SOME REMARKS ON 
Oxaluria and its Relations to 
Certain Forms of Nervous 
Disease 
BY 
I. ADLER, M.D. 
VISITING PHYSICIAN TO THE GERMAN HOSPITAL PROFESSOR OF CLINICAL 
PATHOLOGY AT THE NEWYORK POLYCLINIC 
Reprinted from the Medical Record, June 3, 1893 
NEWYORK 
TROW DIRECTORY, PRINTING AND BOOKBINDING CO. 
20X-213 East Twelfth Street 
1893 SOME REMARKS ON 
Oxaluria and its Relations to Certain 
Forms of Nervous Disease.1 
I. ADLER, M.D., 
VISITING PHYSICIAN TO THE GERMAN HOSPITAL ; PROFESSOR OF CLINICAL PA- 
THOLOGY AT THE NEW YORK POLYCLINIC. 
Reprinted from the Medical Record, June 3, 1893. 
Ever since Prout2 in 1820 first called attention to the 
occurrence of oxalic acid, principally as oxalate of lime, 
in the urine of persons suffering from a variety of diseases, 
and in later publications sought to establish oxaluria as a 
disease sui generis and characterized by well-marked symp- 
toms, the excretion through the urine of oxalic acid in 
health and in disease has been a subject of much discus- 
sion. While Prout based his assumptions rather on hy- 
pothesis than on facts, Golding Bird3 first demonstrated 
the occurrence of oxalate of lime crystals in the urine, 
which indeed had been seen and described by Brugnatelli 
in 1787, but not recognized by him as to their true chem- 
ical composition. 
Numerous investigators took up the subject, and in Eng- 
land at least oxaluria obtained a place of its own in the 
nosological system. The symptoms were chiefly disturb- 
ances of the nervous and digestive systems. Mental de- 
pression, taedium vitae, headaches, neuralgic pains, espe- 
cially in the back and in the limbs, tremor, insomnia, im- 
pairment of vision even to complete amaurosis, loss of 
1 Read before the New York Neurological Society, January 3, 1893. 
2 For a very complete survey of the older literature on oxaluria, see- 
Smoler, Studien über Oxalurie. Prager Vierteljahresschrift, xviii. 
Jahrg., Bd. i. & ii. 
3 Lectures on Physiological and Pathological Characters of Urinary 
Deposits. 1846. 2 
appetite, constipation, emaciation, are some of the many 
symptoms claimed as characteristic of this disease ; the 
physical sign, the occurrence of more or less oxalate crys- 
tals in the urine. 
In France the theory of oxaluria could not obtain a 
sure footing, and it was principally Gallois1 who, after 
most careful investigation of the urine of healthy and of 
sick persons, maintained the temporary occurrence of ox- 
alate of lime in the urine of perfectly healthy subjects of 
all ages and both sexes. He showed, furthermore, that 
oxalate sediments can occur in the most varied forms of 
disease and also after ingestion of certain kinds of food 
and certain drugs. Similar results were obtained by 
Bence-Jones.2 
In Germany, Lehmann,3 and especially Beneke,4 studied 
the occurrence of oxalate of lime in the urine under the 
most varied conditions, and also came to the conclusion 
that oxalic acid is excreted under manifold conditions of 
disease, and that oxaluria as a distinct nosological type 
does not exist. A like result was reached by Smoler 5 
who studied the urine in a very large number of persons 
suffering from all kinds of disease. 
It is well to note here that all these investigations were 
made mainly with the microscope. The urine was al- 
lowed to stand for twenty-four hours or longer, and the 
sediment then examined for oxalate of lime crystals. A 
rough estimate of their number and size as they appeared 
in the microscopic field was considered all that was 
needed. After the studies of Beneke6 and Neubauer,7 
who showed that acid sodic phosphate when present in 
the urine wall hold the oxalate of lime in solution and 
prevent its sedimentation, it was frequently found neces- 
1 Memoir sur I’oxalate de chaux dans les sediments de Purine, dans 
la gravelle et les calculs. Soc. de Biologic, 1859. 
2 Medico-Chirurgical Transactions, vol. xvii. 
3 JLehrbuch der physiol. Chemie, 1850. 
4 Zur Physiologic und Pathologic des phosporsauren, und oxalsauren 
Kalks. 1850. s Loc. cit. 3 Loc. cit. 
7 Archiv fur gemeinschaftl. Arbeiten, Bd. iv., 1856. Ueber Oxal- 
saurebildung. 3 
sary to add certain chemicals (calcium chloride and acetic 
acid) before making the microscopical examination. 
Though this rapid procedure gives results incomparably 
more trustworthy than the older and simpler method, 
it is nevertheless at best but a rough approximation and 
can in no wise take the place of exact quantitative deter- 
mination. 
All these investigations, and other and more exact ones, 
to which I shall have briefly to refer later on, while they 
opened up many new lines of research and left many 
points of fundamental importance unsettled, nevertheless 
appeared to establish one fact beyond doubt: the non- 
existence of oxaluria as an independent type of disease. 
