjustifiable any nephrectomy which has not been pre- 
ceded by an examination of the comparative functional 
values of each kidney, the urine being drawn directly from 
each ureter by means of ureteral catheters introduced 
through a special cystoscope, or else being collected sepa- 
rately by means of a *' segregator." 

The data of ordinary urinalysis, etc., may give a clue 
to the anatomic conditions present or to the extent of the 
anatomic lesions, but do not give a ready means of cal- 
culating the actual amount of work a kidney can do. 
" For the fate of a patient does not depend upon the ana- 
tomic changes in the kidneys. It depends upon the in- 
terference with the function of this organ which is produced 
by these lesions" (Cooper). A kidney may be diseased, 
yet very nearly perfect in function, as enough healthy 
parenchyma may be left to do its work. 


We shall assume that the reader is acquainted with the 
anatomy, minute structure, and physiology of the kidneys. 
A few words must be said, however, as regards the mode 
of secretion of the urine by these organs. There are 
two principal theories as to the mode in which the urine is 
excreted. The first of these is the theory of Ludwig, who 
regards the kidneys essentially sls fillers, through which the 
waste-products pass from the blood out of the body, and 
who considers the process as a purely physical one, de- 
pending upon the principle of diffusion or osmosis. 

Ludwig assumes that the blood-pressure is relatively 
greatest in the glomerular tufts as a result of the resistance 

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to the'efiFerent circulation; and consequently a free exuda- 
tion of water takes place from the tufts, with, perhaps, 
some dissolved salts. This concentrates the blood that 
reaches the convoluted tubules through the capillaries 
about these canals, while within the tubules flows the thin 
aqueous filtrate from the tufts. These conditions — a, thin, 
watery fluid on one side of a membrane (the tubular wall) 
and a thickened blood on the other side — ^are the ideal con- 
ditions for osmosis, and so an interchange of elements oc- 
curs in the kidney, whereby water from the urinary tubules 
passes into the blood, while the products of tissue waste — 
urea and salts — pass from the blood into the tubules, where 
they mix with the watery fluid and so form the urine. 

The second theory is that of Bowman-Heidenhain. Ac- 
cording to this theory, the kidney is essentially a secreting 
gland and the urine is a mixture of certain characteristic 
elements, such as urea, etc., which are secreted by the epi- 
thelial cells of the urinary tubules, and of water and in- 
organic salts, such as sodium chlorid, which are filtered 
through the glomeruli from the blood. According to Bow- 
man, therefore, the glomeruli are filters which send water 
and salts into the urine, while the tubules are true secretory 
structures. This theory has been confirmed by certain 
interesting experiments by Heidenhain, who injected 
methylene-blue into the blood of an animal and found soon 
afterward that the blue color appeared in the urine, and 
that epithelium of the tubules was stained blue, while 
the glomeruli were free from stain, thus showing that the 
tubular epithelium possesses selective powers like those of 
a secreting gland. The most important proof of the Bow- 
maa-Heidenhain theory, however, is the fact that when the 
epitheliimi of the tubules is destroyed by disease, urea and 

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certain toxic products ( ?) are retained in the blood, pro- 
ducing uremia, while the urine is more watery and contains 
a smaller percentage of its characteristic solids. 

Koranyi, of Budapest, to whom we shall refer later, 
has combined the theories of Ludwig and of Heidenhain. 
He admits, with Heidenhain, that water and salts are fil- 
tered through the glomeruli, while the other constituents 
of urine are secreted by the tubular epithelium, but he 
believes that there is a perfect balance maintained between 
the number of molecules of urea and allied products se- 
creted by the epithelium of the tubules, on the one hand, 
and the number of molecules of sodium chlorid and other 
salts filtered into the lumen of the tubules through the 
glomeruli, on the other. The epithelium of the tubules, 
therefore, acts not only as a secreting cell with special 
properties but also as a living membrane, through which 
osmosis constantly takes place from the blood into the 
tubules, and vice versS,, so that for every molecule of urea, 
etc., that passes from the blood into the tubule there is 
reabsorbed a molecule of sodium chlorid or other salts 
through this living membrane of epithelium into the blood. 
For this reason any changes in the epithelium wrought by 
disease will be reflected in changes in the proportion 
between the urea and the salts.* 


How many theories of urinary secretion are there at present? By 
what names are they known ? 

What is Ludwig's theory, in your own words? 

* The above is a very brief synopsis of the theories of the secretion 
of the urine ; for further details the student is referred to the more ad- 
vanced text-books on physiology. 

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On what physical principles does Ludwig's theory of secretion 
depend ? 

What is Bowman-Heidenhain 's theory? How does this theory re- 
gard the kidney essentially? 

What part of the urine is secreted by the tubular epithelium? 
What part filtered by the glomeruli? 

Mention experiments to confirm this theory. 

What is the most important pathologic proof of this theory? 

What is Kordnyi's teaching as regards the number of molecules of 
urea, etc., and of sodium chlorid, etc., filtered? 

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The special methods which have been devised for 
measuring the functional eflSciency of the kidneys, or of 
each of these organs separately, are as follows: 

I. By determining the molecular concentration of the 
urine — i. e., the relative number of molecules in a 
given volume: 
{a) By measuring the freezing-point (cryoscopy). 
{h) By measuring the electric conductivity of the urine. 
II. By measuring the rate of excretion of urine in the 
(a) The methylene-blue test (Achard and Castaigne). 
{b) The indigo-carmin test (Voelcker and Joseph). 

III. By measuring the chemic activity of the kidneys : 

The phloridzin test (Casper and Richter). 

IV. By measuring the rate of excretion under abnormal 

The experimental polyuria test of Albarran. 

Cryoscopy is the study of dissolved substances by ob- 
serving the freezing-point of their solutions. The physical 
laws which underlie cryoscopy were discovered by Raoult 
in 1882, although they had been partly forecast by 
DeCoppet in 1872 and were later supplemented by laws 


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deduced from experimental researches by Vant' HoflF 
in 1886. The application of cryoscopy to the study of 
urine, blood, and other body-fluids is due to von Kordnyi, 
of Budapest, who first introduced this method into clinical 
work in 1897. 

It would be beyond our scope to enter into the intricacies 
of the physics of solutions upon which the freezing-point 
method is based. It will be enough if we say that the 
freezing-point of a solution varies in proportion to the num- 
ber of molecules of a substance in a given volume of the 
solvent. The more concentrated the solution, the greater 
the number of molecules, the lower the freezing-point. 
This is simply a more exact statement of the well-known 
fact that a solution of salt in water freezes at a lower tem- 
perature than does water alone. The number of hun- 
dredths of a degree Centigrade at which freezing takes 
place below zero represents the ratio of the molecules dis- 
solved in I cc. of the solution. Thus, if urine may be 
found to freeze at 1.30° F., it may be assumed that there are 
130 molecules of solids in i cc. of this urine. This figure 
is merely a conventional way of calculating, and we do not 
rtiean to state the actuM number of molecules, but merely to 
designate the ratio of molecules in this particular solution 
as compared to other solutions. 

Cryoscopy is, therefore, based upon the principle 
established experimentally that for every additional 
molecule of dissolved solids in a solution the freezing-point 
sinks to some extent, and that, therefore, by comparing the 
freezing-point of different solutions we can determine the 
ratio of molecular constitution.* 

* There is, however, a very slight error in this calculation, which 
depends upon the fact that there is a difference between the freezing- 
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The technic of cryoscopy is by no means simple, on 
account of the delicacy of the observations, the variations 
in the freezing-point of urine being in hundredths of 1° C. 
A sample of the whole amount 
passed in twenty-four hours must 
be obtained, and 10 or 15 cc. of 
this are suflicient for the cryoscopic 
test. The latter is performed in 
a special apparatus known as the 
cryoscope, of which there are a num- 
ber of modifications, the original 
types being constructed by Raoult 
and by Beckmann-Heidenhain 
(Fig. 88). Essentially the appar- 
atus consists of an extremely 
delicate thermometer ^ graduated 

point actually observed and the calculated 
freezing-point, expressing the sinking of the 
point of congealing corresponding to the 
molecular constitution of a solution of 
known quantitative composition. This dif- 
ference is very slight, does not amount to 
more than one-sixtieth of the figure obtained, 
and probably depends upon what is known 
as dissociation. In virtue of this phenome- 
non, which takes place to a greater or less 
extent in all solutions of salts, the molecules 
are split up or dissociated into their ions or 
radicles (such as Na and CI in the case of 
NaCt). Each of the ions exerts the same 
influence upon the freezing-point as an inde- 
pendent molecule^ and so the freezing-point is 

lowered more markedly than it should be from the actual number of 
molecules corresponding to the amount of the substance dissolved. 

^ The thermometer used in all cryoscopes was devised by Beckmann. 
The introduction of this instrument into chemic technic may be said to 

Fig. 88. — Beckmann- 
Heidenhain 's apparatus 
for determining the 
freezing-point of a solu- 

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to Yoir ^^ ^ degree, the bulb of which dips into a test-tube 
filled with the urine. Outside of this is another test-tube 
containing alcohol or a solution of glycerin, so that the 
urine is inclosed in a double-walled chamber with one of 
these fluids in the interspace. The outer test-tube is sur- 
rounded by a mixture of ice and salt packed in a jar. 
A spiral of platinum wire or of hard rubber is arranged so 
that by means of it the urine can be constantly stirred 
around the thermometer, thus keeping the temperature 
of all parts of the sample uniform. The mercury begins 
to sink rapidly when the fluid approaches the freezing- 
point. It then rises and fluctuates for a time until it 
finally settles at a point below zero, which is read accurately 
as the freezing-point of the urine. Various mechanic im- 
provements, such as automatic stirrers moved by clock- 
work, etc., have been devised, and in France the evapora- 
tion of ether or carbon disulphid is used instead of ice 
for the purpose of freezing.* 

Clinical Applications of Cryoscopy. — The total num- 
ber of molecules in a given urine is expressed by the freez- 
ing-point thereof, J. The normal freezing-point of urine 
ranges between — 1.30° and — 2.20° C. When there are 

have marked an era in the history of physical chemistry. The Beckmann 
thermometer is unlike the ordinary instrument in that it has a reservoir 
of mercury at the top of the capillary, and by shaking the thermometer one 
can add to or subtract from the length of the column of mercury. In this 
manner the thermometer may be "set" to read at any temperature. It is 
graduated so as to cover only a few degrees, thus giving a long scale which 
is subdivided into hundredths, and these, with the aid of a magnifying 
glass, may be read to thousandths. Before using, the freezing-point of 
water should be determined with it, and any deviation from o° C. should 
be noted as a correction. 

^ Not because of any advantage of this method, but because of the 
scarcity of ice. 

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lesions in the kidneys interfering with the functional activity 
of these organs the freezing-point rises — i. e,, approaches 
zero Centigrade — ^because the total number of molecules 
excreted is diminished. A urine freezing at above — i ° C. 
is usually considered as abnormal. In extremely severe 
cases of chronic nephritis, with uremia, the freezing-point 
is close to or actually at zero. The symbol J, by com- 
mon consent, stands for the number of dissolved molec- 
ules in I cc. of urine, as expressed by the freezing- 
point in tenths and hundredths of a degree Centigrade. 
If V stands for the amount of urine eliminated in twenty- 
four hours, and P for the weight of the patient in kilograms, 
then the formula J X y represents the total number of 
molecules eliminated in the urine per kilogram of body- 
weight in twenty-four hours. The comparison of the value 
of J X ^ in different persons makes the freezing-point 
method more exact as a measure of functional activity 
than the mere comparison of the cryoscopic coeflicient, 
J, alone. 

The foregoing is a summary of the theoretic basis of 
cryoscopy. Unfortunately, the beautiful structures built up 
by Koranyi and his school, by Claude and Balthazard, 
and others, who vied with each other in devising complete 
mathematic formulae for determining the functional con- 
dition of the kidneys, have not stood the test of time and 
experience. Cryoscopy is a troublesome method, is sub- 
ject to many errors, and even when performed with ac- 
curacy is not clinically conclusive. A normal freezing- 
point has been found with anatomic lesions of the kidney, 
and an abnormal freezing-point may occur with healthy 
kidneys, Cryoscopy of the urine of each kidney sepa- 
rately has more value, as it may be used for comparison, 

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but even then the freezing-point tells very little, if anything, 
more than the specific gravity, which is much more easily 

The relation oj the specify, gravity of urine to its freez- 
ing-point has been the subject of extended studies during 
the past ten years. Theoretically there should be a 
marked difference between the specific gravity and the 
freezing-point. The latter indicates the number of mole- 
cules, the former the weight of the same molecules. Thus, 
if a trace of albumin be present, its heavy molecules 
would theoretically influence the specific gravity more 
than the freezing-point. Yet in practice this difference is 
of no importance.^ There is, therefore, a fairly constant 
parallelism between specific gravity and J. Fuchs 
proposes that the last two figures of the specific gravity 
(carried out to the third place) be multiplied by 0.075 ^^ 
determine the freezing-point of normal urine in degrees 
Centigrade. In practice, therefore, we can usually do with- 
out cryoscopy, but can employ advantageously an accurate 
determination of the specific gravity of the urine from each 
kidney. This may be done with the aid of a pyknometer 
and an accurate balance or, more easily, with the writer's 
urinopyknometer (see p. 44). 


This method is a complicated one, and consists in 
measuring the power of the urine to conduct or carry a 
current. This power varies with the molecular concen- 
tration of the urine. The method has not gained head- 
way in practice because it gives no information that may 

* Bugarszky, Fiodoroff, Kiss, etc., Kapsammer, Casper. 

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not be obtained by measuring the specific gravity or by 
determining the freezing-point. 


Kutner^ was the first to conceive the idea of giving 
methylene-blue internally and watching the flow of urine 
from the ureters through a cystoscope to determine the 
functional activity of the kidneys. The method, however, 
which is at present used was worked out by Achard and 
Castaigne (1900). 

The test consists in injecting 0.02 gm. of methylene- 
blue ^ intramuscularly (Kapsammer), though some authors 
recommend larger doses — 0.05 gm. (Albarran). Normal 
kidneys begin to excrete the dye within fifteen or twenty 
minutes and the excretion is complete within forty-eight 
hours. The excretion must normally begin not later than 
within half an hour and reach its maximum in the third 
or fourth hour (Kapsammer). 

Clinical Value. — ^When the kidneys are in a state of 
functional inefficiency due to anatomic lesions, they are 
unable to excrete methylene-blue properly: 

(a) The excretion may be delayed and may be prolonged 
when it does occur (impermeability, said to be indicative 
of interstitial lesions — Bard). 

(6) The excretion may be premature and the total dura- 
tion short (said to mean parenchymatous changes — Bard 
and others). 

{c) The excretion may be premature and prolonged 

^ Deutsche med. Wochenschrift, 1892. 

^ Merck's or Griibler's " medicinal " chemically pure methylene- 
blue should be used in sterile water. 

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(said to mean compensatory hypertrophy of a kidney — 
Albarran and Bernard). 

It is claimed by Achard and Castaigne that methylene- 
blue excretion is always delayed when there are lesions in 
the kidney. ChaufiFard, Kovesi, and Kapsammer, and 
with them many other observers, including the present 
writer, find that methylene-blue is retained only in the 
presence of marked renal lesions. When methylene-blue 
appears within half an hour the kidney is functionally 

Sources of Error. — The most important difficulty with the methylene- 
blue test is the fact that the dye is often not excreted as such, but as a 
leuko-derivative or chromogen, a colorless substance from which the 
blue color may be obtained only by oxidation. This oxidation frequently 
takes place in the kidney, but sometimes a urine may appear unchanged 
in color although it contains methylene-blue in the form of a chromogen. 
By boiling with a little acetic acid the blue color is unmasked. 

A further source of error lies in administering the methylene-blue and 
the phloridzin test in the same patient on the same day. If the phloridzin 
test (see below) is used first and the methylene-blue test used afterward, 
while sugar is still present, the sugar excreted interferes with the blue dye 
and the latter is excreted as a chromogen, hence is invisible. On the other 
hand, if the methylene-blue test is used first and the phloridzin test is 
applied while the urine is still blue, the sugar decolorizes the urme and 
converts the blue dye into an invisible chromogen. 

Retention of methylene-blue and its late excretion, months or even 
years after the injection of the dye, may occur. E. Beer, of New York, 
has suggested that such retention of the dye may be used as a diagnostic 
sign of pyelonephritis with abscesses in which the dye is lodged. The 
subsequent excretion of the dye is due to the bursting of these abscesses. 

To sum up, the methylene test is not absolutely 
reliable for the determination of the functional value 
of the kidneys. Its chief value, as that of several other 
methods, is in contrasting the function of one kidney with 
that of the other (urethral catheterization or separation of 

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urines) when the lesions are marked on one side. The 
indigo-carmin test is more satisfactory in many respects. 

In 1903 Voelcker and Joseph showed* that indigo- 
carmin was superior to methylene-blue in testing the 
rate of excretion of the kidneys, because the former dye, 
unlike methylene-blue, was not excreted as a chromogen, 
but always as a blue pigment. 

