kidneys' but they may also be found in the interior of the gland, chiefly, however, in the cortical substance. They are surrounded by a thin, delicate wall of connective tissue, lined with polygonal pavement epithelium2, and contain a clear colorless, or pale-yellow liquid, watery, and rarely gelatinous, which yields albumen phosphates, carbonates, leucin, tyrosin, sometimes a large amount of cholesterine, but no urinary constituents. This latter statement is made with great positiveness by Rindfleisch, but Roberts more prudently remarks that urea and uric acid are found in them very rarely. In other respects the renal substance is healthy, except possibly from the effects of pressure of the cysts upon their immediate surroundings.

Very little is known as to the origin of this variety of renal cysts. They are said to not arise from changes in the uriniferous tubes and to be, like congenital cystic degeneration of the kidneys, entirely unassociated with previous inflammation.

But, as, according to Roberts, urinary constituents may be found in their contents, and as, according to Virchow, congenital cysts originate in intra-uterine inflammation of the tubes, it is possible that further investigation may show the connection of these cysts with the uriniferous tubes and antecedent inflammation.

A second class of renal cysts is found in "Bright's disease," with a small and contracted or granular kidney. Here, as in the first variety, the cysts present great diversity of dimension. They may reach the size of a pea, or even of a hazelnut, but very many are so small as to be microscopic, and of the calibre of the uriniferous tubes. They are scattered singly through the parenchyma, or crowded close together in rows, like beads strung on a thread. Their seat is in the medullary substance. According to Rindfleisch it is especially in the second-fourth, counting from the apex, that they are most frequently found; from here toward the cortical portion they gradually lose themselves. The contents are an albuminous and saline fluid, free from urinary constituents. Rokitansky and Simon held that the origin of these cysts is in germs, or cells which undergo an enormous increase in size; but this theory has found few adherents. The generally accepted opinion, I believe, is that the cysts are formed by circumscribed dilatations of the uriniferous tubes, induced by localized obstructions of the

Roberts, Urinary and Renal Diseases.

2 Rindfleisch, Pathological Histology.

latter by exudation matter, or by obliteration of the tubes at intervals from compression by new and contracting tissue. In Bright's disease with a small contracted kidney there may also be cysts in the cortical substance; like those already described, they vary in number and magnitude. Their beginning is often enough in the convoluted tubes which in some regions become dilated in spots; the walls of these parts merge together, and the whole mass has the appearance of a single cyst divided into compartments by their septa. These after a while give way, and the whole forms one large cavity, in which the shreds of the original partition wall may long be discerned. The presence of these two varieties of disseminated cysts, is of no clinical interest, as they give rise to no symptoms; hence, a further elaboration of this part of the subject would be rather beyond the scope of this paper, in which it is my purpose to deal especially with those varieties of renal cysts which may be recognized at the bedside.

General Cystic Degeneration of the Kidneys.-Here the morbid formative process is so active, and these little globular cells become so exceedingly numerous, that the glandular parenchyma of the kidneys almost or entirely disappears.

This form of cystic degeneration is either congenital or acquired. In the congenital form of the disease, and as a result of it, the infant may die during parturition; or, in consequence of the disproportionate size of the abdomen, embryotomy may have to be performed, and has been already resorted to; in still another class of cases this disease of the foetus appears to have been the cause of premature labor.

But even when carried to the full term the child, if not stillborn, dies after a few unsuccessful efforts to breathe. Both kidneys are always affected; they may be as large or even larger than the normal kidneys of an adult, and have been found to weigh as much as four or even six ounces. The enlarged glands fill the abdominal cavity, push up the liver and the diaphragm, and thus mechanically prevent expansion of the lungs. On opening the kidneys they are seen to be composed of cysts, and little or nothing of the secreting substance remains.

These cysts are formed by dilatations of the convoluted tubes, as already described; that is the view of Virchow and Förster. Rindfleisch expresses a different opinion, and holds that, although the tubuli may undergo this degeneration in their continuity, still it is constantly but one, and the cysts here never arise or grow by

the confluence of several; the partition walls rather appear to become thicker the larger the cysts grow. All the authorities consulted admit that the point of departure in this variety of cystformation is often in the Malpighian capsules, which become obstructed and dilated, the vascular coil is compressed, and the capsule recedes, the interspace being filled with fluid which at first is urinous and later becomes albuminous. Various other deformities usually coexist in congenital cystic degeneration of the kidneys. In one case the foetus was anencephalous, and some of the fingers on both hands and soine of the toes on one foot had grown together and were united by a web-like membrane. In another case there was encephalocele (hernia cerebri), club-foot and club-hand, six fingers on the left hand and six toes on each foot. In almost all cases of this kind there has also been malformation of the urethra, bladder, ureter, or of the pelvis of the kidney, and it has been the exception to find these lower urinary passages open. The renal artery at its origin from the aorta is greatly contracted, and the veins proportionately increased in calibre.'