Some years ago, however, Cantani1 again raised the stan- 
dard of oxaluria. On the basis of a number of clinical 
histories, the microscopic examination of the chemically 
prepared urine, and the effect of certain therapeutic 
measures, he elaborates an extremely plausible theory of 
the excretion of oxalic acid under normal and morbid 
conditions. 
His theory it briefly this: Under normal conditions 
mainly such oxalic acid appears in the urine as is directly 
introduced into the system with the food. Under ab- 
normal conditions the excreted oxalic acid may be de- 
rived from incomplete oxidation of the proteids ; of uric 
acid and—and this is, according to Cantani, the prin- 
ciple source of pathological oxaluria—from incomplete 
oxidation of the carbohydrates. He asserts that when 
the system has been overcrowded for a length of time 
with an excess of carbohydrates, the organs and tissues 
whose duty it is to gradually transform these substances 
into the ultimate products of oxidation—water and C02, 
become in a measure exhausted and are rendered incap- 
able of carrying oxidation further than the oxalic acid 
stage. An excess of oxalic acid, in the shape chiefly 
of oxalate of lime, is thus thrown into the blood and 
voided into the kidneys and urine, and morbid symptoms 
1 Specielle Pathlogie und Therapie der Stoffwechsel-krankheiten. 
Deutsch von Dr. Hahn, Bd. 11., Berlin, 1880. 4 
necessarily follow. That oxaluria does not follow in 
every instance of habitual abuse of carbohydrates, nor 
even in the majority of cases, is explained by Cantani on 
the assumption of individual predisposition, in which 
heredity, lesions of the digestive and nervous systems, 
corpulency, and indolent and pampered modes of living 
are leading factors. 
It is interesting to note the parallelism of this view of 
oxaluria with the same author’s theory of diabetes; the 
difference between the two diseases being mainly this, 
that in diabetes mellitus the exhausted tissues cannot 
tranform sugar at all, and it is voided as such; in oxalu- 
ria sufficient energy remains to transform the carbo- 
hydrates as far as the oxalic acid stage. 
Cantani himself has not infrequently found oxaluria a 
concomitant of diabetes, and, in several instances in the 
case of diabetic patients, oxaluria alternating with glyco- 
suria. Similar and very exact observations have been re- 
corded by Fiirbringer.1 
The symptoms of pathological oxaluria are, according 
to Cantani, manifold, but in their aggregation sufficiently 
characteristic to admit of certain diagnosis. First and 
foremost is the excess of oxalate of lime in the urine, 
when not due to direct ingestion of oxalic acid with the 
food. This excess Cantani estimates by the aid of the 
microscope, but does not determine it by exact quantita- 
tive analysis. In a number of instances he succeeded by 
a complicated procedure2 in obtaining oxalate of lime 
crystals from the blood serum. Prominent among other 
symptoms are those relating to the nervous system : men- 
tal depression, melancholia to the verge of suicide, ex- 
treme nervous irritability, impairment of memory and 
intellectual vigor, insomnia, sexual impotence, etc. Be- 
sides these and other nervous symptoms there are always 
disturbances of the vegetative functions. In almost all 
cases more or less rapid emaciation, loss of appetite, dys- 
peptic symptoms, such as eructations, flatulence, consti- 
1 Zur Lehre von Diabetes mellitus. Deutsches Archiv f. klin. 
Medicin, Bd. xvi., 1875. 2 Loc. cit., p. 8. 5 
pation, etc. In most of these cases there was dull pain 
in the back and in the region of the kidneys, and quite a 
number at various times passed oxalate gravel or calculi. 
The therapeutic measures consisted, in all cases, in the 
enforcement of an absolute milk and meat diet, with al- 
kaline waters as a drink. 
Under the influence of this diet which was maintained for 
weeks and even months, nearly all patients rapidly recov- 
ered. The oxalate disappeared from the blood and urine 
and did not reappear, when, in the course of time, a 
mixed diet was again permitted. With the disappearance 
of the oxalate in the urine the patients regained flesh and 
recovered their normal healthy functions of the digestive 
and nervous organs. Those few that were not entirely 
cured, either owing to remissness in diet or because they 
withdrew from observation, were, nevertheless, materially 
improved. 
It is not my object to enter into a detailed criticism of 
Cantani’s most interesting and suggestive work. Permit 
me only very briefly to state a few of the objections that 
can be advanced. 
In the first place, the absence of quantitative determina- 
tions leaves the whole superstructure of ingenious specu- 
lation without a solid foundation of facts comparable 
among themselves or with other similar ones. Further- 
more, none of the other important constituents of the 
urine, such as urea and uric acid, have, it would appear, 
been taken into account. And yet it seems that these 
also, especially in cases of emaciation and grave metabolic 
disturbance, should claim a most careful consideration. 