Normal kidneys begin to excrete a solution of indigo- 
carmin injected into the muscles in about five minutes. 
The urine turns blue and the color reaches its maximum 
in one-half or three-quarters of an hour. The excretion 
lasts about twelve hours. The dose usually given (Kap- 
sammer) is 4 cc. of a 4 per cent, suspension in normal 
NaCl (=0.16 gm.). The site of injection may be into 
the gluteal muscles, but as the dye is excreted rapidly, 
there may not be time to turn the patient and put him 
into position for cystoscopy. Kapsammer, therefore, in- 
jects the dye into the quadriceps muscles about 4 inches 
above the knee-cap. (The ureteral catheters should be in 
their places before the injection.) 

Delayed excretion and lessened excretion of indigo- 
carmin used in this way means a functional renal dis- 
turbance. If the color does not appear for ten or twelve 
minutes after injecting 0.16 gm. of the dye, and then only 
as a greenish tint, and if the color never becomes blue, but 
remains greenish, there is renal insufficiency. Kapsammer 
emphasizes the trustworthiness of tJie time oj onset oj the 
excretion with indigo-carmin. The longer the appearance 
of the blue color is delayed, the more severe the lesion. 

* Munch, med. Wochenschrift, 1903. 

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The intensity oj the color is also a criterion. The dose 
used by Kapsammer takes twenty-four hours to be com- 
pletely eliminated, but as this time varies normally, it is 
not so valuable as the other criteria mentioned. 


Phlorid^in is a glucosid discovered by Koninck, in 1855, 
in the root-bark of apple, pear, and cherry trees. Von 
Mering, in 1885, found that phloridzin caused glycosuria 
when injected subcutaneously in normal persons. The 
glucose excreted after injections of this drug is manufac- 
tured in the kidney itself, but just where or how is not as 
yet definitely known. That interstitial nephritis interferes 
with the excretion of sugar in cases of diabetes had been 
known for some time (Klemperer, Fiirbringer, Senator), 
and we have referred to this fact in the chapter on this 
disease (p. 383). In 1896 Klemperer showed that patients 
with chronic Bright's disease did not have glycosuria after 
the injection of" phloridzin, as did normal persons. 

It remained for Achard and Delamarre, in 1899, to apply 
these ideas to the functional diagnosis of renal affections. 
These authors were the first to use the phloridzin test as 
such for the purpose of determining whether or not the kid- 
neys were functionally efficient, measuring this efficiency 
by the capacity of the kidneys to excrete sugar after in- 
jections of phloridzin. 

Preparation of the Patient. — ^The patient should not have received 
any of the following drugs within a reasonable time before the test: 
Antipyrin, glycerin, sodium salicylate, piperazin, or jambul. All these 
retard sugar excretion. Furthermore, the administration of diuretics 
before the test is not advisable, although practised by some in order to 
accelerate the collection of urine after the test. Diuretics interfere with 
the quantitative relations of the excretion. 

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The patient's kidneys should not be massaged or otherwise forcibly 
manipulated for at least three days before the test. 

Technic of the Injections. — The phloridzin used should be of the 
best quality, Merck's being preferred. Cases have been reported of 
failure of the test due to the use of impure phloridzin. 

Phloridzin is insoluble in cold water and is precipitated on cooling from 
its solutions in hot water. Solutions may be made in hot water and the 
requisite amount drawn into the syringe while the fluid is hot and before 
the glucosid has had time to precipitate. A better way, however, is to 
make a solution of phloridzin in alcohol, and to add to it the required 
amount of water. No precipitate occurs in such solutions. The solu- 
tions should, in all cases, be freshly prepared. 

The best method of preparing the solution, therefore, is to dissolve 
I part of phloridzin in 30 parts of 95 per cent, alcohol and add 70 
parts of warm water. This will make a i per cent, solution, and 
from 10 to 20 minims (usually 15 minims) is a convenient dose of this 
solution, which should be injected warm. The syringe should have been 
boiled and washed with alcohol before each injection. The solution 
should be injected suhcutaneously into the arm, care being taken not to 
inject intradermally nor too deeply into the adipose layers, as the rate of 
absorption varies according to the character of the tissue into which phlor- 
idzin is injected. In metric weights the dose usually used may be ex- 
pressed as 0.0 1 gm., although some workers use higher doses. 

The sugar should appear in the urine ten or fifteen 
minutes after the injection of phloridzin. If the function of 
the kidneys is insuflicient, the excretion of sugar is delayed, 
appearing twenty minutes or a longer time after the in- 
jection. If no sugar appears within forty-five to fifty 
minutes after the injection, the kidney is in a state of 
marked insufficiency. The sugar normally disappears in 
about twelve hours, after reaching a maximum excretion 
at the end of one and a half hours. 

Method of Observing the Result. — Inasmuch as the phloridzin 
test is now almost always applied as a means of comparing the function 
of one kidney with that of the opposite organ, the urine being collected 
for this purpose through ureteral catheters, or with the aid of a 

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" separator," a few words might be said as to the manner of 
conducting this test under these conditions. The cystoscope is intro- 
duced before the injection, and the catheters are inserted into the 
ureters. The phloridzin is injected, and the time of injection noted. 
Ten minutes are allowed to elapse, during which the urine is allowed to 
drop through the catheters into graduated test-tubes. The first portion 
of urine is used for the purpose of a general examination. At the end of 
ten minutes the tubes are changed, a new tube being substituted on each 
side. The tubes are changed after each succeeding five minutes. It is 
convenient to have a series of test-tubes, properly marked in series, ready 
for each side. The first sugar reaction normally appears in the second 
tube, i. e., after fifteen minutes. The third tube represents the urine up 
to twenty minutes, etc. In this way the exact time of appearance of the 
sugar can be noted, and the progress of the excretion can be accurately 

Interpretation of the Result. — Although it seems to be well established 
both clinically and experimentally that functional inefficiency interferes 
with the excretion of sugar, there is still a question as to what criteria are 
to be applied to the excretion of sugar in order to make out an insufficiency. 
There are practically two views at present. Casper and Richter orig- 
inally held and still hold that it is necessay to determine the percentage 
of sugar excreted after phloridzin injections, and for this purpose make 
a quantitative determination of sugar in the urine obtained at maximum 
excretion. This view is now gradually becoming obsolete, owing to the 
many sources of error which obtain in judging the quantity of sugar under 
these conditions. First, the percentage of sugar is affected by the polyuria, 
which is ordinarily produced by the mere act of ureteral catheterization, 
and second, there is always some leakage alongside the catheter, which 
makes a difference in the quantity of sugar excreted in a given time. 

The second view, brought forward some years ago by Kapsammer, 
seems more simple and more practical in its application. According to 
this author, it is merely necessary to watch for the time of appearance of 
the sugar in the manner described above. The time of appearance of 
sugar is a more trustworthy criterion as to the functional capacity of the 
kidney than the variable factor of quantity of sugar excreted. Kapsam- 
mer's method is sufficiently accurate for practical purposes, and, indeed, 
seems to lead to fewer errors than the method of Casper and Richter. 
If the appearance of sugar is delayed for forty-five minutes on the "un- 
affected side, " Kapsammer rules out the possibility of performing nephrec- 
tomy, as the functional capacity of the remaining kidney is then not suffi- 
cient to allow the patient to live. If the appearance of sugar is delayed 

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for thirty minutes, marked renal lesions are present, but before final 
decision is made other confirmatory tests, such as the indigo-carmin test 
and the polyuria test of Albarran (see below), are recommended. 

Value of the Method. — ^While the phloridzin test, 
on the whole, is the best and most trustworthy single 
method of functional diagnosis we have, it is not infallible. 
It is very delicate, and errs perhaps in this direction. More- 
over, it is not conclusive in cases in which there is a paren- 
chymatous nephritis with few or no interstitial changes. 
In these cases there is commonly a normal excretion of 
sugar, although there are many casts, and albumin is 
present in considerable amount. In interstitial nephritis 
or in diffuse nephritis with considerable interstitial changes 
the phloridzin method is of the greatest value. The reason 
for its failure in parenchymatous types is that in these the 
function of the kidney may long remain comparatively 

The failure to excrete sugar when the kidneys are comparatively 
healthy has been recorded by a number of observers. Beer^ found that 
this interference with sugar excretion occurred at times in the "unaffected 
kidney" when the other Was surgically diseased, and attributes this in- 
terference to the influence of the diseased kidney upon the healthy or 
healthier organ. He reported several cases in which the phloridzin test 
showed normal function in the kidney which remained after nephrectomy 
of its fellow, although previous to operation the test had been negative up 
to fifty minutes in the unaffected organ. While more evidence is needed 
to confirm this. Beer's work certainly throws a shadow of doubt upon 
some of the negative findings with the phloridzin test, and in this sense 
considerably diminishes its value. When the test is positive, however, 
every observer agrees that its interpretation of good function can be 
relied upon, with the possible exception, already noted, of parenchyma- 
tous nephritis. It is because of these occasional failures of the phloridzin 
test that a control by means of the method about to be described may 
be desirable. 

^ Journal Am. Med. Assoc, 1908, II, 1876. 

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When an increased amount of water is taken by a patient 
with normal kidneys, there occurs a corresponding in- 
crease in quantity and a proportionate dilution of the urine. 
On the other hand, when the water intake is increased in a 
person with parenchymatous nephritis, the quantity and 
concentration of the urine remain more or less unchanged. 
This was experimentally proved by Kovesi and Roth- 
Schulz, in 1900, by F. Strauss, in 1902, and by Albarran, 
in 1905. The last-mentioned observer has published a 
considerable amount of evidence as to the value of what he 
terms "experimental polyuria '^ in determining the func- 
tional capacity of the kidneys.* 

Albarran gives the patient from 400 to 600 cc. of a mineral water 
known as "Evian." The urine is then collected every half-hour, and its 
quantity, its freezing-point, the amount of urea, and of chlorids are deter- 
mined. Albarran found that, as a rule, in healthy kidneys the freezing- 
point, the percentage of urea, and the amount of chlorids were diminished 
in about the same degree as the quantity of urine was increased. This was 
true, however, of the percentages of solids, but when their absoltUe quatUi- 
ties were determined, it was found that normal kidneys could at times 
excrete during an experimental polyuria not only more water, but also 
a larger quantity of urinary solids. In other cases, however, there was also 
a reduction in the absolute quantity of the solids along with the polyuria. 

In diseased kidneys the decrease in the percentages of the solids ex- 
creted was much less marked, with the same amounts of urine, and the 
more severe the anatomic lesion of the kidney the less markedly altered 
were the percentages of solids in proportion to the total amount excreted. 

In addition to the factors mentioned above, the specific gravity of the 
urine may also be employed as a criterion in connection with this test. 
Griinwald used Albarran's method, substituting the specific gravity for 
the freezing-point, and came to the same conclusions. In healthy kid- 
neys the polyuria was noteworthy for a marked lowering of the specific 
gravity, while in parenchymatous nephritis the specific gravity was low- 
ered to a lesser extent and the change in density appeared later than in 

' * Albarran, Exploration des Fonctions R^nales, Paris, Masson, 1905. 

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normal cases. In interstitial nephritis no polyuria of any account was 
produced and the specific gravity was not affected by the increased intake 
of water. 

The experimental polyuria test is simple in technic and 
may be employed as a corroborative method in connection 
with other means of functional renal diagnosis. 


To sum up what has been said in the preceding pages 
as to the value of the various methods of functional renal 
diagnosis, the following brief statement may serve as a 
guide to those who are at a loss to select a suitable method 
for this purpose: A careful estimation of the specific grav- 
ity, of the urea, and, if need be, of chlorids in each of the 
separated urines gives for practical purposes as trustworthy 
results as cryoscopy, without the sources of error to which 
the latter is subject. 

Of the other functional test, the phloridzin method 
stands highest in accuracy and delicacy, but its limitations 
must be understood and its results must be corroborated, 
if necessary, by the indigo-carmin test. The latter is to 
be preferred in every instance to the methylene-blue test. 
Finally, the method of experimental polyuria may be re- 
sorted to as an additional safeguard. 

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It has been known for a long time that suppression 
of urine is followed by systemic poisoning of a definite 
type. In 1881 Felt2 and Ritter showed that normal 
urine was poisonous by injecting it into animals and finding 
that a certain dose of urine was fatal. Later, Bouchard 
investigated the poisonous properties of normal urine more 
thoroughly. In order to be able to compare the toxicity 
of urine under various conditions, Bouchard established 
what is known as the urotoxic coefficient, which is the weight 
of rabbit in kilos that is killed by the quantity of urine 
excreted by one kilo of the person experimented upon in 
twenty-four hours. According to Marfan this coefficient 
is from 20 to 35 in health. 

The toxic symptoms produced by the intravenous in- 
jection of normal urine include contraction of the pupil, 
which dilates just before death, somnolence, coma, marked 
polyuria, frequent micturition, a lowering of the tempera- 
ture, diminished reflexes of the conjunctiva and cornea, 
and death in coma or convulsions. 

The toxicity of the urine, according to Bouchard, is 
greater during the day than at night. The day urine is 
strongly narcotic and but feebly convulsive, while the 
night urine is the reverse. The toxicity is diminished by 
active exercise in the open air. Bouchard found that in 

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acute uremia the urine becomes non-toxic. He concludes 
that the urine's toxic properties are due to a number of 
substances which he could not isolate completely, but is not 
due to urea, uric acid, creatinin, etc., since these are 
non-toxic in large doses when injected into the blood. 

Some observers — e, g,, Stadthagen, Beck, and v. d. 
Bergh* — deny that any specific poisonous substance occurs 
in normal urine. They claim that the poisonous action of 
the urine is due partly to the potassium salts and partly 
to the other normal constituents — urea, creatinin, etc. — 
which have very little toxic effect individually. 

In disease the toxic power of the urine may be either 
increased or diminished. It is generally increased in 
acute infectious diseases and fevers, provided the kidneys 
remain healthy. The toxic powers of the urine become 
more or less diminished according to the extent of the dam- 
age done to the kidneys, and in extensive renal lesions the 
urine may become almost non-toxic. In uremia the kid- 
neys no longer eliminate the poisons from the system, and 
the urine is non-toxic. The toxicity of the urine, however, 
is considerably raised in most diseases — e, g., in tetanus 
(Labbe), in cholera (Bouchard), in septicemia (Feltz), 
in diphtheria (Roux and Yersin), etc. 

Bouchard has shown that from 30 to 60 cc. of normal 
urine injected intravenously will kill a rabbit weighing 
I kilograrrt A man weighing 60 kilos and passing 
1200 cc. of urine daily secretes enough poison to kill 24 
kilos of animal, if 50 cc. are necessary to kill one kilo of 
living matter. This standard is used in determining the 
relative value of the "urotoxic coefficient" referred to 

^ Quoted by Hammarsten, loc, cit. 

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In connection with the subject of urinary toxicity we 
may briefly consider the two classes of substances that 
have been found in the urine, and that are responsible 
for this toxic action — ptomains and leukomains. 


Ptomains are complex organic substances, basic in 
character, resembling alkaloids in many respects, and 
formed by the action of bacteria upon nitrogenous matter, 
which may be either animal or vegetable in origin. Some 
ptomains are highly poisonous and are styled toxins 
(Brieger), while others are harmless. 

According to Bouchard, Pouchet, and others, ptomains 
occur in normal urine and are increased in quantity in 
disease (Bouchard, Lepine, and Guerin, etc.). Villiers 
found a constant increase of these substances in measles, 
diphtheria, and pneumonia. Pouchet found them in chol- 
era; Feltz, in cancer; Lepine, in pneumonia, and Griffiths 
and Albu have isolated a series of ptomains in a great va- 
riety of diseases. Baumann and von Udrdnszky showed 
the presence of two ptomains, first described by Brieger 
— ^putrescin (C4H12N2) and cadaverin (C5H14N2) — in the 
urine in a case of cystinuria and cystitis. 


Leukomains are basic substances found in living tissues, 
which do not result from the action of bacteria, but are the 
product of fermentation or of retrograde changes in the 
organism. While leukomains are the products of normal 
life-processes, ptomains are the results of putrefaction. 

Leukomains in the urine are divided into two groups — 
the uric-acid group and the creatinin group. The uric-acid 

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group includes bases related to uric acid — viz,, adenin. 
hypoxanthin, guanin, xanthin, heteroxanthin, etc., carnin, 
episarkin, pseudoxanthin, etc. The creatinin group, 
according to Gautier, includes creatinin, creatin, cruso- 
creatin, xanthocreatin, amphicreatin, and two unnamed 

Brieger and von Udrdnszky and Baumann and Stad- 
thagen^ deny the occurrence of ptomains and leukomains 
in normal urine, and present very strong objections to 
Bouchard's teachings. 

The clinical interest in the presence of ptomains and 
leukomains in the urine lies in the fact that these sub- 
stances are the chemic bases of infectious diseases, and 
that possibly specific substances may be isolated from the 
urine in various maladies. The subject, however, has 
not yet been sufficiently well worked out to bear direct 
application in clinical work.^ 

^ Quoted by Hammarsten, Physiological Chemistry (Mandel), third 
edition, New York, 1901, p. 463. 

^ For details regarding the chemistry of ptomains and leukomains, see 
Vaughan and Novy, Cellular Toxins, Philadelphia, 1902. For a 
bibliography of ptomains and leukomains in the urine, see Neubauer and 
Vogel, Analyse des Harnes (Huppert), Weisbaden 1898. 

