A CONTRIBUTION TO THE STUDY OF 
CYSTIC KIDNEY. 
MY 
LUDVIG HEKTOEN, M.D. 
Reprinted from the Chicago M w»ia i, Recokdke, September, 1892} Jf 
PRESS OF 
THE M. H. KAUFFMANN MEDICAL PUBLISHING COMPANY, 
340-344 DEARBORN ST., CHICAGO. A CONTRIBUTION TO THE STUDY OF CYSTIC KIDNEY. 
LUDVIG HEKTOEN, M.D., Chicago 
The development of cystic kidney is still in many instances 
obscure, although it has been made the subject of much study, many 
explanations and theoretical considerations. Individual instances of 
cystic kidney should always be accurately described and studied so 
that sufficient reliable and well prepared material can be accumulated 
from which general deductions could be correctly drawn. 
As the matter now stands cysts occurring in the kidney may be 
divided into the following varieties, for the purpose of orientation: 
1. Small cysts found in the kidney of chronic interstitial inflam- 
mation and arterio-sclerotic atrophy; these cysts are usually situated 
in the cortex and are caused by dilatation of the tubules or glomerular 
capsules on account of compression and obstruction by fibrous tissue. 
They are not often larger than a big pea. Their contents may consist 
of retained urine changed by resorption, colloid material from the 
degeneration of the epithelial lining, blood from hemorrhage into the 
cavity of the cyst, and these various substances may be present singly 
or combined, unchanged or, usually, degenerated, giving us variety in 
color, in consistence, and in microscopic findings. The characteristic 
epithelial lining may be absent from the larger cysts. 
2. Sometimes there is found in an otherwise perfectly healthy 
kidney a single cyst which may be of the capacity of several litres, 
projecting prominently from the surface of the organ, or, more fre- 
quently, much smaller and then situated either in the cortex or in the 
medulla; the origin of these cysts is exceedingly difficult to explain; 
they are obviously retention cysts, and yet the absence of any inflam- 
matory changes in the kidney renders the assignment of any definite 
cause for the obstruction impossible.1 
1 Orth. Lehrb. der speciellen Path. Anat., iv. Lief, Berlin, 1889, p. 141. 
3 4 
3. In the cystic kidney proper—the total cystic degeneration of 
the kidneys of the Germans and the gros rein polykystique of the 
French—the entire renal substance, cortex as well as medulla, is 
crowded with cysts which may be quite large and very small; no 
distinction between cortical and medullary portions can be pointed out 
in the very much enlarged kidney. The fluid contents vary much in 
color, depending on the quantity of pigment, blood, fat, cholestearin, 
etc., present; chemically the fluid usually contains urea, uric acid, 
oxalate of lime, albumen and other urinary constituents. Micro- 
scopically it is shown that the cyst wall is lined with epithelial cells 
which often are absent in part or totally in the large cysts; the inter- 
cystic tissue is, as a rule, the seat of an advanced chronic interstitial 
inflammation, but it may contain some quite normal renal parenchyma. 
Cystic kidney may be unilateral, but oftenest bilateral. It is spoken 
of as congenital when found in the newborn, in which it may be so 
voluminous as to constitute a serious obstruction to birth, or death may 
ensue soon after birth from diaphragmatic impediment, or from renal 
insufficiency. On the other hand, life may be continued for an indefinite 
number of years, the cystic kidney remaining latent, the amount of 
useful renal parenchyma being sufficient to carry on the renal function 
until gradually advancing interstitial changes, to which the overworked 
remnants of tissue are predisposed, cause death by ursemia. It is quite 
plain that the duration of life under these circumstances will depend 
upon the amount of normal kidney tissue present, and whether the 
cystic kidney is unilateral or bilateral. All writers suggest the 
theoretical possibility of congenital cystic changes persisting into 
middle, or past middle life, and that a considerable number of cystic 
kidneys in the adult date from birth. The cystic kidney of the adult 
and old, sometimes spoken of as acquired, resembles in all essentials 
the congenital, both as to the composition of the cystic fluid and as to 
the histological structure of the cyst wall and the extra-cystic paren- 
chyma which, however, is almost invariably the seat of chronic inter- 
stitial inflammation. 