Again, the clinical histories are not sufficiently detailed 
and explicit, and might often be construed in quite a dif- 
ferent sense from that adopted by the author. The dem- 
onstration of a few oxalate crystals in the blood serum 
should be accounted a proof of pathological oxalsemia only 
after it has been established by numerous experiments that 
the like can never be found in healthy persons. Oxalate 
gravel and calculus can by itself not be accepted as proof 
of excess of oxalate in the urine, inasmuch as local tissue 6 
changes in kidney and bladder may cause local precipita- 
tion without absolute excess (Hoppe-Seyler), as is the 
case too with uric-acid calculus. 
Lastly, and most important of all, it appears to me that 
Cantani has failed to show that the grave disturbances, 
particularly in the functions of the nervous and digestive 
systems, are due to the excess of oxalic acid as a primary 
cause. It is quite possible that under certain conditions 
very serious changes can take place in the ordinary met- 
abolism of the system, as one of the results of which an 
excess of oxalic acid appears in the urine. That nervous 
disturbances or digestive lesions may possibly be the cause 
of these metabolic changes and the excess of oxalic acid 
an effect or only an incidental symptom, and perhaps an 
innocuous one, is by no means disproven. Nor is the 
effect claimed for the absolute meat and milk diet incom- 
patible with this latter hypothesis. It is in considering 
these questions that the want of quantitative determina- 
tion is most seriously appreciated. 
If now we endeavor to ascertain what is the actual 
knowledge we possess at present concerning the excretion 
of oxalic acid and the physiological data relating thereto 
at our command, we will find a rather unsatisfactory 
state of affairs. On very few even of the funda- 
mental points has unity of opinion been obtained, 
while the very large majority of questions pertaining 
to this subject are still enveloped in obscurity and 
doubt. It is certain that most plants and nearly all veg- 
etables used for food contain oxalic acid; some of the 
latter, like tomatoes, rhubarb, rumex, bananas, apples, 
spinach, carrots, etc., a comparatively large percentage. 
It seems tolerably certain also, especially through the ex- 
periments of Gaglio,1 that all or very nearly all the ox- 
alic acid thus taken into the system reappears again un- 
transformed in the urine, and some perhaps in the faeces, 
principally as oxalate. From this it follows that oxalic 
1 Ueber die Unveranderlichkeit der Kohlenoxyds und der Oxalsaure 
im thierischen Organismus. Archiv fur experimentelle Pathologic 
und Pharmacologic, Bd. xxii. 1886 and 1887. 7 
acid can and does occur in the urine of perfectly healthy 
persons, and that it may occur in quite large quantities 
if the diet is one rich in oxalic acid. Oq this point all 
authors are now agreed. 
Is oxalic acid a constant component of the normal 
urine, like urea and uric acid ? Is the oxalic acid in the 
urine due altogether to oxalic acid ingested, or are there 
chemical transformations and reactions normally going on 
which result in the production of certain, perhaps very 
minute, quantities of oxalic acid ? These questions have 
been much discussed, but still await a conclusive answer. 
The fact that oxaluric acid (C3H4N204) has been found 
in normal urine 1 and that Auerbach 2 found oxalic acid 
in traces in the urine of dogs that were fasting, would 
seem to indicate that oxalic acid may originate in the 
course of normal metabolism. Even the fundamental 
question, What are the normal quantitative limits of ox- 
alic acid excretion in the urine ? has not been satisfacto 
rily settled. Schultzen,3 working with a method of his 
own, found an average of o.i in twenty four hours. Fiir- 
bringer4 undertook a large and most laborious and exact 
series of analyses after Neubauer’s method. He found 
that, while the normal urine could contain mere traces, 
i. e., less than o.ooi pro die, the normal maximum should 
be placed at not more than 0.02. In a later investiga- 
tion in which he modified his method, Schultzen 5 estab- 
lished an average of from 0.02 to 0.07 as about normal. 
Salkowski6 found in a perfectly healthy man o. 144. Lat- 
terly the subject has again been investigated by Wesley 
Mills 7 who, after a careful comparison of the methods 
of Neubauer and Schultzen, finds the results after Neu- 
bauer’s method uniformly too small and the figures ob- 
tained according to Schultzen as approximately correct. 
1 Schunk, Journal f. prakt. Chemie, Bd. 100, p. 125. 
2 Zeitschr. f. Klin Medicin, Bd. ii. 
3 Reichert u. Du Bois-Reymond’s Archiv, 1868, pp. 719 and 720. 
4 Zur Oxalsaureausscheidung durch den Harn. 
6 Zeitschrift f. Analyt. Chemie, Bd. viii., p. 521. 
6 Virchow’s Archiv, Bd. lii., p- 64. 1871. 
7 Virchow’s Archiv, Bd. IC., 1885, p. 305 et seq. “ Ueber die Aus- 
scheidung der Oxalssaure durch den Harn.” 8 
As regards the other questions hinted at above, still less 
unanimity obtains among investigators. It has long been 
ascertained tfigt uric acid (C5H4N403) under the influ- 
ence of artificial oxidation, before finally being resolved 
into carbonic acid and water, will give as intermediate 
products urea (CON2H4) and oxalic acid (C2H204). 