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While a complete urine examination, as may be seen 
from the foregoing pages, calls for a great deal of time and 
labor and a full mastery of technical detail, routine analyses 
which are sufficient for every-day purposes require but a 
few minutes' time and are accomplished with compara- 
tively simple means and with the fewest possible manipu- 

In the following summary I mean to give the student, 
the busy physician, and the medical examiner for life 
insurance a few hints as to the best means of shortening 
the time and lessening the labor of urine analysis, without 
unduly interfering with the trustworthiness or accuracy 
of the results. 

Every one who has a large number of urinalyses to 
perform daily, or who has but a few minutes to devote to the 
examination of urine, will d o well if he hepins bv devjs ing 
a certain routine of work. Such routine examinations 
should be as rapid as is compatible with thoroughness 
and accuracy; they should include everything that is 
necessary for a clinical diagnosis, and exclude everything 
that is unnecessary or of purely theoretic interest. A 
routine of work may, indeed, be so devised that even 

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unnecessary movements are saved, wherever possible, 
by simplifying the methods and arranging the order of the 
tests. Such moments, wasted in unnecessary trifling with 
minor details, are well saved and well invested in a longer 
time allotted to the study of the urine under the micro- 

Selection of Methods. — ^The first thing to be done 
when contemplating the analysis of a number of specimens 
is to determine, once for all, the methods that are to be 
used, and then to adhere to these methods unless forced to 
deviate from them by some special circumstance. This 
does not, of course, mean to exclude experimenting with 
various methods or modifications at our leisure. 

It is the beginner who is usually undecided as to what 
method he shall use for a certain test, etc. The experienced 
man, as a rule, works with one method or, at the most, 
with two, for the same part of the analysis. 

As I have said in speaking of albumin tests, in pract ical 
work the best way is to use one test, always ho lfjjnpr a ^con- 
firmatory test in reserve in case of doub t. This principle 
holds good in all parts of urine analysis. Select, therefore, 
the best method you know of — one that has proved effi- 
cient and practical in the hands of a large number of men — 
and adhere to this method in your routine work. This has 
the obvious advantage that the man who works with one 
method will in a short time know all the vagaries, irregulari- 
ties, possibilities, impossibilities, and sources of error in 
the one method which he uses. 

The next rule to be observed in routine work is: _In 
employing a given method, invariably use the sam e 
amounts of reagents, the same dilution, th e same order, 
heating, i f needed, for the same length of time — m shor t, 

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u sing exactly the same manipulations for the sa mejtest 
in each analys is. This will enable a careful worker, after 
a time, to estimate with fair accuracy the quantity of a 
constituent from the bulk of a sediment or precipitate. 
Of course, such adherence to routine in details can be 
profitable only after one knows with perfect accuracy just 
how to perform a test to the best advantage with whatever 
materials (test-tubes, etc.) one may have on hand. 

Routine of Work. — Necessarily each man must be a 
law unto himself in devising this routine according to his 
tastes, the time at his disposal, and the requirements of 
his cases. The following order of examination is suggested 
as one that is apt to meet the average requirements. The 
tests selected are those which have proved trustworthy 
in my own work and which have been found satisfactory 
by a large number of observers. 

I. Physi cal Examinati on. — ^The urine is poured into 
a small cylinder and a urinometer is immersed in it, to- 
gether with a strip of blue litmus-paper. While the urin- 
ometer is allowed to settle in position, the color of the urine 
is determined by a comparison with VogePs scale, which 
hangs directly opposite on a wall. The same glance tells 
us its transparency, the presence of a sediment, and, before 
the specific gravity is read, the odor is ascertained. These 
characteristics are noted on the record blank (see p. 420) 
and then the urinometer scale is read. A portion of the 
urine is now poured into a small filter, the consistence of 
the fluid being noted as this is done, and the filtered urine 
is used for many of the subsequent tests, a constant supply 
of it being kept up by filling the filter from time to time. 

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2. Chemic Examinatio n,— This should begin with th e 
e5;tirr|atinn of urp.a^ because while the nitrogen gas is form- 
i ng we can attend to the other tests and then r ead the scale 
of the apparatus. 

A Ibumin. — ^While the urea test is under way we proceed 
to look for albumin. For this purpose I usually employ 
first the acetic acid and heat test, after adding saturated 
salt solution. Unless there is a massive coagulation, I 
confirm the result with Heller's ring test (cold nitric acid) 
and the ferrocyanid test. If hyaline casts are found in 
the urine on subsequent examination imder the microscope 
and if all the above albumin tests were negative, I make 
sure of the absence of even the faintest traces af albumin 
by the use of the Roberts magnesium test with the horis- 
mascope or with Spiegler's test. If albumin is found, 
Esbach's or Tsuchiya's quantitative method is applied. 
If time is pressing, Purdy's centrifugal method will suffice 
ordinarily, if performed accurately. 

Sugar , — ^While the test-tube of the albumin test is al- 
lowed to stand for a few moments to show the full develop- 
ment of the ring or reaction, we mix and dilute the Fehling's 
solution and bring it to a boil. Th e^urine is added, and if a 
p ositive reaction is obtained, we at on ce set up the Einhom 
s accharometer. with yeast and urine, and allow it to sta nd 
for t wenty-four hou rs. If a polariscope is available, the 
urine is at once prepared for polarimetry by mixing with 
basic lead acetate and filtering. If albumin is present it 
must, of course, be removed first. 

Indican is the next substance looked for. Here I am 
in the habit, in routine work, of employing Obermeyer's 
simple and efficient method. The same amount of urine 
and of the reagent is always used, and a fair estimate is 

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obtained of the amount of indican in the urine. For 
routine quantitative work Robin's method of estimating 
indican is useful. 

Bile. — In testing for bile we may use the filter-paper, 
which has become in the meanwhile well saturated with 
the filtering urine. Whil e the in dican test is allowed t o 
reach its completion, a drop of pure nitric acid is placed on 
themter, proaucmg a g reen spot which changes to red if a n 
excess ot biie is present . Often this test is not necessary, 
as in Heller's test for albumin an excess of bile-pigments 
will give a play of colors (green, blue, violet, red, and 
yellow) at the point of contact of the two fluids (see 
Gmelin's Test, p. 190). When small traces of bile-pig- 
ments are present, Mar^chaPs test (p. 191) should be used 
to confirm the above-mentioned method. 

The remaining chemic tests are used only when special 
indications require. 

Acetone and diacetic a cid are tested for if there vyp .s 
glucose in th e urine, or in cases of suspected toxemia, in 
pregnancy, etc. For acetone the Jackson-Taylor modi- 
fication of the nitroprussid test is useful. For diacetic 
acid the ferric chlorid method is most convenient. 

The diazo-redctio n is next tested for if necessary. 

The estimation of uric acid may be clinically simplified 
by the use of Ruhemann's method. The estimation of 
chlorids, phos phates, a nd sulpha tes may be made con- 
venient by Purdy's centrifugal method. For accurate 
work, however, these methods are not sufficiently exact. 

The microscopic examinatio n follows: The centrifuge 
is set going, and in the meanwhile the amount of urea is 
read off, and the changes, if any, in the various test-tubes 
that have been allowed to stand are noted. The sediment 

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is then examined microscopically according to the methods 
already outlined. 

Finally, a word of warning: Do not rely upon the find- 
ings of laboratories that do their work upon " the quick- 
lunch-counter plan.'' Such laboratories unfortimately 
exist in some of our large cities. Urine analysis may 
mean life or death, and should not be intrusted to incom- 
petent persons. If the patient cannot pay for an exami- 
nation by an expert, let the physician make the principal 
tests himself, rather than allow the work to be "railroaded" 
through by one of the concerns that apply the "factory sys- 
tem" to clinical pathology. 

Forms for Recording Analyses. — The following blank 
form (p. 420) is used by the writer in reporting analyses 
of urine when the specimen or the patient has been re- 
ferred to him by other physicians. Naturally, this blank 
provides merely for the essential points of an examination 
in an average case. Space is provided, however, for ad- 
ditional data, quantitative and qualitative. The tabular 
form of expressing the principal quantities is recommended 
as very convenient. 

For use in his own private practice the writer has de- 
vised an index card, which is shown on p. 421. These 
cards are filed with the histories of the cases. 

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Report No. Date. 

Dr. Name. 


Transparency Reaction 

Color Specific Gravity 

Amount voided in twenty-four hours, cc, 




Diacetic acid 
Other constituents 

at i5«> C. 

Per Cent, 
by Weight. 

Per MiUe 
by Weight. 

Grains per 

Amount in 
24 hours. 

Total solids 





{Obtained by Centrifuge at 1800 Revolutions for Five Minutes) 
Amorphous sediment 








Red blood-cells 


Other elements 

Respectfully submitted, 

M. D. 

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Dr Name . 





Specific gravity 




Indican . 


Diazo-reaction . . . 


Diacetic acid 



Amorphous deposit . 

Crystals . . , 








From kidney 
" pelvis 
" bladder 
" vagina 

Other elements . . . . 


Reagent bottles of appropriate sizes (250 cc. for liquids 
and 125 cc. for solids) are made by firms supplying chemic 
apparatus, and should be made of glass free from lead and 
other impurities. The bottles should be fitted with glass 
stoppers, and those for solutions of salts, such as sodium 
hydrate, etc., should have stoppers coated with a mixture of 
paraflBin and vaselin. 

All reagents should be purchased chemically pure, 
unless otherwise specified. All standard solutions for 
chemic analysis are described by the United States Phar- 
macopoeia, and should conform to its standard unless 
otherwise mentioned in the text of this book. 

The following list includes the principal reagents needed 
in urine analysis. The list is intended chiefly for the use 
of teachers intending to follow the methods outlined in 
the present book. Practitioners will find it convenient to 

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select from this list the reagents they require in their 
routine analyses. 


Distilled water (H3O). 

Acid, Acetic (c. p.), U. S. P. (HC3H3O,). 

Acid, Acetic, Glacial, U. S. P. 

Acid, Boric (c. p.) (H3BO3), sat. sol. 

Acid, Hydrochloric (c. p.) (HCl). 

Acid, Hydrochloric, Commercial (for cleaning glassware). 

Acid, Nitric (c. p.) (HNO3). 

Acid, Nitric (brown, fuming; nitrosonitric). 

Acid, Picric (CqH2(N02)30H), 8 gr. to i oz. = sat. sol. 

Acids, Picric and Citric (Esbach's solution, see p. 71). 

Acid, Salicylsulphonic, sat. sol. 

Acid, Sulphuric (c. p.) (H^SOJ. 

Ammonium Hydrate, U. S. P. (NH.OH). 

Ammonium Chlorid, sat. sol. 

Ammonium Sulphate, sat. sol. 

Sodium Hydrate, U. S. P. (NaOH). 

Sodium Hydrate Solution for Urea (Knop's). 

Sodium Hydrate Solution for Urea (Rice's). 

Sodium Chlorid (NaCl), sat. sol. 

Sodium Nitroprussid [NaFe(NO)(CN)5 + 2H3O]. 

Potassium Hydrate, U. S. P. (KOH). 

Potassium Ferrocyanid (K^Fe(CN)Q), i: 20. 

Potassiomercuric lodid (Tanret's, see p. 67). 

Potassium and Sodium Tartrate (Fehling's, see p. 10 1). 

Magnesium Fluid (see p. 218). 

Magnesium Sulphate and Nitric Acid (Roberts, see p. 64). 

Barium Chlorid (BaClj, 4 oz.; H^O, 16 oz.; HCl, i oz.). 

Copper Sulphate (Fehling's, see p. 10 1). 

Silver Nitrate (AgNO,), 1:8. 

Iron Chlorid (FejClg), i: 10. 

Obermeyer's Solution, see p. 179. 

Lead Acetate (PhOjiC^lifil), 1:4. 

Lead Acetate, Basic (PbaC2H3032PbO) i : 4. 

Mercuric Chlorid (Spiegler's, see p. 66). 

Mercuric Nitrate (Millon's, see p. 80). 

Hydrogen Peroxid (HjOj), U. S. P. 

Bromin (c. p.) (Br). 

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Bromin (Rice's solution, see p. 139). 

Tincture lodin, U. S. P. 

Tincture Guaiac, U. S. P., fresh. 





Formalin, 40 per cent. 

Also the following standard volumetric solutions: 

Decinormal Potassium Hydrate. 

Decinormal Sodium Hydrate. 

Decinormal Silver Nitrate. 

Decinormal Potassium Bichromate (KjCrjO^). 

Standard Uranium Nitrate. 

Standard Sodium Acetate. 

Potassium Ferrocyanid. 

Standard Barium Chlorid. 

Potassium Sulphate (K2SOJ, 20 per cent. 


Acid, Citric. Potassium Chromate. 

Acid, Picric. Potassium Ferrocyanid. 

Ammonium Chlorid. Potassium Hydrate. 

Ammonium Sulphate. • Potassium lodid. 
Copper Sulphate. Sodium Acetate. 

Lead Acetate. Sodium Carbonate. 

Litmus-paper. Sodium Chlorid. 

Magnesium Sulphate. Sodium Hydrate. 

Mercuric Chlorid. Sodium Nitrite. 

Phenylhydrazin. Sodium Nitroprussid. 

Potassium Chlorate. Yeast. 


1. Methylene-blue, sat. sol. in 95 per cent, alcohol (i part in 3 of water 
for staining bacteria). 

2. Carbol -gentian violet, see p. 333. 

3. Gram's solution (iodin, i; potassium iodid, 2; water, 300). 

4. Bismark brown, see p. 333. 

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5. Carbol-fuchsin (Ziehl-Neelsen's: Fuchsin, sat. alcoholic sol., 10; 
carbolic acid solution, 5 per cent., — 90). 

6. HCl 3 per cent, in 95 per cent, alcohol. 

7. Alcohol, absolute. 


Test-tubes, 2 or 3 dozen, assorted 

Pipets, plain glass, J dozen. 
Pipets, graduated, 5, 10, 25 and 50 

Glass rods, 8 inches long each. 
Beakers, thin glass, with lip, nest of 

Florence flasks, 250 cc, 500 cc. 
Distilling flask, 100 cc, see p. 166. 
Watch-glasses, nest of 6. 
Porcelain evaporating dishes, nest 

of 6. 
Conic glasses, 4. 
Wineglasses, 2. 
Ground-glass covers, square. 
Cylinders for urinometer, 4 ounces, 

and for urine, 12 ounces. 

Funnels, glass, 3 assorted sizes. 
Balance, accurate, with weights. 
Test-tube rack. 

Test-tube brushes, sponge end. 
Filter-paper, round, assorted sizes, 

white "c p." quality. 
Water-bath, copper, fitted with 

Filter and buret stand, metal with 

solid base. 
Wire gauze, several squares, 4 by 4 

inches each. 

Droppers, nipple. 

Graduates for 100, 500, and 1000 
cc, marked also in ounces. 

Graduate for 15 cc, marked also in 

Urinometer (Squibb's, etc). 

Urinopyknometer (see p. 44). 

Saccharometer, Einhom's. 

Doremus' or Hinds* urea appa- 

Esbach^s albuminometer. 

Horismascope (albumoscope). 

Uricometer, Ruhemann's. 

Purin apparatus, Camerer's. 

Thermometer, Centigrade. 

Burets, 50 cc. each, graduated in 
y<j cc 

Tripod and triangle for heating. 

Bunsen burner and tubing; or 


Test-tube holder, wood or wire. 

Platinum foil. 

Platinum wire in glass-rod handle. 

Centrifuge (see p. 237). 

Slides and cover-glasses. 

Microscope (see p. 242). 

Syracuse watch glasses, 6. 

Glass tray for staining, 

Ultzmann polariscope. 

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44 1 1 1.2 

43 109-4 

42 107.6 

Fahr. Cent. 

Fahr. Cent. 







. 167 



. 140 

. 122 


40 . 
39 . 
38 . 
37 • 
36 . 
35 • 
34 . 
33 . 
32 . 

. 104.9 
. 104.0 
. 100.4 

• 99-5 
. 98.6 

• 97-7 
. 96.8 

• 95-9 

• 93-2 

• 91-4 
. 89.6 





— 10 

— 20 

. .87.8° 








. . o 



= 1.8 
= 3.6 


I grain = 64.8 milligrams. 

I ounce = 28.3 grams. 

I pound =453-6 " 

I gram = i5'432 grains. 

I kilo = 2 pounds, 3 ounces. 

I minim = 0.059 cubic centimeter. 

I fluidram = 3.5 cubic centimeters. 