Of sixty-three instances of cystic kidney in the old, collected from 
medical literature by Lejars/ there were in seventeen cases cysts in the 
liver as well. The relative frequency of contemporaneous cysts in 
these two organs is so marked that intra-uterine conditions must be 
looked to for the explanation. It is, of course, true that in many cases 
the occurrence of kidney and liver cysts in the same person is, so to 
say, accidental, the hepatic and renal cysts both being easily explained 
as due to demonstrable local and special causes. 
In order to throw all light possible upon the question of etiology 
2 Lejars, Du gros rein polykystique de I’adulte, 1889. 5 
and development it will be well to briefly consider the various theories 
suggested from time to time as explaining the growth of cystic kidney. 
A review of the more recent contributions to the literature on this 
subject at once demonstrates that the explanations offered by the 
students of the genesis of cystic kidney naturally divide themselves 
into three sets, namely, the retention, the cyst-adenomatous, and the 
teratological theories. 
1. The theory of retention and dilatation, resulting in the forma- 
tion of cysts, is based upon the study of a number of cases of cystic 
kidney in the old as well as in the newborn, in which there was actu- 
ally demonstrated various causes of obstruction in the uriniferous 
tubules at the papillae or elsewhere in their course. Mere mention of the 
various possible modes of obstruction suggested, but not demonstrated, 
will be enough; occlusion by the impaction of fibrinous casts, des- 
quamated epithelium, blood, precipitated salts, etc. Virchow3 assumes 
a papillary atresia or stenosis due to a foetal inflammation in order to 
explain the congenital cystic kidney. Durlach4 describes an instance 
in an infant six months old, with large cystic kidneys, the pelvis of 
which were the seat of a fibrous pyelitis; thick bands of connective 
tissue passed taperingly up through the columns of Bertini to the sur- 
face of the kidney; in the lateral portions of the pyramids was consid- 
erable formation of connective tissue and here the development of 
characteristic retention cysts was beautifully shown. 
Complete obliteration or absence of the pelvis is mentioned by 
Thorn0, Sutton0 and others as capable of causing cystic kidney. Thorn 
describes a kidney removed by Bardenheuer from a man forty-five 
years old, in which there was a nodular, fibrous pyelitis which attacked 
by continuity the lateral aspects of the pyramids where there were 
found many cysts while the central parts of the pyramids were healthy. 
There were many cysts in the cortex also, but the tissue between the 
cysts was healthy. Leichtenstern7 describes a bilateral cystic kidney 
from a woman forty-eight years old, and selects the name nephro- 
papillitis fibrosa obliterans as descriptive of the lesion demonstrated 
as the cause of the degeneration; he assumes that the inflammation 
originated in the coats of the arterise rectse and then passed out among 
the papillary ducts causing stenosis and retention cysts. Arnold8 
3 Wurzburger Yerhandlungen, V. p. 461 and Gesammelte Abhandlungen, 
p. 139-64. 
4 Ueber Entstehnng der Cystenniese, 1885. 
5 Beitrag zur Genese der Cystenneisen, 1882. 
6 Sutton, London Lancet, 1887, I. p. 254. 
7 Deutsche med. Wochenschrift, 1884, No. 51. 
Ziegler’s Beitrage, viii, p. 521. 6 
describes an ascending pyelo-papillitis. Ewald9 in briefly reviewing 
the literature on the etiology states that many authors believe that 
chronic interstitial nephritis with desquamation and impaction of epi- 
thelial cells or strangulation of the tubules by connective tissue may 
cause cystic kidneys in some cases; the peculiarities which would deter- 
mine the instances in which total cystic degeneration and not merely 
small cortical cysts should take place are not described. He assumes 
that in the case described by himself, of a woman, sixty-eight years old, 
with double polycystic kidney, precipitation of uric acid within the 
tubules resulted in obstruction and cystic dilatation, because he found 
in the cysts calculi with uric acid nuclei; he considered the interstitial 
changes in this case as secondary. Mackenzie10 reports a case of a 
woman, sixty-nine years old, with slight double cystic degeneration; in 
one kidney the cysts contained calculi, in the other there were no 
stones; he does not consequently place the calculi in any causative 
relation to the cysts. Smith11 cites Commandeur’s12 case as one of 
secondary origin to calculous pyelitis. Lastly it may be stated that 
the vast majority of cystic kidneys in the old are reported as instances 
of cystic degeneration accompanying chronic instertitial changes, the 
relation of the one to the other being left an open question. 