This fact gave rise to the very plausible and at one time 
generally accepted theory that under pathological con- 
ditions oxalic acid in the urine resulted from incomplete 
oxidation of uric acid. In support of this theory Fre- 
richs and Wohler asserted that introduction of uric acid 
into the stomach was followed by increase of oxalic acid 
in the urine ; an assertion which the very careful experi- 
ments of Fiirbringer could not substantiate. As a nec- 
essary consequence of this theory it was claimed by many 
authors that an excess of oxalic acid in the urine is found 
in such diseases as are accompanied by disturbances of 
the respiratory system and increase of carbonic acid in 
the blood, and in which, therefore, the oxidations are sup- 
posed to be diminished. (Pneumonia, phthisis, emphy- 
sema, valvular lesions of the heart, etc., etc.) We shall 
see that careful analysis furnishes no basis for these as- 
sumptions. The fact that uric acid can be separated into 
urea and oxalic acid in the test-tube by no means proves 
that this ever actually occurs in the living body. It is 
not impossible that oxalic acid can be derived from pro- 
teids, so, according to Kiihne, from kreatine. On the 
other hand, the slow oxidation of sugar with uric acid 
can also produce oxalic acid, and Cantani, as we have 
seen, bases his entire theory on the assumed derivation of 
oxalic acid from the incomplete oxidation of the carbo- 
hydrates. The experiments bearing on these questions 
are comparatively very few and altogether unsatisfactory. 
So, for instance, while Burggrave, on the one hand, finds 
no oxalic acid whatever in the urine of dogs fed exclu- 
sively on meat, and sees the oxalic acid appear on the 
addition of even minute quantities of sugar to the meat, 
Wesley Mills, on the other hand, finds most oxalic acid 
(n.i milligr. on the average) when the dogs are fed Number. I 
Name, disease, etc. 
Date. 
Quantity of 
urine in 24 
hours. 
Specific 
gravity. 
Reaction and 
acidity. 
Microscopic 
examination. 
Urea. 
Uric acid. j 
Relation of 
uric acid 
to urea. 
Oxalic acid. 
Phosphoric 
acid. 
Chlorides. 
Albumin. 
Sugar. 
Remarks. 
Mr, N. H., age 63 
years ; melancholia. 
Sept. 30, 
1889. 
1.024 
Urates and triple 
phosphates. 
I 
etc. 
Jan. 15, 
1890. 
March 5, 
1890. 
• 
. 1 1 1 
30 = 2.5 
r» 
2 
Mr. N. H., age 63 
years; melancholia, 
etc. 
Mr. N. H., age 63 
years; melancholia, 
1,200 
1.028 
Strongly acid, 
3-iS- 
numerous. 
Indican. 
3 
etc. 
April 5, 
1890. 
Sept. 30, 
1889. 
Oct. 14, 
1889. 
Nov. 4, 
1889. 
Nov. 27, 
1889. 
Dec. 20, 
1889. 
Jan. 17, 
1890. 
Nov. 6, 
1889. 
Sept. 16, 
1889. 
Very acid, 3.9. 
Oxalate crystals... 
32.5 = 2.6 % 
26.4 = 2.2 % 
1 : 29^ 
4 
Mr. N. H., age 63 
years; melancholia, 
etc. 
Mr. B., age 26 years; 
neurasthenia. 
1.25° 
1.022 
5 
1,200 
1.028 
Very acid, 5 .. 
Acid, 2.89 .... 
Large and numer- 
ous oxalate crys- 
tals. 
Oxalate crystals... 
1 ; 66 
O.46 
O.063 
6 
Mr. B., age 26 years; 
neurasthenia. 
!,37° 
7 
Mr. B., age 26 years; 
neurasthenia. 
Mr. B., age 26 years; 
neurasthenia. 
Mr. B., age 26 years 
neurasthenia. 
1,000 
I.O3O 
1.026 
43.2 = 3.6$ 
32,4 = 2.7 g 
8 
1,200 
1 : 67 
0.056 
9 
1.026 
Acid, 2.9 
Acid, 2.5 
Slightly acid.. 
Strongly acid, 
. 4-'?- 
IO 
Mr. B., age 26 years; 
neurasthenia. 
1,450 
19.8 = 2.2 % 
None. 
Indican in- 
II 
Mr. B. C., age 52 years ; 
neurasthenia. 
900 
1.020 
Urates ; no oxa- 
lates. 
creased. 
12 
Mr. B. C., age 52 years; 
neurasthenia. 
1,190 
1.020 
0.06 
13 
Mr. S., age 25 years; 
neurasthenia. 
l*eb. 11, 
1890. 
Feb. 19, 
1891. 
Dec. 16, 
1889. 
2,400 
I.O24 
lates. 
40.5 = 3 
14 
Dr. T„ age 47 years; 
melancholia. 