I fluidounce = 28.39 " " 

I pint =567-9 

I cubic centimeter = 16.9 

I liter = 35.2 

I inch = 2.54 

I foot = 30.48 

I yard = 91.44 

I centimeter = 0.39 

I meter = 39.37 





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Abnormal states of metabolism, 

urine in, 380 
Abscess of kidney, 364 
Accidental albuminuria, 51 
Acetate, sodium, solution, 220 

uranium, standard solution, 219 
Acetic acid, 206 

and salt and heat test for 

albumin, 59 
test for Bence-Jones' body, 86 
Aceto-acetic acid, 170 
Acetone, 165 

clinical significance, 165 
Frommer's test for, 169 
group, 165 

Gunning's iodoform test for, 168 
Jackson-Taylor's modification 

of Legal 's test, 167 
Legal's nitroprussid test for, 167 
Lieben's iodoform test for, 168 
nitroprussid test for, 167 
Reynold's test for, 169 
Taylor's modification of Legal's 

test for, 167 
tests for, 167 

preparation of urine for, 166 
Acetonuria, 165 
Achard and Delamarre phloridzin 

test, 404 
Acid fermentation, 23, 251, 252 
urine, sediments of, 251, 252 
Acidimetry, 34 
Acidity of urine, 33 
apparent, 33 
clinical significance, 37 
decreased, 39 
degree of, 34 
diet and, 38 
fever and, 39 
hot baths and, 38 

Acidity of urine, increased, 38 

perspiration and, 38 

real, 33 

total. See Total acidity. 

uric-acid diathesis and, 39 

variations in, 37 
Acidosis, diabetes mellitus and, 384 
Adenin, 155 

Adolescence, albuminuria of, 53 
Air bubbles in sediment, 249 
Albarran's method for experimen- 
tal polyuria, 408 
Albumin, 50 

acetic acid and salt and heat test, 

beta-naphthol-sulphonic acid 

test for, 68 
boiling and acidifying test for, 70 
Carrez's test for, 68 
centrifugal estimation, 73 
citric acid and mercuric chlorid 

test for, 68 
Esbach's estimation, 71 
estimation, 70 
Goodman and Stern's estimation, 

gravimetric method, 70 
Hastings' test for, 60 
heat and acetic acid and salt test 

and nitric acid test for, 57 
Heller's test, 61 

precautions, 62 
Hofmeister's method for remov- 
ing, 75 
Johnson's test for, 66 
Jolles' test for, 66 
M^hu and Millard's test for, 68 
mercuric chlorid and citric acid 
test for, 68 


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Albumin, mercuric chlorid test for, 
nitric acid and heat test for, 57 
test, 61 

precautions, 62 
nitric-magnesium test for, 64 
phenic-acetic acid test for, 68 
phosphotungstic acid estimation, 

picric acid test for, 66 
potassio-mercuric iodid test for, 

^7 . 

potassium f errocyanid test for, 64 
sulphocyanid test for, 67 

Purdy's test, 60, 73 

table of percentages, 75 

quantitative tests for, 70 

Raabe, Grosstern, and Fudakov- 
sky's test for, 67 

removal from urine, 76 

resorcin test for, 68 

Riegler's test for, 68 

Roberts' test for, 64 

Roch and Mac Williams' test for, 

salicyl-sulphonic test for, 66 

Spiegler test for, 66 

Stiitz and Fiirbringer's test for, 68 

sulpho-salicylic acid test for, 66 

table of, in various conditions, 55 

Tanret's test for, 67 

tests for, 56 

clinical estimation, 70 
comparative delicacy of, 69 
quantitative, 70 

titration method for estimation, 

trichloracetic acid test for, 67 
Tsuchiya's estimation, 72 
Vassiliefif's titration method for, 


Zouchlos' test for, 67 
Albuminometer, Esbach's, 71 
Albuminuria, 50 

accidental, 51 

after muscular exertion, 53 

after proteid food, 53 

after shock, 53 

after vasomotor changes, 53 

alimentary, 53 

blood-pigments and, 195 

casts and, 299 

Albuminuria, cyclic, 53 • 

during labor, 53 
essential, 53 
false, 51 
febrile, 54 
functional, 52 
hematogenous, 54 
intermittent, 53 
minima, 54 
nephritic, 55 
nervous, 54 
of adolescence, 53 
of newborn, 53 
of puberty, 54 
of renal stasis, 54 
orthostatic, 53 
orthotic, 53 
physiologic, 52 
postural, 53 
pseudo, 52 
renal, 52 
spurious, 52 
tests for, 56 
toxic, 54 
traumatic, 54 
true, 52 
Albumoscope, 65 
Albumoses, 80 
classification, 82 
definition, 81 
in body-fluids, 81 
peptones and, dififerentiation, 81 
primary 82, 83, 85. See also 

Bence-Jones' body, 
secondary, 83 

biuret test for, 85 

clinical meaning, 83 

diagnostic value, 84 

from destruction of red cells, 83 

Hammarsten-Bang's test for, 


Hofmeister's test for, 85 
tests for, 85 
Albumosuria, 81, 83 

Bence-J ones', 85 

diseases present in, 83, 84 

in liver diseases, 84 

in nephritis, 84 
Alimentary albuminuria, 53 

glycosuria, 97 

pentosuria, 124 
Alkali, 39, 40 

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Alkali, fixed, 40 

volatile, 40 
Alkaline fermentation, 23, 251, 253 

phosphates, 216 
tests for, 218 
Ultzmann's estimation, 218 

urine, 38 

sediments of, 251, 252 
Alkapton, 128, 206 
Alkaptonuria, 127 

clinical significance, 128 
Allantoin, 161 

AUoxur bases, 155. See also Purin 

bodies, 145 
AUoxuric bases, 146 
Amino-acid nitrogen, 387 
Ammonia, 159 
Ammoniacal urine, 23, 28 

deposits in, 253 
Ammoniomagnesium phosphate, 

216, 254, 263 
Ammonium carbonate, conversion 
of urea into, 253 

urate crystals, 257 
Amorphous urates in sediments, 

Amount of urine, 25 
Amyloid bodies, 312 

ki^iney, 356 

differentiation, 358 
urine in, 357 
waxy casts in, 357 

reaction with waxy casts, 303 
Analysis, 17 

blank for, 419, 420, 421 

clinical, 19 

forms for recording, 419, 420, 421 

index-card, 421 

routine of, 414 

selection of methods, 415 
Animal gum, 126 

inoculation with tubercle bacil- 
lus, 336 
Anuria, 25 
Apparatus for examination, 414, 

Arabinose, 124 

Areosaccharometer, Schutz*s, 118 
Aromatic oxyacids, 204, 206 

substances, 18, 204, 206 

sulphates, 223, 224 

Aromatic sulphates, estimation, 228 
Arteriosclerotic nephritis, chronic, 

Ascarides, 338 

Bacillus coli, 330 

Gram's stain for, 330, 332 
Bacteria, 327, 328, 329 
cloudy urine from, 30 
smears of, 329 
Bacterial casts, 309 

stains, 423 
Bacteriuria, 30 
Balance, Westphal, 43, 44 
Ball-bearing water-motor centri- 
fuge, 237, 238 
Baths, hot, acidity and, 38 
Beckmann-Heidenhain cryoscopy 

apparatus, 397 
Beckmann's cryoscopic thermom- 
eter, 397 
Beer-yeast fungus, 328 
Bence-Jones' body, 82, 83, 85 
acetic acid test for, 86 
Boston's test for, 87 
clinical meaning, 86 
nitric acid test for, 86 
tests for, 86 
Benzidin test for blood-pigments, 

^95. . 
Benzoic acid, 205 
Betanaphthol-sul phonic acid test 

for albumin, 68 
Beta-oxy butyric acid, 172 
clinical significance, 172 
tests for, 172 
Bial's test for pentoses, 125 
Bicarbonates, 229 
Bile-pigments in urine, 28 
Biliary acids, 189, 191 

clinical significance, 191 
Pettenkofer's test for, 192 
tests for, 192 
insufficiency, indicanuria and, 

pigments, 189 
Bilirubin, 189 

clinical significance, 190 
Gmelin's test for, 190 
in sediments, 270 
Mar^chal's test for, 191 

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Bilirubin, Rosenbach's test for, 

tests for, 190 
Bismark brown, 333 
Bismuth tests for glucose, 104 
Biuret test for albumose, 8$ 
Black urine, 27, 28 
Bladder, blood in sediment from, 
epithelium from, 290 
fibroma of, 373 
fibromyxoma of, 373 
inflammation of, 369 
malignant growths of, 373 
papilloma of, 373 
pus from, 283 
stone in, 373 
tuberculosis of, 371 
tumors of, 373 
Blanks for recording analyses, 419, 

Blood concretions, 232 
in sediments, 274 
abnormal cells, 275 
clinical significance, 277 
from bladder, 280 
from kidney, 277 
from pelvic hemorrhage, 280 
from ureteral hemorrhage, 280 
guide to origin, 278 
normal cells, 274 
removal, 277 

Teichmann's test for, 276 
tests for, 276 
Blood-casts, 306 

Blood-cells, abnormal, in sedi- 
ments, 275 
crenated, 275 
mulberry, 275 
normal, in sediments, 274 
red, destruction of, albumosuria 
from, S^ 
Blood-pigments, 193 
albuminuria and, 195 
clinical significance, 193 
tests for, 195 
Blue urine, 28 

Body-fluids, albumoses in, 81 
Boric acid as preservative, 236 
Boston's test for Bence-Jones' 

body, 87 
Bottcher's crystals, 313 

Bottger's test for glucose, 105 

Briicke's modification, 105 
Bowman-Heidenhain theory of 

renal secretion, 392 
Brick-dust sediment, 256 
Bright's disease, acute, 346. See 
also NephrUiSf acute disuse. 
chronic, 353 
false, 262 
Bromids, 231 
Brown granules, 304 

urine, 27 
Briicke's modification of Bottger's 

glucose test, 105 
BrUckner's table of pseudoreactions 

for glucose, 106 
Burgundy-red reaction with indi- " 

can, 180 
Butyric acid, 206 

Cadaverin, 412 
Calcium carbonate calculi, 232 
crystals, preservation, 243 
in sediments, 256 
oxalate, 205 
calculi, 232 
casts, 309 

crystals, 259, 260, 261 
clinical significance, 261 
preservation, 243 
dumb-bell crystals, 260, 261 
phosphate, acid, 215 

crystals, preservation, 243 
in sediments, 264 
sulphate crystals, preservation, 


in sediment, 266 
urate crystals, 257 
Calculi, 232 
analyses, 234 
analytic table, 233 
calcium carbonate, 232 

oxalate, 232 
cystin, 232 
fusible, 234 
hemp-seed, 234 
in kidney, 360 
indigo, 178 
mixed-phosphate, 234 
mulberry, 232 
prostatic, 232 

Digitized by VjOOQIC 



Calculi, uric-acid, 232 

urostealith, 232 

xanthin, 232 
Camerer's estimation of purin 

bodies, 157 
Cammidge's reaction, 128 
Cancer of pancreas, Cammidge's 
reaction in, 128, 130 

of prostate, 376 
Cane-sugar, 126 
Carbohydrates, 96 
Carbol-gentian violet, 333 
Carbon dioxid gas, 229 
Carbonates, 229 
Carcinoma of kidney, 362 
Carmin, 155 

C^arrez's test for albumin, 68 
Casts, 298 

albuminuria and, 299 

bacterial, 309 

blood, 306 

brown granules, 304 

calcium oxalate, 309 

classification, 300 

clinical significance, 299 

crystalline, 309 

cystin, 309 

diagnostic value, 299, 300 

epithelial, 305 

false, 309 

fatty, 307 

fibrinous, 303 

glycerin solution for, 244 

granular, 304 

hyaline, 301. See also Hyaline 

mounting, 244 

mucous, 309 

Miiller's fluid for, 243 

preservation, 243 

pus-, 308 

searching for, 241 

theory of, 298 

urate, 309 

vesicular, 315, 318, 319 

waxy, 303, 357 
Catarrhal nephritis, chronic, 353 
Cellulose in sediments, 248, 250 
Centrifugal estimation of albumin, 

of chlorids, Purdy's, 212 
of phosphates, Purdy's, 221 

Centrifugal estimation of sulphates, 
Purdy's, 226 
method for sediments, 237 
staining for sediments, 245 
Centrifuge, hand, 236, 238 
Purdy electric, 237, 238 
tubes, Purdy's, 238 
water-motor, 237, 238 
Cervix uteri, epithelium from, 297 
Chemic examination, 50, 417 
Childbirth, albuminuria in, 53 
Chloral as preservative, 237 
Chlorids, 208 

after operation, 209 
centrifuge method for, Purdy's, 
table, Purdy's, 213 
clinical significance, 209 
diminished, 208, 209 
prognostic value, 209 
table, 210 
increased, 209 

table, 210 
normal, 208 

Purdy's centrifuge method, 212 
quantitative test, 211 
Salkowski's modification of Vol- 

hard's test, 211 
silver nitrate test for, 210 
tests for, 210 

diagnostic value, 209 
Volhard's test for, Salkowski's 
modification, 211 
Chloroform as preservative, 237 
Cholesterin, 203 
crystals, 204, 272 
preservation, 243 
Chondroitin-sulphuric acid, 205 
Chyluria, 33, 271 
fat in urine in, 203 
parasite of, 337 
Cirrhosis, renal, 353 
Citric acid and mercuric chlorid 
test for albumin, 68 
test for euglobulin, 91 
for Moerner's body, 91 
Clinical phosphaturia, 217 
Cloudy urine, 29 

table of causes, 32 
Cochineal tincture for estimating 

phosphoric acid, 221 
Coffin-lid crystals, 254, 263 

Digitized by VjOOQIC 



Collodion film fixing method for 

sediments, 244 
Colon bacillus, 330 
Color of urine, 27 
Coloring-matters, 186 

normal, 186 
Columnar epithelium, 287 
Comma shreds, 324 

chemical significance, 325 
false, 321, 324 
Comparative density method for 

glucose, 117 
Comp)osition of healthy urine, 17 
Concretions, 232 

Conductivity of urine, electric, 400 
Congestion of kidney, active, urine 
in, 343 
acute, urine in, 343 
chronic, urine in, 345 
passive, urine in, 345 
Conjugate sulphates, 223, 224 

estimation, 228 
Connective-tissue shreds, 284 
Consistence of urine, 29 
Constipation, indicanuria and, 177 
Constituents of urine, 17 
Copper tests for glucose, 97 
precautions, 99 
for uric acid, 151 
Cork in sediments, 249, 250 
Corpora amylacea, 312 
Cotton fibers in sediments, 245, 246 
Creatin, 160 
Creatinin, 160 

leukomains, 413 
Creatinin-zinc chlorid crystals, 161 
Crenated blood-cells, 275 
Cresol, 223, 224 
Cryoscope, 397 
Cryoscopy, 395 

clinical applications, 398 
error in calculation, 396, 397 
technic, 397 
thermometer for, 397 
Crystalline casts, 309 

sediments, dry method of pre- 
serving, 242 
mounting, 243 
preservation, 242 
Cuboid epithelium, 287 
Cyclic albuminuria, 53 
Cylindric epithelium, 287 

Cylindric graduate, 22 
Cylindroids, 309 
Cystin, 223, 226 

calculi, 232 

cast, 309 

crystals, 268, 269 

clinical significance, 270 

preservation, 243 
Cystinuria, 226, 268-270 

diamin elimination in, 270 
Cystitis, 369 

acute, 369 

chronic, 369 

pyelitis and, differentiation, 370 

tuberculous, 371 
Cysts of kidney, 364 

Dark brown urine, 27 

urine, 27 
Decomposition of urine, 22 
Degree of acidity of urine, 34 
Del Spine's method for preserving 

crystalline sediments, 242 
Density estimation of glucose, 117 
Desamidation, 387 
Deutero-albumoses, 83. See also 

AlbumoseSj secondary. 
Dextrin, 126 
Diabetes insipidus, 385 
mellitus, 380 

acetonuria in, 383 

acidosis in, 384 

albuminuria in, 383 

amount of urine, 380 

color of urine, 381 

creatinin in, 383 

diacetic acid in urine, 384 

diagnostic value of glycosuria, 

glycosuria m, 381 

oxybutyric acid in urine, 384 

specific gravity of urine, 381 

testing for sugar in, 381 

uric acid in, 383 
phosphatic, 217 
Diabetic pentosuria, 124 
Diacetic acid, 170 

clinical significance, 170 

tests for, 171 

von Jaksch's test for, 171 
Diaceturia, 170 

Digitized by VjOOQIC 



Diagnosis, urinary, 342 

Diamin elimination in cystinuria, 

Diazo-reaction, Ehriich's, 182 

clinical significance, 184 
Diet, acidity and, 38 
Dififuse nephritis, acute, 346. See 
also NephritiSy acute disuse. 
chronic, 349 

interstitial type, 353 
parenchymatous type, 351 
Diluting urine for Fehling's quan- 
titative test, 112 
specific gravity and, 44 
Diminished amount of urine, 25, 26 
Diplococci, 334 
Dissociation, 397 
Distilling urine, 166 
Distoma haematobium, 337 
Donne's test for pus in urine, 31 
Doremus' method for estimating 
urea, 137 
ureometer, 137 

Hinds' modification, 139 
Drugs, odor of urine and, 28 
Dry method of preserving crystal- 
line sediments, 242 
Dumb-bell crystals, 260, 261 

Earthy phosphates, 215 

phosphoric acid with, estima- 
tion, 221 
in sediments, 262 
tests for, 218 . 