2. The cyst-adenomatous theory is based upon the demonstration in 
cases of cystic kidney of the appearances characteristic of adenomata. 
In these cases the chronic interstitial changes are usually held to be 
secondary, although Sabourin13 concludes his study as follows: Renal 
cysts in cirrhosis develop from tubules, whose epithelium is reduced to 
an indifferent state; by fusion cysts are formed, which merit the name 
of adenoma. Hommey,14 Lejars,15 Cornil et Brault,16 Brigidi and Sevin,17 
Phillippson18 adopt the same view. Orth10 calls attention to the fact 
that in those cases in which the epithelium of the uriniferous 
tubules is proliferating, and lateral projections form the process 
is undoubtedly allied to cyst-adenomatous changes. Phillippson 
saw papillary excresences in the interior of the cysts and solid 
outgrowths from the uriniferous tubules. The classical adenomas 
of the kidney are, I believe, usually solid tumors, no matter 
9 Berliner kl. Wochenschr, 1892, No. 1, p. 7, and Deutsch. Id. Wchnschsf., ’9l, 
No. 51, p. 1883. 
lu Trans. London Path. Society, xxxix. 
11 SajOtis’ Annual, 1892, Yol. I, L. 63. 
12 Revue pratique d’obstetrique et d’hygihne de I’enfance, Apr. 5, 1891. 
13 Contribution a I’etude de lo degenerescence kystique des rein.set du foie. 
14 Contribution a I’etude anatomique des kystes du rein, 1886. 
15 Loc. cit. 
16 Etudes sur la pathologic des reins. 
17 Lo sperimentale, 1886. 
18 Yichow’s Arohiv. Mr Path. Anat. etc., 111, page 510, 1889. 
19 Lehrb. der Path. Anat., Lief. IY, Berlin, 1889, p. 114. 7 
what variety it may concern. In the majority of instances of 
cystic kidney it appears that the epithelium is entirely passive; in 
adenomatous cysts it would, of course, be active and proliferating, and 
unless this is demonstrated there seems to be no other criterion by 
means of which the nature of the process could be established as cyst- 
adenomatous. 
3. Theoretically, the kidney should be the organ of all others, 
able to furnish instances of the teratoid origin of tumors from per- 
sistent embryonic rudiments, but few renal growths have been 
regarded from this point of view.20 S. G. Shattock21 concludes that 
the congenital cystic kidney is formed by a combination of the meso- 
and meta-nephros, the remnants of the Wolffian body developing 
into cysts scattered through the proper renal tissue; the tension upon 
the intertubular tissue by the enlarging cysts might cause the inter- 
stitial changes; the presence of urinary constituents in the cysts does 
not mean according to Shattock that they originate from the kidney 
proper, because the meso-nephros in the fishes and the amphibia per- 
form the function of the permanent mammalian kidney. Bland 
Sutton22 adopts and advances this view enthusiastically. He says the 
microscopical appearances of a congenital cystic kidney and of the 
meso-nephros at its fullest development, the sixth week, agree 
completely. 