1.350 
IS 
Mrs. R. M., age 28 
years; anaemia ; neu- 
rasthenia. 
750 
1.030 
Strongly acid, 
3-8. 
Slightly acid, 
1.8. 
Strongly acid, 
. 4G 
few and small. 
Uric acid crystals. 
Small oxalate crys- 
tals. 
35-3 
24 = 3 $ 
0.25 
16 
Mr. O. T., age 32 
years ; neurasthenia; 
hypochondriasis. 
Nov. 14, 
1892. 
1,260 
1.023 
0.016 
17 
Mr. M. A. J., age 48 
years; tabes dorsalis. 
Jan. 27, 
1890. 
8co 
1.026 
18 
Mrs. G. M., age 60 
years; gouty diathesis. 
Mrs. G. M., age 60 
years; gouty diathesis. 
l>ec. 7, 
1889. 
Oct. s> 
1890. 
April 10, 
1890. 
1,465 
1,600 
1.021 
0.8 
i9 
, 
20 
Mrs. G. M., age 60 
years: gouty diathesis. 
1.550 
1.022 
Acid, 3.7 . ... 
Slightly acid, 
3- 
Slightly acid, 
1.8 
Hardly sediment.. 
53.2 = 3.8 % 
Only 
trace. 
Indican in- 
21 
K., German Hospital; 
typhoid fever. 
Nov. 6, 
1889. 
1,400 
1.024 
i-33 
creased. 
22 
23 
K., German Hospital; 
typhoid fever. 
Nov. 15, 
1889. 
1,200 
1.018 
K. (male), German 
Hospital; phthisis 
pulmon. 
Nov. 29, 
1889. 
Feb. 9, 
1890. 
March 12, 
1890. 
Feb. 20, 
1890. 
March 13, 
1890. 
950 
1.021 
I.Ol8 
1.026 
18.9 = 2.1 % 
0.028 
24 
W. (female), German 
Hospital; phthisis 
pulmon. 
900 
600 
o.S4 
0.9 
Trace. 
25 
W. (female), age 12 
years, German Hos- 
pital ; pleuro - pneu - 
monia; endocarditis. 
24.8 — 1.6 % 
26 
N., German Hos- 
pital ; carcinoma 
hepatis. 
1. SSo 
Indican in- 
27 
Mr. A., age 72 years; 
carcinoma flexurm sig- 
moideee. 
!,I7° 
Slightly acid, 
0.36. 
14.9 = 1.3 i 
35.2 = 2.2 % 
17.5 = 1.4 % 
So 
42 = 3 $ 
Mere 
trace. 
0.29 
Trace. 
creased. 
28 E. (female), German 
j Hospital; cat. gastric, 
chron. 
March 3, 
1890. 
1,150 
1,600 
I.Oil 
1.016 
. 
29 
Mrs. J. E. A., age 38 
years; healthy, occa- 
sional renal colic. 
Jan. 4, 
1890. 
Pus; no crystals.. 
trace. 
30 
Mrs. W., age 85 years ; 
cystitis : pyelitis. 
Nov. 6, 
1889. 
Oct. 6, 
1890. 
1,250 
1.010 
3i 
Mr. H. A. S., age 35 
years; healthy, ure- 
thritis. 
1,775 
i : 30 
S2 
Mr. H. A. S., age 35 
years; healthy, ure- 
Oct. 13, 
1890. 
1,400 
1.030 
Acid, 2.5 
Acid, 3.7S 
No crystals 
Uric acid crystals. 
2.9 
x-S 
33 
Mr. H. A. S„ age 35 
years; healthy, ure- 
thritis. 
Dec. 1,. 
1890. 
1,500 
1,028 
3i-5 
43.2 = 3.6$ 
1 : 28.8 
0.080 
0 060 
Indican in- 
34 
Mr. O. M., age 45 years ; 
cat. intest chron. 
Oct. 20, 
1889. 
Dec. 2, 
1889. 
1,200 
1.022 
creased. 
No i n d i- 
35 
Mr. O. M., age 45 years ; 
cat. intest. chron. 
1,15° 
Acid, 1.4 
Phosphate crystals. 
48 = 2.4 %.. 
2 8 
can. 
36 
Dr. K„ age 45 years; 
renal hemorrhage occa- 
sionally. 
Oct. 28, 
1890. 
2,000 
1.022 9 
exclusively on meat, less (5.4 miliigr.) when fed on 
meat and increasing quantities of bread. Ido not pro- 
pose to enter here into chemical and physiological de- 
tails, nor to attempt to unravel the contradictions and 
obscurities with which all these fundamental questions 
are beset. I desire simply to ascertain whether, on the 
basis of careful quantitative analyses, any relations can be 
established between certain forms of disease, particularly 
of the nervous system, and the excretion of oxalic acid in 
the urine. My most sincere thanks are due to Dr. E. 