According to Virchow the following is the order of events culminating in congenital cystic degeneration: first there is an impaction of uric acid and urates in the straight tubes; the irritation set up by the presence of these substances terminates in inflammation, and, as a late result, adhesion of the walls with obliteration of the lumen of the tubes and the development of large quantities of connective tissue between the calices and the papillæ.

These conditions he found existing in every case he examined. Retention and accumulation of fluid are the consequences of closure, the final result being dilatations of the tubuli and Malpighian capsules which form the cysts.

Acquired Cystic Degeneration of the Kidneys in Adults.-This is probably the rarest of all the affections to which the kidneys are liable. Many works on medical pathology merely mention the disease by name, and others omit it altogether.

The rarity of the disease is almost as forcibly illustrated by the fact that Roberts has endeavored to collect all the cases published as by the small number, only fifteen, which he could obtain. In this as in the congenital form both kidneys are always affected, though not unfrequently in different degrees. They sometimes attain huge dimensions, weighing several pounds, and their pres

1 Rindfleisch, op. cit.

ence may be detected during life. The place of the normal kidneys, and, indeed, much more than their normal space, is occupied by an immense number of cysts, the whole resembling somewhat the shape of a kidney. The cysts vary in size from the smallest microscopic vesicle to a bladder as large as an orange. They do not communicate with each other or with the pelvis of the kidney, though several cysts may become fused together by the breaking down of the septa. The contents are urinous in the early stages, and even later, when the cysts are quite large, urea has been found in "tolerable amount." Some, however, deny that urinary constituents are ever present. The fluid is always more or less albuminous; cholesterine plates and leucocysts are often found in it, and blood-corpuscles are often so abundant that some of the cysts. acquire a dark brown color. The cyst wall is similar in structure to that of the varieties already described, viz., it consists of connective tissue and is lined with epithelial cells.

The parenchyma of the kidney is always greatly diminished, and often entirely lost.

The mode of origin of the cysts in this is very much the same as in the congenital type of the disease. Virchow thinks circumscribed spots in the region of the convoluted tubes are the points of departure, others hold that the straight tubes, as already described, give origin to the cysts; and dilatations of the Malpighian capsules, no doubt, also contribute to the formation of a certain. number. Unlike the preceding variety, the pelvis of the kidney, the ureters, and urethra are here open and healthy.

As to the determining cause of this morbid process by which the secreting substance is so extensively destroyed, nothing is posi-tively known. It has been attributed to "an inflammatory hyperplasia of the connective tissue, which has particularly attacked the environs of the larger renal vessels at the medullary limits."

Whether this be a correct interpretation or not, there certainly is an excessive development of connective tissue in these cases.

The relations of cystic degeneration to Bright's disease is a question of practical import. They have some features in common, and, as the distinguished Dr. Austin Flint has remarked, "under certain circumstances this affection will be treated as Bright's disease prior to the autopsy." Cysts occur with sufficient. frequency in kidneys with Bright's disease, and both affections are, under some circumstances at least, so far referable to antecedent inflammation as to make this a possible common origin. But.

what causes determine one line of development in some cases and another line of development in other cases, of these we are entirely ignorant.

The access of cystic degeneration is insidious and its progress slow. Men appear to be more frequently attacked than women in the proportion of two to one. Age is a factor of some weight, and, so far as I can learn, the disease has not been observed in persons of less than thirty years. Most of the cases have been between forty and fifty years of age. Data are almost entirely wanting as to the duration of the disease, but its course is regarded as essentially chronic.

Clinical observations have been very limited; hence our knowledge of even the symptoms is rather scant and imperfect. On analysis of recorded cases, and on consulting authorities within reach, the following symptoms appear all that have been noted:SYMPTOMS.-1. Dyspepsia, which is often of a very severe and distressing character.

2. Lumbar pains.

3. The urine is usually abundant until very late in the disease, when it becomes scanty or its secretion is suddenly arrested. 4. It is of low specific gravity.

5. There is usually albuminuria, though very variable in amount 6. Hæmaturia at intervals occurs in a certain proportion of cases. 7. Edema of the feet and legs is not uncommon. Austin Flint and others have noted that there may be general dropsy, but death may occur without even puffiness of the ankles.

8. The most important symptom is the presence of a tumor in each flank, which sometimes attains a very large size.

It is probable that with an increase of recorded cases our knowledge of the symptomatology of this disease will become more ample and complete. The above brief abstract of symptoms, however, is not entirely inadequate to meet the wants of the clinician. For when one considers their character, their peculiar grouping, and the manner and course of development, a diagnosis can in most cases be reached, at least after the appearance of the tumors in the flanks.

The differential diagnosis of cystic degeneration of the kidneys is not always easy.

In the early stages, before the appearance of tumors, a differentiation from Bright's disease must sometimes be impossible. How