Sutton23 believes that congenital cystic kidney, cystic testicle and 
parophoron cysts are identical, developmentally, structurally and in 
their pathology. It is proper to state in connection with this that in 
many cases of congenital cysts in the kidney other anomalies in develop- 
ment have been found as, for instance, hydrocephalus and hydren- 
cephalocele; horse-shoe or misplaced kidney with congenital cystic 
change; kidneys without any pelves or ureters; absence of the female 
genital organs in cases of unilateral cystic kidney. Cases are recorded 
of the same mother giving birth in succession or interruptedly to 
several children with cystic kidney.21 The simultaneous occurrence of 
cysts in the kidney and in the liver not explainable by local conditions 
in each organ would naturally be referred, as stated, to intra-uterine 
conditions in order to account for their origin. This view of Shattock 
and Sutton is certainly quite fascinating. It is plain however that in 
the cystic kidney of the old the histological structure in the majority 
of instances permits no definite conclusion with reference to the possi- 
20 Bell and Johnston, Montreal Medical Journal, February, 1891. 
21 London Pathological Society’s Transactions, xxxvii, 1886, p. 287. 
22 London Lancet, 1887, I, page 254 and Gen. Pathology, 1886, 176. 
23 Loc. Cit. 
24 Orth. Loc. Cit. 8 
ble congenital origin of the cysts in persistent meso-nephrotic rem- 
nants, because of the advanced changes in the tissue between the cysts 
and the usual absence of the epithelial lining in the larger cavities. 
This theory is not mentioned by Ewald.2IJ 
Conclusions: 1. The common cystic kidney in the old is best 
explained as due to retention caused by a chronic interstitial inflam- 
mation of the pyramids, and the medullary rays especially, as well as 
of the labyrinthine structure of the cortex. The epithelial lining of 
the cysts is entirely passive and often absent. There is no epithelial 
proliferation and new cyst formation demonstrable. A congenital or 
adenomatous origin for the cysts can only be inferred and not demon- 
strated. 
The etiology of the chronic inflammation is obscure in many 
cases; in others it may be referred to an ascending pyelo-papillitis 
from calculi or to the same causes that produce the ordinary chronic 
interstitial nephritis. 
2. Cystic kidneys presenting a proliferating epithelial lining with 
evidences of new cyst formation by budding from the old cysts or from 
uniferous tubules are plainly instances of renal cyst-adenomata. 
Reasoning by analogy from other organs in the body, occasionally 
the seat of cystic adenomta, it would be expected that this variety of 
cystic kidney would most frequently be unilateral. 
3. Congenital cystic kidney, without any demonstrable cause for 
obstruction and urinary retention in the tubules and presenting the 
structure characteristic of the meso-nephros, as described by Shattock 
and Sutton, is most reasonably to be regarded as coming from mis- 
placed meso-nephrotic remnants. To look upon all cystic kidneys as 
congenital cannot be considered proper in view of the instances cited 
of cysts developing directly as the result of compression of the tubules 
and the papillae by fibrous tissue, and cystic adenoma of the kidney 
can occur at any time of life. 
As a typical instance of cystic kidney in the adult I beg to 
describe the following case: 
Unknown woman, about fifty, found in uraemic condition, autopsy 
showing bilateral large cystic kidney due to a universal chronic inter- 
stitial inflammation. 
The cystic kidneys to be described were removed from a woman 
who was picked up in the street by the police, conveyed to the Cook 
County Hospital, to which she was admitted in an unconscious condi- 
tion. Judging from her apparel and personal appearance she must 
have been living in poverty and in unfavorable hygienic surroundings. 
She was about forty-five or fifty years old. There was deep coma with- 
25 Loc. Cit. 9 
out any convulsive seizures, a foul breath and a furred tongue. The 
pulse was rapid. Examination of the urine showed this to contain a 
large amount of albumen, and a diagnosis of uraemic coma was made 
by Dr. Visser. Death ensued in a few hours. 
The post-mortem examination showed quite fair general nourish- 
ment. The body bore evidence of imperfect personal hygiene. The 
great cavities were empty and their lining membranes smooth. The 
heart showed no valvular lesion, a healthy myocardium with a con- 
siderable increase in the thickness of the left ventricular wall. There 
was a moderate amount of arterio-sclerosis in the aorta. The lungs 
were oedematous and congested. The spleen, liver and pancreas were 
quite healthy; there were no cysts in the liver. Both kidneys were 
greatly enlarged, measuring 18x8x4 cm. in their various diameters; 
Fig. 1.—Longitudinal Section of Cystic Kidney—Photograph. 