Rosenberg, of this city, to whose skill and scientific enthu- 
siasm I am indebted for all the analyses made use of in 
this investigation. The method we employed was that 
of Schultzen.1 In all cases the twenty-four hours’ quantity 
was examined. In the majority of cases the acidity was 
determined by titration with yL- normal alkali solution, and 
expressed in grammes of oxalic acid for the entire quan- 
tity. Nearly always a careful microscopical examination 
was made. In all cases the urea and uric acid were deter- 
mined, besides oxalic acid. Every urine was examined 
for albumin and sugar, and in a number of instances 
phosphoric acid and the chlorides were also determined 
(see Table of Analyses). 
We will now briefly review the cases and consider in 
the first place the nervous disturbances. 
Mr. N. H (Table, Nos. 1, 2, 3, 4), about sixty- 
three years of age, when first seen by me complained of 
great nervous depression, increasing frequently to par- 
oxysms of downright melancholia; sleeplessness, occa- 
sional rheumatic pains in the back and limbs, various 
dyspeptic symptoms, such as loss of appetite, eructation 
and distress after meals, constipation, loss of weight. A 
brother of Mr. H had died of general paresis, and 
the haunting dread of brain disease irresistibly overpow- 
ered our patient in his spells of depression. Though al- 
ways “nervous,” he had never had any serious physical 
1 Loc. cit., and E. Rosenberg, Quantitative Bestimmung der Oxal- 
saure im Harn. N. Y. Medicinische Monatsschrift, Bd. iii., 1891, p. 
484. illness. Syphilis was denied absolutely. He had always 
been a lover of the good things of the table and fond of 
sweets and many vegetables. He never drank to excess, 
but was fond of champagne and good wines with his 
meals. Repeated and careful examination failed to de- 
tect any evidence of organic lesion of any kind. His 
urine was rather concentrated, acid, free from albumin 
and sugar, but showed under the microscope numerous 
large and small oxalate of lime crystals. Here, then, was 
a case in all essential respects identical with the cases re- 
ported by Cantani as pathological oxaluria, and it was 
determined to investigate it analytically. The first an- 
alysis showed only 900 c.c. for twenty-four hours’ quan- 
tity, specific gravity of 1.024, acid reaction, a sediment 
consisting of urates and triple phosphates, 30 grammes of 
urea and 0.135 °f oxalic acid. It is possible that, owing 
to some mishaps in the manipulation, the figures for the 
oxalic acid may have turned out too large ; nevertheless 
there was a decided excess, and I am willing, for the sake 
of further discussion, to accept the figures as correct. 
The patient was put on Cantani’s diet; sweets, vegetables, 
and amylaceous matter were strictly prohibited, and in- 
stead of wines he drank alkaline waters. Nevertheless 
the patient did not improve until ordered away from the 
city, when he rapidly regained spirits and sleep. On 
January 15, 1890, the urine was 1,200 ctgms. for twenty- 
four hours, specific gravity 1.024, acid 2.5, showed under 
the microscope numerous octahedra, urea three per cent.; 
uric acid, 0.6; oxalic acid, 0.05. This amount comes 
well within Schultzen’s normal limits. The patient felt 
well and had not kept very strictly to his diet. About six 
weeks later Mr. H had one of the worst paroxysms 
of melancholia that he ever passed through. All the 
symptoms above detailed were exaggerated to the utmost, 
and well-marked suicidal tendencies were noted. An 
analysis made during that time showed only 0.01 of 
oxalic acid, but a decided increase in the urea. A still 
later analysis, after the paroxysm had passed and Mr. 
H was feeling tolerably well, showed 0.035 °f oxalic acid, but a very marked increase (i.i) of uric acid. 
These figures evidently give no basis to the assumption 
of a direct connection between the excretion of oxalic 
acid and the nervous symptoms in this case. We evi- 
dently have here a case of general neurasthenia with hy- 
pochondriacal and melancholic paroxysms based perhaps 
on slight hereditary taint. That certain morbid meta- 
bolic changes were going on is shown by the urea and 
uric acid determinations. Nevertheless the quantities of 
oxalic acid, with the exception of the first analysis, kept 
well within the normal, though, if the microscope had been 
relied on, an excess would no doubt have been assumed. 
Let me add that for the last two years the patient has 
been abroad, and that, while attention is no longer paid 
to the oxalic acid in the urine, he has been very bene- 
ficially influenced by absence from business and the 
diversion of travelling. Though, at rare intervals, still 
slightly nervous, he has gained in weight, enjoys himself 
thoroughly, and considers himself a healthy man. 
Mr. B , aged twenty-six. Loss of appetite, loss of 
sleep, distress after meals, all sorts of rheumatoid pains, 
particularly in the back and in the loins, emaciation, 
mental depression, loss of intellectual vigor and of sex- 
ual desire, general debility. Has complained of these 
symptoms for several years; no syphilis, no organic lesion 
of any kind. (Table, Nos. 5, 6, 7, 8, 9, and 10.) The 
first analysis gave 0.422 oxalic acid in 1,200 c.c. This 
amount is manifestly too large, owing to an accident in 
the manipulations. The second analysis again showed o. 46 
oxalic acid. This may be also too high a figure, but we 
will assume a very decided excess of oxalic acid, especi- 
ally as the urine was very acid (5), and showed large and 
numerous oxalate octahedra under the microscope. Par- 
ticular attention is called to the amount of urea, which in 
this analysis was 46.5. The patient was put on a diet that 
had no special reference to oxalic acid. He was permit- 
ted to eat certain kinds of farinaceous food and vegetables. 