Ultzmann's estimation, 218 
Echinococcus, 338 
Echtgelb, 74 
Eclampsia, 386, 387 
Ehriich's diazo-reaction, 182 
clinical significance, 184 
Einhorn's saccharometer, 114, 115 

test for glucose, 114 
Ejaculatory ducts, epithelium from, 

Electric conductivity of urine, 400 
Embolism of kidney, 365 
Emerson's method for melting 

point of crystals, 109 
Endogenous purin bodies, 156 
pus-corpuscles, 291 
uric acid, 147 


English and metric systems, rela- 
tions, 425 
Eosin, 334 
Epiguanin, 155 
Episarkin, 155 
Epithelial casts, 305 

shreds, 322, 324, 325, 326 
clinical significance, 325 
Epithelium, 285 

adherent, hyaline with, 305 

columnar, 287 

cuboid, 287 

cylindric, 287 

differential table, 288 

differentiation of origin, 285 

extraneous, 298 

flat-cells, 287 

from bladder, 290 

from cervix uteri, 297 

from ejaculatory ducts, 296 

from kidney, 292 

from mucosa of uterus, 297 

from pelvis of kidney, 291 

from prostate, 296 

from seminal vesicles, 296 

from ureters, 291 

from urethra, 294 

from uterus, 297 

from vagina, 297 

origin, 285 

preservation, 243, 244 

renal, 292 

squamous-cell, 287 
Esbach's albuminometer, 71 

estimation of albumin, 71 

reagent for albumin, 71 
Essential albuminuria, 53 
Ethereal sulphates, 174, 181, 223, 
as index to intestinal putre- 
faction, 225 
clinical significance, 182 
diminished, 225 
estimation, 228 
increased, 225 
ratio to total sulphates, 225 
tests for, 182 
Ethyldiacetic acid, 170 
Euglobulin, 77, 89 

citric acid test for, 91 

clinical meaning, 91 

Heller's test for, 63, 91 

Digitized by VjOOQIC 



Euglobulin, tests for, 91 
" Evian" water, 408 
Examination, chemic, 417 

microscopic, 235, 418 

physical, 416 

routine of, 414, 416 

selection of method, 415 
Exogenous purin bodies, 156 

uric acid, 147 
Extra-intestinal indicanuria, 175 
Exudative process, test for chlorids 

in diagnosis, 209 

False albuminuria, 51 

Bright's disease, 262 

casts, 309 
Fat, 203 

in chyluria, 203 

in lipuria, 203 
Fat-globules in sediment, 271 
Fatty acids, 204, 206 

casts, 307 

degeneration of kidney, 351 

substances in urine, 18 
Feathers in sediments, 247 
Feathery crystals, 263 
Febrile albuminuria, 54 
Fecal matter in sediment, 249 
Fehling's qualitative test for glu- 
cose, 100 

quantitative test for glucose, 112 

solution, 100, loi 
Female urethra, epithelium from, 

Fermentation, acid, 23, 251, 252 

alkaline, 23, 251, 253 

test for glucose, 114 
Ferments, 204, 206 
Ferrocyanid, potassium, saturated 

solution, 220 
Fever, acidity and, 39 
Fibrin, 79 

clinical significance, 79 

concretions, 232 

Millon's reaction, 80 

tests for, 79 
Fibrinogen, 79 
Fibrinoglobulin, 77, 91 
Fibrinous casts, 303 
Fibroma of bladder, 373 
Fibromyxoma of bladder, 373 
Filaria sanguinis, 203, 337 

Filaria sanguinis, chyluria from, 33 

Filariasis, 203, 337 

Filter theory of renal secretion, 391 

Fixed alkali in urine, 40 

Flat-cell epithelium, 287 

Flaws in glass slide, 249 

Florence's reagent for spermatozoa, 

Fluorin, 230 
Folin-Hopkin's estimation of uric 

acid, 154 
Folin's method for total acidity, 37 
Food, proteid, albuminuria after, 

Formalin as preservative, 236 
Formic acid, 206 
Freezing-point of urine, 395 

law of, 396 

specific gravity and, 400 
Frequent urination, 26 
French's test for leucin, 201 

for tyrosin, 201 
Freund and Topfer's method for 

total acidity, 36 
Frohn*s reagent, 105 
Frommer's test for acetone, 169 
Fruit-sugar, 123 
Fuchsin, 334 
Functional albuminuria, 52 

renal diagnosis, 389 
Furfurol test for tyrosin, 202 
Fusible calculi, 234 

Galacosazon crystals, 109 

Cxases in urine, 18, 229 

Genital organs, diseases of, urine 

in, 369 
Globulin, 50, 77 

diseases occurring in, 77 

qualitative tests for, 78 

quantitative tests for, 78 

Roberts' test for, 78 

tests for, 78 
Glomerular nephritis, chronic, 349, 

subacute, 351 
Glucosazon crystals, 108 

melting point, 109, no 
Glucose, 96 

areosaccharometer for, 118 
bismuth tests for, 104 
Bottger's test for, 105 

Digitized by VjOOQIC 



Glucose, Briicke's modification of 
Bottger's test for, 105 
Brllckner's table of pseudoreac- 

tions, 106 
clinical significance, 96 
comparative density estimation, 

copper tests for, 97 
precautions, 99 
density estimation, 117 
Einhorn's test for, 114 
Fehling's qualitative test for, 100 

quantitative test for, 112 
fermentation test for, 114 
Haines' test for, 103 
Lohnstein's estimation, 115 
Nylander's test for, 104 
Pavy's test for, 103 
phenylhydrazin test for, 106 
polarization estimation, 119 
pseudoreactions for, 106 
Purdy's estimation, 114 
Roberts' comparative density 

estimation of, 117 
Rubner's test for, 108 
saccharometer for, 1 1 4- 1 1 7 
Schiitz's estimation, 118 
Stern's urinoglucosometer for, 

117, 118 
substances allied to, 125 
tests for, 97 
qualitative, 97 
quantitative, no 
Trommer's test for, 98 
urinoglucosometer for estimating, 
117, ij8 
Glycerin solution for casts, 244 
Glycerophosphoric acid, 205 
Glycogenic reaction with pus, 281 
Glycosuria, 96 
alimentary, 97 
medicinal, 97 
secondary, 97 
Glycuronic acid, 126 
Gmelin's test for bilirubin, 190 
Gonococci, 331 

Gram's stain for, 318, 319, 320 
staining, 33i . . 
Gonorrheal urethritis, 377 
Goodman and Stern's estimation of 

albumin, 73 
Gout, uric acid and, 149 

Graduate, cylindric, 22 

stoppered, 22 
Gram-negative germs, 332 
Gram-positive germs, 332 
Gram's solution, 332, 333 

stain for bacillus coli, 330, 332 
for gonococci, 318, 319, 320, 

for proteus vulgaris, 332 
for staphylococcus aureus, 332 
for streptococci, 318, 319 
for streptococcus pyogenes, 332 
technic, 333 

Granular casts, 304 

Graphic expression of urinary 
analysis, 20 

Gravel, 232, 255, 361 

Gravimetric method for albumin, 70 
for sulphates, 227 

Gravity method of obtaining sedi- 
ments, 235 

Greenish urine, 28 

Greenish-blue urine, 28 

Guaiacum test for blood-pigments, 


Guanin, 155 

Guinea-pig, inoculation of, with 
tubercle bacillus, 336 

Gum, 126 

Gunning's iodoform test for ace- 
tone, 168 

Haeser's coefficient, 47 
Haines' solution, 103 

test for glucose, 103 
Hairs in sediments, 246 
Halogens, 231 
Hammarsten-Bang test for albu- 

mose, 85 
Hand centrifuge, 236, 238 
Harley's test for urobilin, 188 
Hastings' test for albumin, 60 
Healthy urine, composition, 17 
Heat and acetic acid and salt test 
for albumin, 59 

and nitric acid test for albumin, 

Hedge-hog crystals, 258 
Heidenhain-Bowman theory of 

renal secretion, 392 
Heintz's estimation of uric acid, 152 

Digitized by VjOOQIC 



Heitzmann's method for renal cells 

in urine, 292 
Heller's analytic table for calculi, 

test for albumin, 61 
precautions, 62 
for blood-pigments, 197 
for euglobulin, 63, 91 
for indican, 178 
for Moerner's body, 63, 91 
for nucleo-albumin, 63, 91 
uroglaucin, 177 

urophaein test for urobilin, 187 
urrhodin, 177 
Hematin, 193 

benzidin test for, 195 
clinical significance, 194 
crystals, preservation, 243 
guaiacum test for, 195 
Heller's test for, 197 
spectroscopic test for, 196, 197 
Teichmann's hemin crystal test 

for, 197 
tests for, 195 
Hematogenous albuminuria, 54 
Hematoidin crystals, preservation, 
in sediments, 270 
Hematoporphyrin, 186, 197 
Hematuria 194, 274 

guide to origin of blood, 278 
Hemin crystals, Teichmann's, 276 

test for blood-pigments, 197 
Hemoglobin, 193 
benzidin test for, 195 
clinical significance, 193 
guaiacum test for, 195 
Heller's test for, 197 
spectroscopic test for, 196, 197 
Teichmann's hemin crystal test 

for, 197 
tests for, 195 
Hemoglobinuria, 193 
Hemorrhage from bladder, blood 
in sediment from, 280 
from kidney, blood in sediment 

from, 277 
from pelvis, blood in sediment 

from, 280 
from ureter, blood in sediment 
from, 280 
Hemp-seed calculi, 234 

Hepatic insufl&ciency, indicanuria 

and, 177 
Hetero-albumoses, 82, 83, 85 
Heteroxanthin, 155 
Highly colored urine, 27 
Hinds' modification of Doremus' 

ureometer, 139 
Hippuric acid, 162 
crystals, 162 
tests for, 163 
Hoffmann's test for tyrosin, 202 
Hofmeister's method for removing 
albumin, 76 

test for albumose, 85 
Homogentisic acid, 206 
Horismascope, 65 
Hot baths, acidity and, 38 
Hiifner's estimation of urea, 139- 
apparatus for, 140 
Hyaline casts, 301 
pure, 301 

with adherent epithelium, 305 
Hydrobilirubin, 186 
Hydrochloric acid secretion, indi- 
canuria and, 176 
Hydrofluoric acid, 230 
Hydrogen peroxid, 230 

sulphid, 230 

sulphocyanid, 205 
Hydronephrosis, 366 

intermittent, 367 
Hydroparacumaric acid, 206 
Hydroquinon, 206, 223, 224 
Hydruria, 385 
Hypernephroma, 362 
Hypobromite estimation of urea, 
Rice's solutions for, 139 

Knop's solution of, 138 

method for estimating urea, 136 
Hypoxanthin, 155 
Hysteria, phosphaturia in, 217 

Idiopathic diabetes insipidus, 385 
pentosuria, 124 

Increased amount of urine, 26 

Indican, 174, 225 
approximate estimation, 179 
Burgundy-red reaction with, 180 
clinical significance, 174 
estimation, 179 

Digitized by VjOOQIC 



Indican, Heller's test for, 178 

Jaffa's test for, "178 

Obermeyer's test for, 179 

origin, 175 

Robin's estimation, 179 

Rosenbach's test for, 180 

tests for, 177 
precautions, 180 
Indicanuria, 174, 175 

biliary insufficiency and, 177 

constipation and, 177 

extra-intestinal, 175 

hepatic insufficiency and, 177 

hydrochloric acid secretion and, 

intestinal, 175 

putrefaction ^nd, 175, 176 
Indicator in titration of urine for 

acidity, 34 
Indigo calculi, 178 

crystals, 271 

preservation, 243 
Indigo-blue, 174, 177 
Indigo-carmin test, 403 
Indigo-red, 174, 177 
Indol, 174, 223, 224 
Indoxyl-potassium-sulphate, 1 74, 

225. See also Indican. 
Injections of normal urine, toxic 

symptoms, 410 
Inoculation, animal, with tubercle 

bacillus, 336 
Inorganic constituents, 208 
accidental, 231 

salts of urine, 18 
Inosite, 125 
Insect wings, scales of, in sediment, 

247, 248 
Insipid diabetes, 385 
Intermittent albuminuria, 53 

hydronephrosis, 367 
Interstitial nephritis, 349 

chronic, 353 
Intestinal indicanuria, 175 

putrefaction, ethereal sulphates 
as index, 225 
indicanuria and, 175, 176 
Intravenous injections of normal 

urine, toxic symptoms, 410 
Introduction, 17 
lodids, 231 
lodin, 231 

lodin solution. Gram's, 333 
Iodoform crystals, 169 
test for acetone. Gunning's, 168 
Lieben's, 168 
Iron, 229 

Jackson-Taylor's modification of 

Legal 's acetone test, 167 
Jaffa's test for indican, 178 
Johnson's test for albumin, 66 
Jolles' test for albumin, 66 

Kidney, abscess of, 364 
amyloid, 356. See also Amyloid 

blood from, in sediments, 277 

causes, 279 
calculi in, 360 
carcinoma of, 362 
congestion of, active, urine in, 


acute, urine in, 343 

chronic, urine in, 345 

passive, urine in, 345 
cysts of, 364 
degeneration of, chronic, 351 

cystic, 364 

fatty, 351 

waxy, 356 
diseases of, functional, diagnosis, 


urine in, 342 
efficiency of, determination, 395 
embolism of, 365 
epithelium from, 292 
functions of, efficiency of, tests 
for, 40 T 

objects of determining, 389 
in origin of uric acid, 147 
inflammation of, 365, 366 
lardaceous, 356 
pelvis of, diseases of, urine in, 342 

epithelium from, 291 

inflammation of, 365, 366 
pus from, 283 
sarcoma of, 362 
sclerotic, 353 
secretion of, 389 

theories, 391 
stone in, 360 

Digitized by VjOOQIC 



Kidney, stone in, differentiation, 

urine in, 360 
sufl&ciency of, 389 

surgical diseases and, 390 

tests for, 401 
tuberculosis of, 358 

urine in, 359 
tumors of, 362 

differentiation, 363 

urine in, 362 
Kjeldahl's estimation of urea, 144 
Knop's solution of hypobromite, 


test for urea, 136 
Kollmann five-glass test for comma 

shreds, 324 
Kor^nyi's theory of renal secretion, 

Kiihne's definition of peptone, 81 
Kutner's methylene-blue test, 401 
clinical value, 401 
sources of error, 402 

Labor, albuminuria during, 53 
Lactic acid, 205 
Lactose, 122 
Lactosuria, 122 
Laiose, 123 

Lardaceous kidney, 356 
Lateritious sediment, 256 
Legal's nitro-prussid test for ace- 
tone, 167 
Leo's sugar, 123 
Leucin, 201 

crystals, 203, 267 

French's test for, 201 

in sediment, 267 

platinum-foil test for, 202 

tests for, 201, 202 
Leukocytes in sediments, 281 
Leukomains, 412 
Levosazon crystals, 109 

melting point, 109, no 
Levulose, 123 
Lieben's iodoform test for acetone, 

Linen fibers in sediments, 245, 246 
Lipaciduria, 206 
Lipuria, 271 

fat in urine in, 203 

Liquid reagents, 421 

Liver diseases, albumosuria in, 84 

in origin of uric acid, 147 
Litmus with oxalic acid for total 

acidity, 35 
Lohnstein's estimation of glucose, 


saccharometer, 115, 116 
Lower urinary tract, diseases of, 

urine in, 369 
Ludwig's magnesia mixture, 158 

theory of renal secretion, 391 
Lycopodium in sediments, 248, 249 

Magnesia mixture, Ludwig's, 158 
phosphate crystals, neutral, 263 

Male urethra, epithelium from, 294 

Maltose, 126 

Mar^chal's test for bilirubin, 191 

Massage-urine, 314 

Matsumoto's work with nucleo- 
albumin, 91 

Medicinal glycosuria, 97 

M6hu and Millard's test for albu- 
min, 68 

Melanin, 199 
crystals, 271 
tests for, 199 
von Jaksch's test for, 199 
Zeller's test for, 199 

Mercuric chlorid and citric acid 
test for albumin, 68 
test for albumin, 66 

Metabolism, abnormal states of, 
urine in, 380 

Metals, 231 

Methemoglobin, 193 

Methylene-blue test, 401 
clinical value, 401 
sources of error, 402 

Methylxanthin, I-, 155 

Metric and English systems, rela- 
tions, 425 

Microchemic reactions, 242 

Micrococcus ureae, 328 

Micro-organisms, 327 

Microscope, kind needed, 242 

Microscopic examination, 235, 418 

Milk-sugar, 122 

Millon's reaction with fibrin, 80 

Mineral sulphates, 223 

Digitized by VjOOQIC 



Mineral sulphates, estimation, 228 
Mixed-phosphate calculi, 234 
Moerner's body, 89 

citric acid test for, 91 
clinical meaning, 91 
Heller's test for, 63, 91 
tests for, 91 

mucoid, 87 
tests for, 89 

work with nucleo-albumin, 90 
Moerner-Sjoqvist estimation of 

urea, 144 
Monosodic acid phosphate, 216 
Moulds, 327, 328 
Mucin, 87 

clinical meaning, 88 

soluble, 90 

tests for, 89 

threads, 310 
Mucin-like body, 90 
Mucoid, 87 

clinical meaning, 88 

tests for, 89 
Mucopus shreds, 321, 322 

clinical significance, 325 
Mucous casts, 309 

cloud, 29, 251 

shreds, 322, 323 

clinical significance, 325 

threads, 310 
Mulberry blood-cells, 275 

calculi, 232 
Muller's fluid for casts, 243 
Murexid test for uric acid, 151 
Muscle-sugar, 125 
Muscular exertion, albuminuria 

after, 53 
I-Methylxanthin, 155 

Nephritic albuminuria, 55 
Nephritis, acute diffuse, 346 
albumin in, 55, 56 
amount of urine in, 26 
differentiation, 348 
fatty stage, 348, 349 
urine in, 346 
albumosuria in, 84 
catarrhal, chronic, 353 
chronic, 353 

arteriosclerotic, 349 
diffuse, 349 

Nephritis, chronic diffuse, chronic 
parenchymatous nephritis 
and, differentiation, 353 
interstitial type, 353 
parenchymatous type, 351 
urine in, 350 
glomerular, 349, 351 
interstitial, 353 
urine in, 355 
parenchymatous, 349, 351 
differentiation, 353 
urine in, 352 
with exudation, 349 
without exudation, 353 
interstitial, 349 
subacute glomerular, 351 
Nervous albuminuria, 54 
Neurasthenia, phosphaturia in, 217 
Neutral magnesium phosphate crys- 
tals, 263 
sulphates, 223, 226 
estimation, 228 
Newborn, albuminuria of, 53 
Nitrate of silver test for chlorids, 
of urea crystals, 136 
uranium standard solution, 219 
Nitric acid, 230 

and heat test for albumin, 57 
test for albumin, 61 
precautions, 62 
for Bence-J ones' body, 86 
Nitric-magnesium test for albumin, 