the left weighed 280, the right 297 grammes. The external surface 
presented a large number of cystic nodules varying in size from that 
of a pea to a hazel-nut approximately; the cysts were situated on the 
flat as well as on the convex surfaces of the kidneys, the capsules of 
which are quite intimately adherent to the cyst walls; there is no nor- 
mal kidney substance to be made out on the external surface between 
the cysts which are quite closely aggregated; in places large cysts pro- 
ject from the surface to such an extent as to be almost pedunculated; 
in other places the cyst barely reaches beyond the surface which is 
consequently very uneven and nodular, and not altogether unlike a 
bunch of grapes, The color of the cysts is a light brown, or some 
modification of brown. On the cut surface there can not be seen any 10 
areas of normal renal substance; all distinction between cortex and 
medulla has been lost; there are no traces of cortical markings; there 
are no pyramids to be pointed out, only occasionally can a much 
changed papillae be seen projecting into the distorted pelvic cavity. 
There is no pelvic dilatation, no pressure atrophy of the medullary 
portion of the kidney, but the cavity of the pelvis is distorted and 
encroached upon by the crowding into it of cysts from the kidney. 
The entire cut surface of the kidney is occupied by a vast number of 
large and small cystic cavities, in equally close apposition near the 
pelvis as at the circumference, so that the kidney presents a honey- 
combed appearance throughout. (Fig. 1.) On the cut surface of 
half of the left kidney two hundred and fifty distinct cysts can easily 
be counted. The wall of the larger cysts is very thin in places, so that 
two cavities may be separated from each other by a transparent and 
Fig. 2.—a. Glomeralus. b. Thickened capsule, c. Smooth fibrillated wall of 
large empty cyst. d. Cyst with colloid masses; imperfect epithelial 
lining, e. Cyst with colloid and granular masses; epithelial lining 
barely recognizable. /. Small, empty cyst. 
Leitz. Obj. 5, Eye-piece 111, Tube-length 160 mm.Xl5O. 
delicate membrane; in other places the walls may show transverse 
ridges and irregularities, undoubtedly the remains of the walls of 
originally independent cavities which have coalesced by atrophy 
of the intervening tissue. In the tissue between the larger cysts 
are many small cavities. The largest cyst measures three cm. in 
diameter, the smallest are barely distinguishable with the naked eye. 
In shape the cysts are all somewhat oval, rounded, or oblong; occasion- 
ally there is one of angular contour. There is no difference in the 
shape and in the size of the cysts upon the surface and of those near 
the pelvis. The cystic contents are all fluid, and quite thin as a rule; 
in some cysts the fluid was thicker and colloid in appearance; the color 11 
was some shade of brown, and, as a rule, the fluid was slightly opaque. 
There was no chemical examination made of the fluid further than to 
demonstrate that it contained albumen and urea. Microscopic examina- 
tion showed it to hold in suspension the following substances: colloid 
masses, a few cholestearin tablets, small granular cells with fat drops 
in their interior in some instances, decolorized red blood-corpuscles, 
granular detritus, free fat drops. 
The pelvic mucous membrane is even, grayish white in color; it 
does appear a little thickened, but it is not nodular. As before stated, 
the pelvic cavity is distorded and diminished because cysts crowd into 
it from the kidney; there does not seem to be much thickening of the 
Fig. 3.—a. Cysts with epithelial lining, b. Tubule with solid outgrowth of cells 
c. Budding mass of cells, d. Round cell infiltration. 
Leitz. Obj. 5, Eye-piece 3, Tube-length 160mm.X150. 
mucous membrane of the greatly distorted calices; in many places the 
apex of a pyramid is replaced by a large globular cyst, and nowhere is 
a typical, normal papilla to be seen. 
The ureters, the bladder, and the urethra are quite normal and 
present no obstruction to the urinary outflow. 