In the next analysis the oxalic acid amounted to 0.063, 
while the urea was forty per cent., equal to four per cent. 12 
of the day’s quantity. The next analysis gave only 0.012 
of oxalic acid, and 3.6 per cent, of urea. A month later 
oxalic acid had risen again to 0.056, while urea had come 
down to 2.7 per cent. Four weeks later again, oxalic 
acid was none; urea, 2.8 percent.; uric acid, 1.0. Dur- 
ing all this time the condition of the patient was about 
the same, sometimes a little better, sometimes a little 
worse, but manifestly independent of the variation in the 
amount of oxalic acid. It was a clear case of general 
neurasthenia and hypochondriasis with nervous gastro- 
intestinal disturbances. The morbid metabolism in this 
case is undoubtedly to be measured by the increase in 
urea and uric acid, and has no relation to the oxalic acid. 
In this case, too, dependence on the microscope alone 
would have led to the assumption of an excess of oxalate, 
where analysis showed normal quantities. 
Mr. B. C (Table, Nos. 11 and 12), aged fifty-two. 
Neurasthenia of many years’ standing, without any or- 
ganic lesion. Shows symptoms more especially of cere- 
bral and spinal neurasthenia, vertigo, pains in limbs, 
pains in back, loss of sexual power, muscular weakness, 
together with gastro-intestinal symptoms, such as loss of 
appetite, distress after eating, diarrhoea alternating with 
constipation, etc. Flis diet consists principally of meat 
and milk food, and small quantities of farinaceous sub- 
stances. The first analysis gave no oxalic acid, but indi- 
can abnormally increased, the second analysis, 0.03 of 
oxalic acid. 
Mr. St (Table, No. 13). Neurasthenia mainly of 
cerebral type. Frequent headaches. Intellectual apathy, 
impairment of memory, great mental depression. No 
evidence whatsoever of organic disease. One analysis, 
specific gravity, 1.024, strongly acid (4.8). Microscope 
shows urates and oxalates. Urea, 2.8 per cent. ; uric 
acid, 1.7; oxalic acid, 0.06. 
Dr. T (Table, No. 14), aged forty-seven. Or- 
ganically perfectly sound. Periodic melancholia of very 
severe type. The attacks sometimes last many months, 
during which the patient is tortured by almost irresistible suicidal impulses. In this condition, insomnia, general 
debility, loss of appetite, and emaciation. One analysis, 
during acme of a paroxysm. Urine strongly acid (0.3), 
three per cent, of urea, only 0.3 uric acid, and 0.017 ox- 
alic acid. 
Mrs. R. M , aged twenty-eight (Table, No. 15). 
General anaemia with well-marked hysterical tendencies ; 
no organic lesion. Microscope shows small oxalate crys- 
tals ; oxalic acid, 0.011. 
Mr. O. T , aged thirty-two (Table, No. x 6). Ner- 
vous dyspepsia and diarrhoea ; well-marked agoraphobia; 
rapid emaciation ; no organic lesion ; mixed diet; acid- 
ity, 3.8 ; urea, 35.3 per cent. ; oxalic acid, 0.008. 
Mr. M. A. J , aged forty-nine (Table, No. 17). 
Tabes dorsalis of ten years’ standing, with frequent gas- 
tric crises ; acidity, 1.8 ; urea, three per cent.; uric acid, 
0.59. Microscope shows numerous small oxalate octahe- 
dra. Oxalic acid, 0.016. 
In all these cases it is shown that the oxalic acid, 
whether increased, whether within normal limits, or even 
if diminished, had no demonstrable influence on the 
course of the disease, and that emaciation or other meta- 
bolic disturbances can be accounted for by tissue waste 
as measured by the excretion of urea and uric acid. 
Besides these cases of nervous disturbance, analyses 
were obtained of the urine of perfectly healthy persons, 
as well as of such suffering from various acute and chronic 
diseases, with the view of studying oxalic-acid excretion 
under varied conditions. I will not enter upon all of 
them in detail, as they can be found in the annexed 
table. I wall single out only a few of the more impor- 
tant ones. As much has been said concerning the rela- 
tions of oxaluria to gout, it will be interesting to note the 
case of Mrs. G. M , aged sixty (Table, Nos. 18, 19, 
and 20), a very corpulent lady, with well-marked gouty 
diathesis. During the year in which the analyses were 
obtained, her diet consisted of a limited quantity of meat, 
small quantities of amylaceous food, no sweets, no pastry, 
a moderate amount of vegetables and fruit, and alkaline drinks. She took also a nightly dose of rhubarb, accord- 
ing to her custom for many years. The analyses show a 
marked increase in the quantity of uric acid, but only 
very small quantities of oxalic acid (0.015, 0.017, 0.019), 
certainly referable in this case only to oxalic acid in- 
gested with food and rhubarb. 