Nitrobenzol, 163 
Nitrogen, amido-acid, 387 
balance, 132 
excretion, 131 
group, 131 
in urine, 229 
partition, 386 

clinical value, 387 
total, 131 

diminished, 132 
in disease, 132 
in pregnancy, 386 
in toxemias of pregnancy, 133 
increased, 132 
normal, 132 
undetermined, 131, 133 
in pregnancy, 386, 387 
Nitrogenous equilibrium, 132 

Digitized by VjOOQIC 



Nitropnissid test for acetone, 

Legal's, 167 
Nitrous acid, 230 
Non-nitrogenous organic acids, 204, 

Normal phosphates, 215 
Nubecula of urine, 29 
Nucleic acid, 161, 205 
Nuclein bases, real, 155 
Nucleo-albumin, 89, 93 

clinical significance, 91 

Heller's test for, 63, 91 

in urine, 59 

Matsumoto's work, 91 

Moerner's work, 90 

Oswald's work, 91 

substances formerly taken for, 


Nucleoproteid, 92 

clinical significance, 93 

definition, 92 

tests for, 93 
Nylander's test for glucose, 104 

Obermeyer's test for indican, 179 
Odor of urine, 28 

putrid, 28 
Oil globules, 203, 249 
Oliguria, 25, 26 
Orcin test for pentoses, 125 
Organic acids, non-nitrogenous, 

204, 205 
constituents, 18, 50 

accidental, 206 
sulphur, suboxidized, 226 
Organized sediments, 235, 274 

table of, 251 
Orthostatic albuminuria, 53 
Orthotic albuminuria, 53 
Oswald's work with nucleo-albu- 
min, 91 
Oxalic acid, 205 

diathesis, 262 

method with litmus for total 
acidity, 35 
Oxaluria, 205, 259, 262 
Oxyacids, aromatic, 204, 206 
Oxyamygdalic acid, 206 
Oxygen in urine, 229 
Oxyhemoglobin, 193 
Oxyproteic acid, 205 

Pale-colored urine, 27 
Pancreatic reaction, Cammidge's, 

Pancreatitis, Cammidge's reaction 

in, 128 
Papilloma of bladder, 373 
Parakresol, 206 
Para-oxyphenylacetic acid, 206 
Para-oxyphenylglycolic acid, 206 
Parasites, 337 
Paraxanthin, 155 
Parenchymatous nephritis, chronic, 

349» 351 
Parkes' rule for total solids deter- 
mination, 47 
table of urinary constituents, 18, 

Pathologic urines, specific gravity 

of, 45 
Pavy's solution, 103 

test for glucose, 103 
Pelvis, hemorrhage from, blood in 
sediment from, 280 
of kidney, diseases of, urine in, 
epithelium from, 291 
inflammation of, 365, 366 
Pentosazon crystals, 109 

melting point, 109, no 
Pentoses, 124 

Bial's test for, 125 
clinical significance, 124 
orcin test for, 125 
tests for, 125 
Pentosuria, 124 
alimentary, 124 
diabetic, 124 
idiopathic, 124 
Pepsin, 206 

Peptones, albumoses and, differen- 
tiation, 81 
Kiihne's definition, 81 
Peptonuria, 81 
Pernicious vomiting of pregnancy, 

386, 387 
Perspiration, efifect on acidity, 


Pettenkofer's test for biliary acids, 

Phenic-acetic acid test for albumin, 

Phenol potassium sulphate, 181 

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Phenolphthalein method for total 

acidity, 36 
Phenols, 223 

Phenylhydrazin test for glucose, 108 
Phenyl-lactosazone, 123 
Phloridzin solutions, 405 
technic of injections, 405 

value, 407 
test, 404 

appearance of sugar, 405 

failure of, 405, 407 

interpretation of result, 406 

observing result, 405 

preparation of patient, 404 
Phosphates, 215 
acid, 215 
alkaline, 216 

tests for, 218 

Ultzmann's estimation, 218 
ammoniomagnesium, 216, 254, 

calcium, acid, 215 
calculi, mixed, 234 
centrifugal estimation, Purdy's, 

clinical significance, 216 
cloudy urine from, 30 
crystals of, 262 
diminished, 217 
earthy, 215 

in sediment, 262 

phosphoric acid with, estima- 
tion, 221 

tests for, 218 

Ultzmann's estimation, 218 
in sediment, clinical significance, 

increased, 216, 217 
monosodic acid, 216 
normal, 215 
preservation, 243 
Purdy's centrifugal estimation, 

table for estimation, 222 
triple, 216, 254 

crystals of, 263 

preservation, 243 
Zueltzer's coefficient, 216 
Phosphatic diabetes, 217 
Phosphaturia, 215, 216, 265 
clinical, 217 
in hysteria, 217 

Phosphaturia in neurasthenia, 217 

true, 216 
Phosphoric acid, 205, 215 
estimation, 219 
excess of, 265 

with earthy phosphates, esti- 
mation, 221 
Phosphotungstic acid test for albu- 
min, 72 
Physical examination, 416 

properties of urine, 25 
Physiologic albuminuria, 52 
Picric acid test for albumin, 66 
Pigments, 186 
biliary, 28, 189 
blood, 193 

albuminuria and, 195 
clinical significance, 193 
tests for, 195 
normal, 186 
Pipet, cleansing, 240 
Piria's test for tyrosin, 202 
Platinum-foil test for leucin, 202 
Pocket-spectroscope for detecting 

urobilin, 187 
Polariscope, 119 

Ultzmann's, 119, 120 
Polarization estimation of glucose, 

Pollakmria, 26 
Polydipsia, 385 
Polyuria, 26 
experimental, 408 
persistent, 385 
Postural albuminuria, 53 
Potassio-mercuric iodid test for 

albumin, 67 
Potassium ferrocyanid, saturated 
solution, 220 
test for albumin, 64 
sulphate, phenol, 181 

skatoxyl, 181 
sulphocyanid test for albumin, 67 
urate crystals, 257 
Pre-eclamptic state, 386, 387 
Preformed sulphates, 223 

estimation, 228 
Pregnancy, eclampsia in, 386, 387 
nitrogen output in, 386 
pre-eclamptic state in, 386, 387 
toxemias of, 386 
total nitrogen in, 133 

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Pregnancy, urea in, 386 

vomiting in, persistent, 386, 387 
Preservation of urine, 23, 24 
Preservatives, boric acid as, 236 
chloral as, 237 
chloroform as, 237 
formalin as, 236 
salicylic acid as, 237 
thymol as, 236 
Primary albumoses, 82, 83, 85 
calcium oxalate crystals, 261 
concretions, 232 
Propionic acid, 206 
Prostate, cancer of, 376 
epithelium from, 296 
inflammation of, 373 
pus from, 283 
tuberculosis of, 375 
Prostatic calculi, 232 

plugs, 311 
Prostatitis, 373 
acute, 373 
chronic, 374 
tuberculous, 375 
Protalbumoses, 83 
Proteid, 50 

food, aJbuminuria after, 53 
Proteus vulgaris. Gram's stain for, 

Pseudo-albuminuria, 52 
Pseudoglobulin, 77 
Ptomains, 412 
Puberty, albuminuria of, 54 
Purdy's centrifugal estimation of 
albumin, 60, 73 
table of percentages, 75 
of chlorids, 212 

table of percentages, 213 
of glucose, 114 
of phosphates, 221 

table of percentages, 222 
of sulphates, 226 

table of percentages, 227 
centrifuge, electric, 237, 238 
tubes, 238 
Pure hyaline casts, 301 
Purin bases, 146, 155 

Camerer's estimation of, 157 
clinical significance, 156 
estimation, 157 
normal, 156 
origin, 155 

Purin bodies, 145 

Camerer's estimation of, 157 
endogenous, 156 
estimation of, 157 
exogenous, 156 
'molecule, 145 
ring, 145 
Purinometer, 157 
Pus, 31, 281 

clinical significance, 282 
cloudy urine from, 31 
Donne's test for, 31 
endogenous, 291 
from bladder, 283 
from kidney, 283 
from prostate, 283 
from seminal vesicles, 283 
from urethra, 283 
from uterus, 283 
from vagina, 283 
glycogenic reaction, 281 
origin, 281 
preservation, 244 
shreds, 320, 321 

clinical significance, 325 
Pus-casts, 308 

Putrefaction, intestinal, ethereal 
sulphates as index, 225 
indicanuria and, 175, 176 
Putrescin, 412 
Putrid odor of urine, 28 
Pyelitis, acute, 365 
suppurative, 365 
chronic, 366 

cystitis and, diflFerentiation, 370 
Pyelonephritis, acute, 365 

chronic, 366 
Pyknometer for specific gravity, 43, 

Pyonephrosis, 367 
Pyrocatechin, 206, 223, 224 
Pyuria, 31 

Raabe, Grosstern, and Fuda- 

kovsky's test for albumin, 67 
Rape, spermatozoa in urine in, 314 
Reaction of urine, 33 

clinical significance, 37 
testing for, 33 
Reagents, 414, 421 
bottles, 421 

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Reagents, liquid, 422 

solid, 423 
Real nuclein bases, 155 
Red blood-cells, destruction of, 

albumosuria from, 83 
Reddish urine, 27 
Renal albuminuria, 52 

calculi, blood in urine from, 279 

cirrhosis, 353 

stasis, albuminuria of, 54 
Resorcin test for albumin, 68 
Reynold's test for acetone, 169 
Rhamnose, 124 
Rice's solutions for hypobromite 

estimation of urea, 139 
Riegler's test for albumin, 68 
Ringing slides, 243 
Roberts' comparative density 
method for glucose, 117 

test for albumin, 64 
for globulin, 78 
Robin's estimation of indican, 179 
Roch and MacWilliams' test for 

albumin, 66 
Rosenbach's Burgundy-red reaction 
with indican, 180 

test for bilirubin, 191 
Rubner's test for glucose, 108 
Ruhemann's estimation of uric acid, 

uricometer, 152 
Rust particles in sediment, 249 

Saccharometer, Einhom's, 114, 

Lohnstein's, 115, 116 
Saccharose, 126 
Sago bodies, 314, 315, 316 

clinical significance, 319 
Salicylic acid as preservative, 237 
Salicylsulphonic acid test for albu- 
min, 66 
Salkowski's method for sulphates, 
modification of Vol hard's chlorid 
test, 211 
Salt and acetic acid and heat test 

for albumin, 59 
Sand, 232, 255, 361 
Sarcina urinae, 329 
Sarcolactic acid, 205 

Sarcoma of kidney, 362 

Saxe's method for urethral shreds, 

specific gravity method for small 

amounts, 44 
staining method for sediments, 

urinopyknometer, 44, 45 
Scales of insect wings in sediments, 

247, 248 
Schutz's areosaccharometer, 118 

estimation of glucose, 118 
Sclerotic kidney, 353 
Scratches in slides, 240, 249 
Secondary albumoses, 83. See also 

AlbumoseSf secondary. 
calcium oxalate crystals, 261 
concretions, 232 
glycosuria, 97 
Secretion of urine, 389 

theories, 391 
theory of renal function, 392 
Sediments, air bubbles in, 249 
ammoniomagnesium phosphate 

in, 263 
ammonium urate, 257 
amorphous urates in, 258 
amyloid bodies, 312 
ascarides in, 338 
bacillus coli in, 330 
bacteria in, 327, 328, 329 
bilirubin in, 270 
blank for, 420 
blood in, 274. — See also Blood 

in sediments. 
Bottcher's crystals, 313 
brick-dust, 256 
calcium carbonate in, 266 

oxalate in, 259, 260, 261 

phosphate in, 264 

sulphate in, 266 

urate in, 257 
casts in, 298 
cellulose in, 248, 250 
centrifugal method for, 237 
cholesterin in, 272 
classification, 250 
cofl&n-lid crystals in, 263 
collodion film fixing method for, 

colon bacillus in, 330 
comma shreds in, 324 

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Sediments, connective-tissue shreds 

in, 284 
cork in, 249, 250 
corpora amylacea, 312 
crystalline, dry method of pre- 
serving, 242 

mounting, 243 

preservation, 242 
cystin in, 268, 269 
diplococci in, 334 
distoma haematobium in, 337 
echinococcus in, 338 
epithelial shreds in, 322, 324, 325, 

epithelium in, 285 
examination, 239 
extraneous materials in, 245 
fat-globules in, 271 
feathers in, 247, 248 
fecal matter in, 249 
filaria sanguinis hominis, 337 
glass, 236 
gonococci in, 331 
gravel in, 361 

gravity method of obtaining, 235 
gross features, 29 
hairs in, 246 
hematoidin in, 270 
high power examination, 241 
in alkaline urine, 251, 252 
indigo in, 271 

insect wings, scales of, 247, 248 
lateritious, 256 
leucin in, 267 
leukocytes in, 281 
low power examination, 241 
lycopodium in, 248, 249 
magnesium phosphate in, 263 
making slides of, 240 
melanin in, 271 
micro-organisms in, 327 
moulds in, 327, 328 
mounting, 242 
mucopus shreds in, 321, 322 
mucous shreds in, 322, 323 

threads in, 310 
normal, 251 
obtaining, 235 
of acid urine, 251, 252 
oil globules in, 249 
organized, 235, 274 

table, 251 

Sediments, parasites in, 337 
pathologic, 254 
phosphates in, 262 
potassium urate, 257 
preservation, 242 
prostatic plugs, 311 
pus in, 281. See also Pus. 

shreds in, 320, 321 
rust particles in, 249 
sago bodies in, 314, 316 
sand in, 232, 255, 361 
sarcina urinae in, 329 
scales of insect wings in, 247, 

shreds in, 319-327 
smegma bacillus in, 335 
sodium urate, 256 
spermatozoa in, 312, 313 
spermin crystals, 313 
staining, 244 

centrifugal, 245 

Saxe's method, 244 

Wolff's method, 245 
starch globules in, 247, 248 
sugar granules in, 315, 317, 319 
textile fibers in, 245 
triple phosphate in, 263 
tubercle bacilli, 335, 360 
tyrosin in, 267, 268 
unorganized, 255 

table of, 250 
urates in, amorphous, 258 

clinical significance, 259 
urethral shreds in, 319 
uric-acid, 252, 255 
vesicular casts in, 315, 318, 319 

elements, 314 

shreds in, 319 

skins in, 315, 317, 319 
yeasts in, 327, 328 
Seminal vesicles, epithelium from, 

inflammation of, 376 

pus from, 283 
vesiculitis, 376 
Serkowski's table of conditions in 
which chlorids are diminished 
and increased, 210 
Serum-albumin, 50. See also 

Serum-globulin, 50, 77. See also 

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Shock, nervous, albuminuria after, 

53 • 
Shreds, 319-327 

clinical significance, 325 
comma, 324 

false, 321, 324 
connective-tissue, 284 
epithelial, 322, 324, 325, 326 
mucopus, 321, 322, 325 
mucous, 322, 323, 325 
pus, 320, 321, 325 
urethral, 319, 325 

Saxe's method, 320 
vesicular, 319 
Silicic acid, 230 
Silk fibers in sediments, 245, 246, 

Silver nitrate test for chlorids, 210 

test for uric acid, 151 
Skatol, 223, 224 

Skatoxyl potassium sulphate, 181 
Skins, vesicular, 315, 317, 319 
Slides, care of, 240 
flaws in, 249 
ringing, 243 
scratches on, 240, 249 
Smears, bacterial, 329 
Smegma bacillus, 335 
Smoky urine, 27 
Sodium acetate solution, 220 
chlorid, 208 
urate, 256 
Solid reagents, 423 
Solids, 19 
total, 46 
average, 47 
determination, 47 
Soluble mucin, 90 
Specific gravity, 40 
determination, 41 
diminished, 46 
freezing-point and, 400 
increased, 45 
of pathologic urines, 45 
of small amounts, 43, 44 
Specimen, selection, 21 

best time for, 21 
Spectroscope, pocket, for detecting 

urobilin, 187 
Spectroscopic test for blood-pig- 
ments, 196, 197 
Spectrum of blood-pigments, 196 

Spectrum of hematoporphyrin, 198 

of urobilin, 188 
Spermatorrhea, 314, 377 
Spermatostasis, 319 
Spermatozoa, 312, 313 

Florence's test for, 314 

rape and, 314 

tests for, 314 
Spermin crystals, 313 
Spiegler test for albumin, 66 
Spleen in origin of uric acid, 147 
Sprengel's tubes for specific gravity, 