Microscopic sections prepared in the usual way—hardened in 
alcohol, imbedded in parafin or colloidin, stained in hmmotoxylin 
and eosine, or in carmine—show the following: The microscopic 
cysts have, as a rule, no epithelial lining, not even a vestige 
in some cases, in others a row of flattened cells remain; in the 12 
interior are found granular masses, brownish nearly homogeneous 
oval bodies, small granular, cells and detritus; the wall of the 
large cysts consists of quite dense, fibrillated tissue with slight 
round cell infiltration; it may contain vessels and capillaries filled 
with blood. The smaller cysts have, as a rule, a more or less per- 
fect epithelial lining of very short, nucleated columnar cells, but very 
small cysts may have no lining at all; they contain a debris consisting 
of amorphous particles and granular cell masses. In a very few places 
this epithelial lining appears to be proliferating, partly filling the cavity 
of the tube with cells and sending projections into the surround- 
ing tissue. In Figure 3is shown a uriniferous tubule with a blind 
Fig. 4.—Artery in longitudinal section, showing complete obliterating endarteritis. 
Leitz. Obj. 5, Eye-piece 1, Tube-length 160 mm. XlOO. 
extremity filled with cells and a small cellular mass projecting from 
its free end to which it is still connected by a rather narrow cellular 
pedicle. The small cysts are round, or oblong, or kite-shaped. In the 
large as well as small districts of tissue between the cysts there is an 
astonishing amount of connective tissue, forming in some places con- 
tinuous fibrous areas enclosing shrunken, dilated, or entirely collapsed 
tubules. 
The portions of the kidney most extensively involved in the inter- 
stitial changes are the medullary portion and the medullary rays in 
the cortex; the pyramidal part shows the intercystic tissue to be almost 
entirely fibrous in structure, the cystic cavities being large, oblong, or 
narrow and long; foci of hemorrhage and of round cell infiltration can 
be seen in these fibrous districts. The labyrinthine portion of the cortex 
does not show such an extensive and universal substitution of renal 
parenchyma with connective tissue and cysts as the medullary rays and 
the medulla; but the cells lining the tubules are granular, without out- 
line or nucleus, apparently entirely disintegrated. (Fig. 5.) There is 
nevertheless also a marked increase in the extra-tubular fibrous tissue. 
In view of these marked changes the number of healthy glomeruli is 
quite surprising, although the glomerular capsule is quite constantly 
thickened; in some places there is granular material between the capsule 13 
and the glomerulus, and there are also quite a number of obliterated 
glomeruli represented by round, dense fibrous masses, and then again one 
finds healthy glomeruli in continuous, intercystic tracts of connective 
tissue. The healthy glomeruli appear larger than usual. Sections from 
the pyramidal part including some of the mucous membranes of the 
pelvis show, as already stated, an almost continuous dense fibrous tissue, 
but no such marked involvement of the pelvic membrane as to infer the 
existence of a fibrous pyelitis which had attacked the papillae by direct 
continuity of tissue. Throughout all parts of the kidney the vessels 
show great thickening of their walls, especially of the intima, amount- 
ing in one instance at least to complete obliteration of the lumen of 
the vessels. (Fig. 4.) 
Recapitulation: The cysts with which these kidneys are honey- 
combed can be plainly traced to dilatation of the straight or collecting 
uriniferous tubules mainly. The only cause of this dilatation demon- 
Fig. 5.—Showing degeneration in cells lining the uriniferous tubules; much 
increase in fibrous tissue and some round cell infiltration. 
Leitz. Obj. Y,Eye-piece 3, Tube-length 1(50 mm.XISO. 
strated by microscopic examination is obliteration in places of the 
tubules by the contraction of the extra-tubular connective tissue, which 
is present to an unusually marked extent. The changes in the tissue 
between the cysts are essentially those of chronic interstitial nephritis. 