Two analyses from a hospital case of typhoid fever 
(Table, Nos. 21 and 22), the first at a time when the 
temperatures were decreasing, but before they had 
reached the normal; the second during convalescence. 
The diet at the time of the first analysis consisted only of 
milk and gruel. The oxalic acid Avas none, but a marked 
increase of uric acid and urea appeared. At the time of 
the second analysis the diet was somewhat more liberal, 
as the fever had meanwhile disappeared. Oxalic acid, 
0.012, and a decrease both in uric acid and urea. 
Two cases of phthisis pulmonum, one male, one fe- 
male, both with moderate fever (Table, Nos. 23 and 24). 
In one oxalic acid, 0.019 1 in the other, 0.028. These 
figures are in marked opposition to the theory Avhich de- 
rives oxalic acid from incomplete oxidation, and confirm 
the results already obtained by Fiirbringer and others. 
A case of a child, twelve years of age, suffering from 
pleuro-pneumonia and valvular disease of the heart (Table, 
No. 25). Analysis was made at a time when febrile symp- 
toms had disappeared and the little patient had begun to 
eat solids. He was, however, still distinctly cyanotic. 
Oxalic acid, 0.025, a result Avhich tends to confirm the 
statements made in the preceding case. 
A case of a Avoman suffering from chronic gastric ca- 
tarrh Avith hyperacidity, on absolutely liquid diet (Table, 
No. 28). Oxalic acid, none. 
Cancer of the liver (Table, No. 26). Moderate ca- 
chexia and very little appetite. Oxalic acid, 0.007. 
Mr. A , aged (Table, No. 27). Can- 
cer of sigmoid flexure; anus praeternaturalis ; cachexia. 
Principally milk diet, but eats some farinaceous and vege- 
table food; increase of urea (three per cent.) and of 
indican ; oxalic acid, 0.018. 15 
Mr. H. A aged thirty-five (Table, Nos. 31, 32, 
and .33). Strong and healthy man; has old chronic 
urethritis and prostatitis, in consequence of which from 
time to time gritty white masses, consisting principally 
of urates, are discharged at the beginning of mictur- 
ition. 
The analyses were made chiefly with a view of deter- 
mining whether the local lesions favored a precipitate ot 
oxalate. The uric acid was found very markedly in- 
creased, the oxalic acid, if anything, rather subnormal 
(0.001, 0.021, 0.0075). 
Mrs. W , aged eighty-five (Table, No. 30). 
Chronic cystitis and pyelitis : lives almost exclusively on 
bread, milk, and meat; urine neutral, contains pus. No 
oxalic acid. 
I am well aware that these observations are too few in 
number, and too defective in many respects, to serve as a 
basis for definite and authoritative general conclusions. 
The subject is an intensely difficult one, and our knowl- 
edge of even its elementary chemical and physiological 
bearings still very uncertain. Only long-continued and 
patient analytical and experimental work can ultimately 
furnish the data for a future physiology and pathology of 
oxalic acid in the human organism. While not pretend- 
ing to solve any of the problems connected with this sub- 
ject, it seems to me, nevertheless, that from the forego- 
ing analyses and observations, as well as from the work of 
other observers and experimenters, the following conclu- 
sions may be provisionally deduced : 
1. Oxalic acid is a normal, though possibly not a con- 
stant, constituent of the urine. 
2. The amount present in a given quantity of urine 
can be determined with any degree of reliability only by 
quantitative analysis. All approximations by means of 
microscopic examination are untrustworthy. 
3. The chief source of oxalic acid in the urine is the 
oxalic acid contained in the food, though it is probable 
that minute quantities are produced in the course of nor- 
mal metabolism. Further investigation will have to 16 
demonstrate if, and under what conditions, morbid met- 
abolism affects the production of oxalic acid. 
4. Impeded respiration, diseases of the heart and lungs, 
do not of themselves tend to produce an excess of oxalic 
acid in the urine. 
5. The establishment of pathological oxaluria as a type 
of disease sui generis is not warranted by the facts at 
present at our command. 
6. The nerve symptoms assumed as characteristic of 
pathological oxaluria are not caused by an excess of oxalic 
acid in the blood and in the urine. Analysis will show 
that such excess is by no means as frequent as has often 
been assumed. 
7. Where such excess does occur not to be accounted 
for by ingesta, it is probably one of several symptoms of 
metabolic alterations primarily caused by disturbances of 
the nervous or digestive organs, or both, but no factor in 
the causation of disease. 
8. In considering the excretion of oxalic acid in the 
urine it is of the utmost importance to take into account 
at the same time the excretion of the other principal 
constituents, particularly urea and uric acid.