43> 44 
Spurious albuminuria, 52 
Squamous-cell epithelium, 287 
Squibb's urinometer, 41 
Staining bacillus coli, 330, 332 

gonococci, 318, 319, 320, 331 

proteus vulgaris, 332 

sediments, 244 

staphylococcus aureus, 332 

streptococci, 318, 319, 332 

tubercle bacilli, 335 
Stains, bacterial, 423 

Bismark brown, 333 

carbol-gentian violet, 333 

eosin, 334 

fuchsin, 334 

Gram's, 333 

iodin, Gram's, 333 
Staphylococcus aureus, Gram's 
stain for, 332 

pyogenes albus, 329 
aureus, 329 
citreus, 329 
Starch globules in sediments, 247, 

Starvation, effect on sodium chlorid 

elimination, 208 
Stern's urinoglucosometer, 117, 118 
Stones, 232 

in bladder, 373 

in kidney, 360 

difi^erentiation, 361 
urine in, 360 
Stoppered graduate, 22 
Streptococcus pyogenes, 329 
Gram's stain for, 332 
staining, 318, 319 
Stiitz and Fiirbringer's test for albu- 
min, 68 
Suboxidized organic sulphur, 226 

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Succinic acid, 205 

Sufficiency of kidneys, tests for, 

Sugar granules, 3i5» 3i7» 3^9 
in urine, 96. See also Glucose. 
cane-, 126 
fruit, 123 
Leo's, 123 
milk, 122 
muscle, 125 
Sulphates, 223 
aromatic, 223, 224 

estimation, 228 
centrifugal estimation, Purdy's, 

conjugate, 223, 224 

estimation, 228 
diminished, 224 
ethereal, 174, 181, 223, 224 
as index to intestinal putre- 
faction, 225 
clinical significance, 182 
diminished, 225 
estimation, 228 
increased, 225 
ratio to total sulphates, 225 
tests for* 182 
gravimetric estimation, 227 
increased, 224 
indoxyl-potassium, 174, 225 
mineral, 223 

estimation, 228 
neutral, 223, 226 
estimation, 228 
preformed, 223 

estimation, 228 
Purdy's centrifugal table, 227 
quantitative test, 226 
Salkowski's estimation, 227 
tests for, 226 
total output, 224 

ratio to ethereal sulphates, 225 
Sulphocyanic acid, 205 
Sulphocyanid, hydrogen, 205 
Sulphocyanids, 223 
Sulphosalicylic acid test for albu- 
min, 66 
Sulphur, 223. See also Sulphates. 
Sulphuretted hydrogen, 230 

urine, 29 
Sulphuric acid, estimation, 228 
preformed, 223 

Superphosphates, 216 
Suppression of urine, 25 

Ti«NiA echinococcus, 338 
Tanret's test for albumin, 67 
Taurin, 223 
Taurocholic acids, 205 
Taylor's modification of Legal's 

acetone test, 167 
Teichmann's hemin crystals, 276 
test for blood-pigments, 197 
test for blood in sediment, 276 
Textile fibers in sediments, 245 
Thermometer, cryoscopic, 397 
Thermometric equivalents, 424 
Thiosulphates, 223, 226 
Thiosulphuric acid, 230 
Thorn-apple crystals, 258 
Thymol as urine preservative, 236 
Tissue fragments, preservation, 244 
Titration method for albumin, 

Vassilieff's, 74 
of urine, 34 
Total acidity, 35 
nitrogen, 131 

diminished, 132 

in disease, 132 

in pregnancy, 386 

in toxemias of pregnancy, 133 

increased, 132 

normal, 132 
phosphoric acid, estimation, 219 
solids, 19, 46, 47 
Toxemias of pregnancy, 386 

total nitrogen in, 133 
Toxic albuminuria, 54 
Toxicity of urine, 410, 411 
Transparency of urine, 29 
Traumatic albuminuria, 54 
Trichloracetic acid test for albumin, 


Triple phosphates, 216, 254 
crystals, 263 
preservation, 243 
Trommer's test for glucose, 98 
True albuminuria, 52 

phosphaturia, 216 
Trypsin, 206 

Tsuchiya's estimation of albumin, 

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Tubercle bacillus, 335, 360 
animal inoculation, 336 
staining, 335 
Tuberculosis of bladder, 371 
of kidney, 358 

blood in urine, 279 
urine in, 359 
of prostate, 375 
Tumors of bladder, 373 
of kidney, 362 

blood in urine, 279 
differentiation, 363 
urine in, 362 
Turbid urine, 29 

table of causes, 32 
Twenty-four hour quantity, 21 
Tyrosin, 201, 267, 268 
crystals, 203, 267 
Frerich's test for, 201 
furfurol test for, 202 
Hoffmann's test for, 202 
Piria's test for, 202 
tests for, 201, 202 
von Udrinszky's test for, 202 

Ultzm ANN'S estimation of phos- 
phates, 218 
polariscope, 119, 120 
Undetermined nitrogen, 131, 133 

in pregnancy, 386, 387 
Unorganized sediments, 255 

table of, 250 
Unoxidized organic sulphur, 226 
Uranium acetate standard solution, 
nitrate standard solution, 219 
Urate casts, 309 
Urates, 154 

amorphous, 258 
cloudy urine from, 30 
in sediments, 256 

clinical significance, 259 
preservation, 243 
Urea, 18, 133 
amount excreted, 133, 134 
analytic methods, absolute, 144 
conversion into ammonium car- 
bonate, 253 
crystals, 136 
diminished, 135 

Doremus' method for estimating, 

Urea, estimation, 135 
approximate, 135 
table for, 142, 143 
Hiifner's estimation of, 1 39-1 41 
hypobromite estimation of, 136 

Rice's solutions for, 139 
in pregnancy, 386 
increased, 135 
Kjeldahl's estimation of, 144 
Knop's estimation, 136 
Moerner-Sjoqvist estimation of, 

nitrate of, 136 
specific gravity estimation of , 135, 

table of variations, 135 
tests for, 134 
Ureometer, Doremus', 137 

Hinds' modification, 139 
Ureteritis, 368 

Ureters, epithelium from, 291 
hemorrhage from, blood in sedi- 
ment from, 280 
Urethra, epithelium from, 294 
inflammation of, 377 
pus from, 283 
Urethral shreds, 319, 325 
Urethritis, 377 
acute, 377 
chronic, 377 
gonorrheal, 377 
Uric acid, 145, 146 
calculi, 232 
compounds, 256 
congeners, 145 
copper test for, 151 
crystals, 255 

preservation, 243 
diathesis, acidity and, 39 
diminished, 148, 149 
dumb-bell crystals, 260, 261 
endogenous, 147 
estimation of, 152 
exogenous, 147 

Folin-Hopkin's estimation, 154 
gout and, 149 
Heintz's estimation of, 152 
increased, 148, 149 
apparent, 150 
true, 150 
kidneys in origin of, 147 
leukomains, 413 

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Uric acid, liver in origin of, 147 

murexid test. for, 151 

normal, 151 

origin of, 146 

pathologic significance, 147 

Ruhemann's estimation of, 152 

sediment, 252 

silver test for, 151 

spleen in origin of, 147 

tests for, qualitative, 151 
Uricometer, Ruhemann's, 152 
Urinary coloring-matters, 186 

normal, 186 
concretions, 232 
diagnosis, 342 
nitrogen, 131 
pigments, 186 
tract, lower, diseases of, urine in, 

Urinoglucosometer, 117, 118 
Urinometer, 41 

Squibb's, 41 
Urinopyknometer for specific grav- 
ity, 44 
Urobilin, 186, 187 

Harley's test for, 188 

Heller's urophaein test for, 187 

spectroscope for detecting, 187 

spectrum of, 188 

tests for, 187 

urophaein test for, 187 
Urochrome, 186 
Uroerythrin, 186 
Uroglaucin, Heller's, 177 
Uroleucic acid, 206 
Urophaein, 186 

test of Heller for urobilin, 187 
Urostealith, 232 
Urotoxic coefficient, 410 
Urrhodin, Heller's, 177 
Uterus, epithelium from, 297 

pus from, 283 

Vagina, epithelium from, 297 

pus from, 283 
Vasomotor changes, albuminuria 

after, 53 

Vassilieff's titration method for 

albumin, 74 
Vegetable foods, odor of urine and, 

Vesicular casts, 315, 318, 319 

elements, 314 

shreds, 319 

skins, 315, 317, 319 
Volatile alkali, test for, 40 

fatty acids, 204, 206 
Volhard's test for chlorids, Sal- 

kowski's modification, 211 
Vomiting, persistent, of pregnancy, 

386, 387 
Von Jaksch's test for diacetic acid, 

for melanin, 199 
Von Udranszky's test for tyrosin, 

Water-motor centrifuge, 237, 238 

Waxy casts, 303, 357 

degeneration of kidney, 356 

Westphal balance for specific grav- 
ity, 43, 44 

Wolff's method of centrifugal stain- 
ing, 245 

Wool fibers in sediments, 245, 246, 

Xanthin bases, 146, 155. See 
also Purin bases. 

bodies, 145 

calculi, 232 

crystals, 156 
Xylose, 124 

Yeasts, 327, 328 
Yellow urine," 27 

Zahor's coefficient, 70 
Zeller's test for melanin, 199 
Zouchlos' test for albumin, 67 
Zueltzer's coefficient, 216 

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Kelly and Cullen's 
Myomata of the Uterus 

Myomata of the Uterus. By Howard A. Kelly, M. D., 
Professor of Gynecologic Surgery at Johns Hopkins University; 
and Thomas S. Cullen, M. B., Associate in Gynecology at 
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with 2i^Z original illustrations by August Horn and Hernciann 
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This monumental work, the fruit of over ten years of untiring labors, will 
remain for many years the last word upon the subject. Written by those men 
who have brought, step Ly step, the operative treatment of uterine myoma to 
such perfection that tlie mortality is now less than one per cent., it stands out 
as the record of greatest achievement of recent times. 

The illustrations have been made with wonderful accuracy in detail by Mr. 
August Horn and Mr. Hermann l>ecker, whose superb work is so well known 
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detail, and as an example of the practical results accruing from the associa- 
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Sur^eiy, Gjmecolo^y, and Obstetrics 

** It must be considered as the most comprehensive work of the kind yet published. It 
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New York Medical Journal 

*' Within the covers of this monograph every form, size, variety, and complication of 
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Uterine Adenomyoma 

uterine Adenomyoma. By Thomas S. Cullen, M. D., 
Associate Professor of Gynecology, Johns Hopkins University. 
Octavo of 275 pages, with original illustrations by Hermann 
Becker and August Horn. Cloth, ;J>5.oo net. 


Dr. Cullen's large clinical experience and his extensive original work along 
the lines of gynecologic pathology have enabled him to present his subject 
with originality and precision. The work t^ives the early literature on 
adenomyoma, traces the disease through its various stages, and then gives the 
detailed findings in a large number of cases personally examined by the 
author. Formerly the physician and surgeon were unable to determine the 
cause of uterine bleeding, but after following closely the clinical course of 
the disease, Dr. Cullen has found that the majority of these cases can be 
diagnosed clinically. The results of these observations he presents in this 

The Lancet, London 

" A good example of how such a monograph should be written. It is an excellent 
work, worthy of the high reputation of the author and of the school from which it emanates." 

Cancer of the Uterus 

Cancer of the Uterus. By Thomas S. Cullen, M. B., 
Associate Professor of Gynecology, Johns Hopkins University. 
Large octavo of 693 pages, with over 300 colored and half-tone 
text-cuts and eleven lithographs. Cloth, j7.5onet; Half 
Morocco, ^8.50 net. 

Howard A. Kelly, M. D. 

Professor of Gynecoh^ic Surgery, Johtis Hopkins University. 

" Dr. Cullen's book is the standard work on the greatest problem which faces the sur- 
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Practice of Gynecology 

The Practice of Gynecology. By W. Easterly Ashton, 
M.D., LL.D., Professor of Gynecology in the Medico-Chirurgi- 
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pages, containing 1058 original line drawings. Cloth, $6.50 
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Four editions of this work have been demanded in as many years. Among 
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vaginismus, Dudley's treatment of cystocele, Montgomery's round ligament 
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Urine, and Moynihan's methods in Intestinal Anastomosis. Nothing is left to 
be taken for granted, the author not only telling his readers in every instance 
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feature of the book is the illustrations, numbering 1058 line drawings made 
especially under the author's personal supervision from actual apparatus, living 
models, and dissections on the cadaver. 

From its first appearance Dr. Ashton's book set a standard in practical 
medical books ; that he has produced a work of unusual value to the medical 
practitioner is shown by the demand for new editions. 

Howard A. Kelly, M. D., 

Professor qf Gynecologic Surgery, Johns Hopkins University 

**\\. is different trom anything that has as yet appeared. The illustrations are particu- 
larly clear and satisfactory. One specially good feature is the pains with which you 
describe so many details so often left to the imagination." 

Chajrles B. Penrose, M. D., 

Formerly Professor of Gynecology y University of Pennsylvania. 

** I know of no book that goes so thoroughly and satisfactorily into all the details of 
everything connected with the subject. In this respect your book differs from the others." 

Geoftfe M. Edebohls, M.D. 

Professor of Diseases of Women, New York Post- Graduate Medical School, 
*' I have looked it through and must congratulate you upon having produced m text* 
book most admirably adapted to teach gynecology to those who must get tneir knowledfe. 
even to the minutest and most elementary details, from books." 

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Medical Gynecology 

Medical Gynecology. By S. Wyllis Bandler, M. D., 
Adjunct Professor of Diseases of Women, New York Post- 
Graduate Medical School and Hospital. Octavo of 702 pages, 
with 150 original illustrations. Cloth, $5.00 net; Half Morocco, 
16.50 net. 


This new work by Dr. Bandler is just the book that the physician en- 
gaged in general practice has long needed. It is truly the practitioner' s gyne- 
cology — planned for him, written for him, and illustrated for him. There are 
many gynecologic conditions that do not call for operative treatment ; yet, 
because of lack of that special knowledge required for their diagnosis and 
treatment, the general practitioner has been unable to treat them intelligently. 
This work gives just the information the practitioner needs. 
American Journal of Obstetrics 

" He has shown good judgment in the selection of his data. He has placed most 
emphasis on diagnostic and therapeutic aspects. He has presented his facts in a manner 
to be readily grasped by the general practitioner." 

Bandler's Vaginal Celiotomy 

Vaginal Celiotomy. By. S. Wyllis Bandler, M.D., New 
York Post-Graduate Medical School and Hospital. Octavo of 
450 pages, with 148 original illustrations. Cloth, J5.00 net. 


The vaginal route, because of its simplicity, ease of execution, absence of 
shock, more certain results, and the opportunity for conservative measures, 
constitutes a field which should appeal to all surgeons, gynecologists, and 
obstetricians. Posterior vaginal celiotomy is of great importance in the re- 
moval of small tubal and ovarian tumors and cysts, and is an important step 
in the performance of vaginal myomectomy, hysterectomy, and hystero- 
myomectomy. Anterior vaginal celiotomy with thorough separation of t?ie 
bladder is the only certain method of correcting cystocele. Dr. Bandler shows 
by original illustrations the various steps in these operations. 

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Kelly and Noble's Gynecology 
and Abdominal Surgery 

Gynecology and Abdominal 5urgery . Edited by Howard 
A. Kelly, M. D., Professor of Gynecology in Johns Hopkins 
University; and Charles P. Noble, M.D., Clinical Professor of 
Gynecology in the Woman's Medical College, Philadelphia. Two 
imperial octavo volumes of 900 pages each, containing 880 illus- 
trations, mostly original. Per volume: Cloth, $8.00 net ; Half 
Morocco, $9.50 net. 



In view of the intimate association of gynecology with abdominal surgery 
the editors have combined these two important subjects in one work. For 
this reason the work will be doubly valuable, for not only the gynecologist and 
general practitioner will find it an exhaustive treatise, but the surgeon also will 
find here the latest technic of ihe various abdominal operations. It possesses 
a number of valuable features not to be found in any other publication cover- 
ing the same fields. It contains a chapter upon the bacteriology and one upon 
the pathology of gynecology, dealing fully with the scientific basis of gyne- 
cology. In no other work can this information, prepared by specialists, be 
found as separate chapters. There is a large chapter devoted entirely to 
medical gynecology^ written especially for the physician engaged in general 
practice. Heretofore the general practitioner was compelled to search through 
an entire work in order to obtain the information desired. Abdominal sur- 
gery proper, as distinct from gynecology, is fully treated, embracing operations 
upon the stomach, upon the intestines, upon the liver and bile-ducts, upon the 
pancreas and spleen, upon the kidney, ureter, bladder, and the peritoneum. 
Special attention has been given to modern technic. The illustrations are the 
work of Mr, Hermann Becker and Mr. Max Br'ddel. 

American Journal of the Medical Sciences 

" It is needless to say that the work has been thoroughly done : the names of the authors 
and editors would guarantee this ; but much may be said in praise of the method of presen- 
tation, and attention may be called to the inclusion of matter not to be found elsewhere." 

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Diseases qf Women 

Diseases of Women. By J. Clarence Webster, M. D. 
(Edin.), F. R. C. p. E., Professor of Gynecology and Obstetrics 
in Rush Medical College. Octavo of 712 pages, with 372 illus- 
trations. Cloth, $7.00 net; Half Morocco, ^18.50 net. 