The obviously enlarged glomeruli must be regarded as the seat of a 
compensatory hypertrophy; and the evidences of epithelial cell pro- 
liferation observed here and there in the sections are also to be regarded 
as the result of compensatory changes in the uriniferous tubules 
similar in nature to like processes described in the classical chronic 
interstitial nephritis,26 as well as in other cases of complete cystic 
degeneration. This would seem more rational than to look upon the 
proliferation as adenomatous, according to the view of Sabourin,27 
because it was not possible to demonstrate the formation of new cysts 
from pre-existing cavities or spaces. To successfully claim a congenital 
26 Orth. loc. cit. page 96. 
27 Loc. cit. 14 
origin of the cysts, regarding the chronic inflammatory changes as 
secondary, demands precedent in specimens from the adult showing in 
some way the meso-nephrotic origin of the cysts in a manner that can- 
not be doubted; no such specimens have as yet been described and 
recorded. It is consequently the chronic fibrous inflammation found 
in all parts of the kidneys, especially around the collecting or straight 
tubules that caused the complete cystic degeneration in this instance 
of cystic kidneys; the etiology of this inflammation remains obscure; 
there were no traces of any ascending process that might attack the 
papillary portions of the pyramids and spread onward into the kidney; 
it cannot be assumed that the changes are secondary to precipitation 
of urinary salts in the tubules as in Ewald’s case. In fact the only con- 
clusion that can be reached is that it concerns a more marked localiza- 
tion than usual of an ordinary chronic interstitial nephritic process in 
the medullary portion of the kidney, obstructing the tubules and result- 
ing in peripheral cystic dilatation; the medulla frequently atrophies and 
suffers from interstitial proliferation in cirrhotic kidney, and in excep- 
tional instances of this disease the process might commence at a very 
early period in the pyramids before destruction of the secreting parts 
of the cortex occurred, and by strangulating the straight tubules result 
in the production of a much greater cystic degeneration than is usually 
the case. The clinical history of cystic kidney in the adult is essen- 
tially that of chronic interstitial nephritis with the occasional addition 
of bilateral swelling, which is sometimes demonstrable by palpation. 
Large cystic kidney, due to chronic interstitial nephritis attacking 
the medulla early or especially, would, as in this case, be expected to 
occur bilaterally, or there might be a unilateral cystic kidney with 
the common cirrhotic atrophy of its fellow organ. 
The further consideration of the clinical history and diagnosis of 
cystic kidney in the old can be best elucidated by adding a brief 
resume of the articles on this part of the subject by Ewald,28 Stiller,29 
and Lejars. Ewald’s article considers exhaustively the clinical course 
of cystic kidney, and he finds that the clinical picture is either one of 
chronic interstitial nephritis, uraemia or complicating inflammations 
elsewhere ending life, or it remains entirely latent until a rather 
sudden, fatal uraemia supervenes. Up to the present time cystic kidney 
has been diagnosed during life only three recorded times: Stiller, veri- 
fied by the operation, in woman thirty-eight years old, in 1886; Duquet, 
bilateral cystic kidney in patient fifty-two years old, one year before 
death, diagnosis based partly on nodularities on the surfaces of the 
29 Berliner kl. Wochenschrift, 1892, No. 215, page 215 and Yerhandl. des vii. 
Congresses fflr innere Medicin, 1888. 
28 Loc. Cit. 15 
tumors, verified by post-mortem examination; Verneuil, in fifty-three 
year old patient with complete anuria. Stiller considers the last as a 
lucky guess rather than a systematically elaborated diagnosis. The 
following is a brief abstract of the conclusions on diagnosis formulated 
by Stiller: The topographical diagnosis must be made first. In so doing 
ovarian tumor will most frequently require exclusion. The topography 
determined upon, malignant neoplasms come up for consideration. 
Carcinoma is excluded when the swelling has existed so long or the 
general health is so good as to be incompatible with presence of this 
tumor. Youth speaks against carcinoma; childhood does not. Sup- 
purating kidney need not be thought of when the swelling has existed 
for years, or has been unaccompanied by fever and other symptoms of 
suppurative nephritis. Nephro-lithiasis, cysto-pyelitis, tuberculosis in 
other organs may co-exist in rare cases with cystic kidney. Large 
sacculated kidney, hydro- or pyo-nephrosis or echinococcus cyst, are 
excluded when the tumor is solid and fluctuation totally or partially 
absent. Ewald does not agree to this last statement, but maintains 
that cystic kidney may occasionally give fluctuation. Sudden uraemia 
or anuria in individuals without history of previous renal disease should 
direct attention to cystic kidney. If there be bilateral tumor the pre- 
sumption will be strengthened. In the majority of instances the quality 
of urine is like that in cirrhotic kidney. 
119 Loomis Street.