Dr. Webster has written this work especially for the general practitioner, 
discussing the clinical features of the subject in their widest relations to 
general practice rather than from the standpoint of specialism. The magni- 
ficent illustrations, three hundred and seventy- two in number, are nearly all 
original. Drawn by expert anatomic artists under Dr. Webster' s direct super- 
vision, they portray the anatomy of the parts and the steps in the operations 
with rare clearness and exactness. 

tfOWard A« Kelly» M.D,» Prqfessorqf Gyngcologic Surgery ^ Johns HopkimUnxoersity. 

" It is undoubtedly one of the best works which has been put on the market within 
recent years, showing from start to finish Dr. Webster's well-known thoroughness. The 
illustrations are also of the highest order." 

Webster's Obstetrics 

A Text-Book of Obstetrics. By J. Clarence Webster, 
M. D. (Edin.), Professor of Obstetrics and Gynecology in Rush 
Medical College. Octavo of 767 pages, illustrated. Cloth, 
$5.00 net; Half Morocco, $6.^0 net. 

Medical Record, New York 

** The author's remarks on asepsis and antisepsis are admirable, the chapter on eclamp- 
sia is full of good material, and ... the book can be cordially recommended as a safe 

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Text-Book of Obstetrics 

The New (6th) Edition 

A Text-Book of Obstetrics. By Barton Cooke Hirst, 
M. D. , Professor of Obstetrics in the University of Pennsylvania. 
Handsome octavo, 992 pages, with 847 illustrations, 43 in colors. 
Cloth, 115.00 net j Half Morocco, i>6.5o net. 


Immediately on its publication this work took its place as the leading text- 
book on the subject. Both in this country and abroad it is recognized as the 
most satisfactorily written and clearly illustrated work on obstetrics in the 
language. The illustrations form one of the features of the book. They are 
numerous and the most of them are original. In this edition the book has 
been thoroughly revised. Recognizing the inseparable relation between ob- 
stetrics and certain gynecologic conditions, the author has included all the 
gynecologic operations for complications and consequences of childbirth, 
together with a brief account of the diagnosis and treatment of all the path- 
ologic phenomena peculiar to women. 


British Medical Journal 

** The popularity of American text-books in this country is one of the features of recent 
years. The popularity is probably chiefly due to the great superiority of their illustrations 
over those of the English text-books. The illustrations in Dr. Hirst's volume are far mwe 
numerous and far better executed, and therefore more instructive, than those commonly 
found in the works of writers on obstetrics in our own countr>'." 

Btilletin of Johns Hopkins Hospital 

** The work is an admirable one in every sense of the word, concisely but comprehen- 
sively written." 

The Medical Record, New York 

"The illustrations are numerous and are works of art, many of them appearing for the 
first time. The author's style, though condensed, is singularly clear, so that it u nerer 
necessary to re-read a sentence in order to grasp the meaning. As a true model of whmt a 
modern text-book on obstetrics should be, we feel justified in affirming that Dr. Hirst's book 
is without a rival." 

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Diseases of Women 

A Text-Book of Diseases of Women. By Barton Cooke 
Hirst, M. D., Professor of Obstetrics, University of Pennsyl- 
vania; Gynecologist to the Howard, the Orthopedic, and the 
Philadelphia Hospitals. Octavo of 745 pages, 701 illustrations, 
many in colors. Cloth, i>5.oo net; Half Morocco, $6.^0 net. 


The new edition of this work has just been issued after a careful revision. 
As diagnosis and treatment are of the greatest importance in considering dis- 
eases of women, particular attention has been devoted to these divisions. To 
this end, also, the work has been magnificently illuminated with 701 illus- 
trations, for the most part original photographs and water-colors of actual 
clinical cases accumulated during the past fifteen years. The palliative treat- 
ment, as well as the radical operative, is fully described, enabling the gen- 
eral practitioner to treat many of his own patients without referring them 
to a specialist. The author's extensive experience renders this work of un- 
usual value. 


Medical Record, New York 

*' Its merits can be appreciated only by a careful perusal. . . . Nearly one hundred pa^^ea 
are devoted to technic, this chapter being in some respects superior to the descriptions in 
many text-books." 

Boston Medical and Surgical Journal 

'* The author has given special attention to diagnosis and treatment throughout the book^ 
and has produced a practical treatise which should be of the greatest value to the student, 
the general practitioner, and the specialist." 

Medical News. New York 

" Office treatment is given a due amount of consideration, so that the work will be as 
aseful to the non-operator as to the specialist," 

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Illustrated Dictionary 

Just Ready— The New (6th) Edition, Reset 

The American Illustrated Medical Dictionary. A new 

and complete dictionary of the terms used in Medicine, Surgery, 
Dentistry, Pharmacy, Chemistry, Veterinary Science, Nursing, 
and all kindred branches ; with over loo new and elaborate 
tables and many handsome illustrations. By VV. A. Newman 
Borland, M.D., Editor of '* The American Pocket Medical 
Dictionary.'' Large octavo, 975 pages, bound in full flexible 
leather. Price, 114.50 net; with thumb index, ^15. 00 net. 


Gives a Maximum Amount of Matter in a Minimum Space 


We really believe that Dorland's Dictionary is the most useful single book 

that the medical practitioner can own. We are confident you will get more 

real use out of it than out of any one book you ever bought. 

Nearly every medical paper to-day contains special words which are new to 

most readers. \i you want to get the best out of your journals and text-books, 

Dorland's Dictionary should be on your desk for ready reference. 

This new edition defines all the new words, and is a safe key to capitalization, 

pronunciation, and etymology. 


Howard A. Kelly, M. D., 

Professor of Gynecologic Surgery ^ Johns Hopkins University ^ Baltimore, 
** Dr. Dorland's dictionary is admirable. It is so well gotten up and of such conve- 
nient size. No errors have been found in my use of it." 

J. Collins Warren, M.D., LL.D., r.RX.S. (Hon.) 

Professor of Surgery, Harvard Medical School. 

" I regard it as a valuable aid to my medical literary work. It is very complete and 
of convenient size to handle comfortably. I use it in preference to any other." 

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Diseases of Women 

Sixth Revised Edition 

A Text-Book of Diseases of Women. By Charles B. 
Penrose, M. D., Ph. D., formerly Professor of Gynecology in 
the University of Pennsylvania ; Surgeon to the Gynecean Hos- 
pital, Philadelphia. Octavo volume of 550 pages, with 225 fine 
original illustrations. Cloth I3. 75 net. 


Regularly every year a new edition of this excellent text-book is called 
for, and it appears to be in as great favor with physicians as with students. 
Indeed, this book has taken its place as the ideal work for the general prac- 
titioner. The author presents the best teaching of modern gynecology, un- 
trammeled by antiquated ideas and methods. In every case the most modern 
and progressive technique is adopted, and the main points are made clear by 
excellent illustrations. 

Howard A. Kelly, M.D., 

Professor of Gynecologic Surgery, Johns Hopkins University, Baltimore. 
" I shall value very highly the copy of Penrose's * Diseases of Women ' received. I 
have already recommended it to my class as the best book." 

Davis' Operative Obstetrics 

Operative Obstetrics. By Edward P. Davis, M.D., Pro- 
fessor of Obstetrics at Jefferson Medical College, Philadelphia. 
Octavo of 463 pages, with 264 illustrations. 


Dr. Davis' new work on Operative Obstetrics is a most practical one and no 
expense has been spared to make it the handsomest work on the subject, as 
well. Every step in every operation is described minutely, and the technic 
shown by beautiful new illustrations. Dr. Davis' name is sufficient guarantee 
for something above the ordinary. 

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Modern Obstetrics 

Modern Obstetrics : General and Operative. By W. A. 

Newman Borland, A. M., M. D., Professor of Obstetrics at 
Loyola University, Chicago. Handsome octavo volume of 797 
pages, with 201 illustrations. Cloth, ;Jl4.oo net. 

Second Edition, Revised and Greatly Enlars(ed 

In this edition the book has been entirely rewritten and very greatly 
enlarged. Among the new subjects introduced are the surgical treatment of 
puerperal sepsis, infant mortality, placental transmission of diseases, serum- 
therapy of puerperal sepsis, etc. 

Journal of the American Medical Association 

" This work deserves commendation, and that it has received what it deserves at the 
hands of the profession is attested by the fact that a second edition is called for within such 
m short time. Especially deserving of praise is the chapter on puerperal sepsis." 

Davis' Obstetric and 
Gynecologic Nursing 

Obstetric and Gynecologic Nursing. By Edward P. 
Davis, A. M., M. D., Professor of Obstetrics in the Jefferson 
Medical College and Philadelphia Polyclinic ; Obstetrician and 
Gynecologist, Philadelphia Hospital. i2mo of 436 pages, illus- 
trated. Buckram, ili.75 net. 


This volume gives a very clear and accurate idea of the manner to meet 
the conditions arising during obstetric and gynecologic nursing. The third 
edition has been thoroughly revised. 

The Lancet, London 

" Not only nurses, but even newly qualified medical men, would learn a great deal by 
a perusal of this book. It is written in a clear and pleasant style, and is a work we can 

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Garri^ues' Diseases of Women Third Editioii 

A Text- Book of Diseases of Womun. By Henry J. Garrigues, 
A. M., M. D., Gynecologist to St. Mark's Hospital and to the German 
Dispensary, New York City, Handsome octavo, 756 pages, with 367 
engravings and colored plates. Cloth, ^^4.50 net ; Half Morocco, 
|6.oo net. 

Thad. A. Reamy» M« D., Professor of Gynecology, Medical College of Ohio. 

** One of the best text-books for students and practitioners which has been published 
in the English language; it is condensed, clear, and comprehensive. The profound 
learning and great clinical experience of the distinguished author find expression in 
this book." 

Macfarlane's Gynecolo^ for Nurses 

A Reference Hand-Book of Gynecology for Nurses. By Cath- 
arine Macfarlane, M. D., Gynecologist to the Woman's Hospital of 
Philadelphia. 32mo of 1 50 pages, with 70 illustrations. Flexible leather, 
j^i.25 net. 

A, M. Seabrook, M. D., IVoman's Medical College of Philadelphia. 

** It is a most admirable little book, covering in a concise but attractive way the sub- 
ject from the nurse's standpoint." 

American Text-Book of Gynecolo^ Edition 

American Text-Book of Gynecology. Edited by J. M. Baldy, 
M. I). Imperial octavo of 718 pages, with 341 text-illustrations and 
38 plates. Cloth, ;j56.oo net. 

American Text-Book of Obstetrics second Edition 

The American Text-Book of Obstetrics. In two volumes. 
Edited by Richard C. Norris, M. D. ; Art Editor, Robert L. Dick- 
inson, M. D. Two octavos of about 600 pages each ; nearly 900 illus- 
trations, including 49 colored and half-tone plates. Per volume : Cloth, 
tZ-So net. 

Mattiiew D. Mann, M. D., 

Professor of Obstetrics and Gynecology, University of Buffalo. 
** I like it exceedingly and have recommended the first volume as a text-book. It 
is certainly a most excellent work. I know of none better." 

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Schaffer and Webster's 
Operative Gynecolo^ 

Atlas and Epitome of Operative Gynecology. By Dr. 

O. Schaffer, of Heidelberg. Edited, with additions, by J. 
Clarence Webster, M. D. (Edin.), F. R. C. P. E., Professor of 
Obstetrics and Gynecology in Rush Medical College, in affili- 
ation with the University of Chicago. 42 colored lithographic 
plates, many text-cuts, a number in colors, and 138 pages of text. 
In Saunders* Hand- Atlas Series. Cloth, 1^3.00 net. 

Much patient endeavor has been expended by the author, the artist, and 
the lithographer in the preparation of the plates for this Atlas. They are based 
on hundreds of photographs taken from nature, and illustrate most faitlifully 
the various surgical situations. Dr. Schaffer has made a specialty of demon- 
strating by illustrations. 

Medical Record, New York 

"The volume should prove most helpful to students and others in grasping details 
usually to be acquired only in the amphitheater itself." 

De Lee's Obstetrics for Nurses 

Obstetrics for Nurses. By Joseph B. De Lee, M. D., 
Professor of Obstetrics in the Northwestern University Medical 
School, Chicago; Lecturer in the Nurses' Training Schools of 
Mercy, Wesley, Provident, Cook County, and Chicago Lying-in 
Hospitals. i2mo of 512 pages, fully illustrated. 

Cloth, ^12.50 net. 


While Dr. DeLee has written his work especially for nurses, the practi- 
tioner will also find it useful and instructive, since the duties of a nurse often 
devolve upon him in ihe early years of his practice. The illustrations are 
nearly all original ami represent p.iotographs taken from actual scenes. The 
text is the result ^f the author's many years' expeiience in lecturing to the 
nurses of five different training schools. 

J. CUfton tAifix. M. Dc, 

Professor of Obstetrics and Clinical Midwifery ^ Cornell University ^ New York. 
** It U far and away the best that has come to my notice, and I shall take great pleasure 
in recommending it to my nurses, and students as well." 

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Schaffer and Ed^arV 

Labor and Operative Obstetrics 

Atlas and Epitome of Labor and Operative Obstetrics. 

By Dr. O. Schaffer, of Heidelberg. From the Fifth Revised 
and Enlarged German Edition, Edited, with additions, by J. 
Clifton Edgar, M. D., Professor of Obstetrics and Clinical Mid- 
wifery, Cornell University Medical School, New York. With 14 
lithographic plates in colors, 139 other illustrations, and 11 1 pages 
of text. Cloth, 112.00 net. In Saunders' Hand- Atlas Series, 

This book presents the act of parturition and the various obstetric opera- 
tions in a series of easily understood illustrations, accompanied by a text 
treating the subject from a practical standpoint. 

American Medicine 

" The method of presenting' obstetric operations is admirable. The drawings, repre- 
senting original work, nave the commendable merit of illustrating instead of confusing.' 

Schaffer and EM^arV 

Obstetric Diagnosis and Treatment 

Atlas and Epitome of Obstetric Diagnosis and Treat- 
ment. By Dr. O. Schaffer, of Heidelberg. From the Second 
Revised German Edition. Edited, with additions, by J. Clif- 
ton Edgar, M. D., Professor of Obstetrics and Clinical Mid- 
wifery, Cornell University Medical School, N. Y. With 122 
colored figures on 56 plates, 38 text-cuts, and 315 pages of text. 
Cloth, $3.00 net. In Saunders'' Hand-Atlas Series. 

This book treats particularly of obstetric operations, and, besides the wealth 
of beautiful lithographic illustrations, contains an extensive text of great value. 
This text deals with the practical, clinical side of the subject. 

New York Medical Jcniraal 

" The iDustrations are admirably executed, as they are in all of these atlases, and the 
text can safely be commended, not only as elucidatory of the plates, but as expounding the 
scientific midwifery of to-day." 

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American Pocket Dictionary „ JS^J^^ 

•^ New (7th) Edition 

The American Pocket Medical Dictionary. Edited by W, A. 

Newman Dorland, A. M., M.D. With 6io pages. Full leather, 

limp, with gold edges, ^i.oo net; with patent thumb index, ^{1.25 net 

Jamet W. Holland, M. D.. 

Professor 0/ Chemistry and Toxicology, ai the Jefferson Medical College, 

" I am struck at once with admiration at the compact size and attractive exterior 
I can recommend it to our students without reserve." 

Cras(in*s Gynecolo|(y New (7th) Ed. 

Essentials of Gynecology. By Edwin B. Cragin, M. D., Pro- 
fessor of Obstetrics, College of Physicians and Surgeons, New York. 
Crown octavo, 240 pages, 62 illustrations. Cloth, %l.QO net. In 
Saunders' Question- Compend Series, 

Galbraith*s Pour Epochs of Woman's Life edition 

The Four Epochs of Woman's Life: A Study in Hygiene. 
Maidenhood, Marriage, Maternity, Menopause. By Anna M. Gal- 
BRAITH, M. D. With an Introductory Note by John H. Musser, 
M. D., University of Pennsylvania. I2mo of 247 pages. Cloth, 
^1.50 net. 

Schaffer and Norris* Gynecolo|(y Saunden' Atiaset 

Atlas and Epitome of Gynecology. By Dr. O. Schaffer, of 
Heidelberg. Edited, with additions, by Richard C. Norris, A. M., 
M. D,, Assistant Professor of Obstetrics, University of Pennsylvania. 
207 colored illustrations on 90 plates, 65 text-cuts, and 272 pages of text. 
Cloth, JJ53.50 net. 

Ashton*S Obstetrics New (/Ui) Ed. 

Essentials of Obstetrics. By W. Easterly Ashton, M. D., Pro- 
fessor of Gynecology in the Medico- Chirurgical College, Philadelphia. 
Crown octavo, 252 pages, 109 illustrations. Cloth, ^i.oo net. In 
Saunders' Question- Compend Series. 

Sotrthern Practitioner 

"An excellent little volume, containing correct and practicalknowledge. An admiV' 
able compend, and the best condensation we have seen." 

Barton and Wells* Medical Thesaurus 

A Thesaurus of Medical Words and Phrases. By Wilfred M. 
Barton, M. D., Assistant to Professor of Materia Medica and Thera- 
peutics, Georgetown University, Washington, D. C. ; and Walter A. 
Wells, M. D., Demonstrator of Laryngology, Georgetown University, 
Washington, D. C. i2mo of 534 pages. Flexible leather, ^2.50 net; 
with thumb index, ^3.00 net. 

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