Again the obstruction of the ureter by a calculus in the pelvis which falls into the infundibuliform entrance, or a stone arrested at any part of the duct (or even of the urethra) or by worms, hydatids, cysts or tumors, throws back on the kidney the secreted urine, which distending the pelvis and uriniferous tubes leads to direct compression and absorption of the secretory parenchyma. Direct compression of the kidney by an adjacent tumor will act in a similar manner. Retention cysts by their gradual increase and augmenting pressure cause absorption of the gland tissue.
The blocking of individual uriniferous tubules by minute calculi, which is so often seen in cattle, kept on dry feeding in winter, is a cause of partial nephritis, and absorption, as noted by Röll.
A somewhat rare cause of atrophy is the diminution of the blood supply by arteritis and embolism of the renal artery, or by pressure of tumors on that vessel. Arteritis and blocking suggests at once the possible agency of the strongylus (sclerostoma) armatus in the horse. Trasbot records a striking instance of compression of the renal artery and kidney by an enormous sublumbar melanoma. This occurred in an aged horse and led to atrophy.
Lesions. In cases due to productive inflammation with sclerosis of the kidney, the firmness, pallor and bloodlessness of the organ is a marked feature. When incised it is found to be composed mainly of fibrous tissue, while the glomeruli and tubuli have to a large extent disappeared.
If there has been simple lack of circulation the kidney becomes flaccid, pale and small in size. The secretory elements (glomeruli and uriniferous tubes) are first absorbed, leaving the fibrous network, which tends to shrink and form a hard resistent mass. In extreme cases there may be absolutely no glandular tissue left, and the dense shrunken mass represents only the hyperplasia of the original fibrous network. In the different successive stages of this process the glomeruli and tubules become flattened, the epithelial cells become granular, or contain colloid casts and refrangent elements like oil globules and finally they are represented by a small mass of fibrous material.
Of all the atrophies caused by the pressure of tumors perhaps that caused by cysts is the most characteristic. There may be a single cyst or they may be multiple; they may range in size from a pea to the size of the two fists the total size exceeding that of the normal kidney. In all such cases the cysts project visibly from the surface of the organ. They vary according to their origin and nature. Congenital cysts are said to have resulted from distension by retained urine of the capsule of the glomerulus. The arterial tuft is atrophied and flattened against the wall. Serous cysts with clear contents are found in the old. Urinous cysts again form by distension of the tubules that are obstructed by cysts or minute calculi. Colloid cysts are found in certain forms of nephritis formed by the dilatation of the capsule of the glomerulus or of the uriniferous tubules. The liquid often contains leucin, tyrosin and cholesterine. In all such cases the walls of the cyst become thick, and the glandular parenchyma is compressed leading to progressive degeneration and atrophy.
Symptoms of atrophy of the kidney are necessarily those of suppression of urine, with, in certain cases, the passage of casts of the uriniferous tubes and of crystals of salts. There are, however, no absolutely pathognomonic symptoms. When the kidney can be reached through the flaccid walls of a comparatively empty abdomen, or through the rectum, its hard, shrunken condition may assist in diagnosis.
Treatment is not successful in advanced cases. Prevention is to be sought by obviating or treating the conditions on which the atrophy depends. Nephritis must be treated on general principles. Calculi must be avoided by a liberal supply of water, by soiling, or by pasturage. Strongylus parasitism should be dealt with by destroying the parent worms in the bowels, and by securing pure drinking water free from their eggs and embryos. Cysts, and tumors are only amenable to surgical measures and not often open even to these.
FATTY DEGENERATION OF THE KIDNEY: STEATOSIS OF THE KIDNEY.
Causes: age, overfeeding, idleness, atony, retention of urine. Lesions: kidney enlarged, pale yellow, capsule loose, cut surface glistening unctuous, oil globules in scrapings, granules soluble in ether. Symptoms: in idle, overfed, obese, improved meat producing breeds, closely confined, starchy or saccharine food, fatty granules in urine, finally dropsies, anæmia, debility, sluggishness. Prognosis unfavorable in advanced stage. Treatment: butcher, restricted regimen, open air exercise, nitrogenous diet, crossing, diuretic food or drugs, oil of turpentine, balsam copiaba. Palliation only.
Fatty degeneration of the kidneys is by no means unknown in the domestic animals. It has been observed in dogs and cats (Rogers, Goubaux, Vulpain, Trasbot). In dogs it has been erroneously set down as a characteristic lesion of rabies. Like fatty degeneration of other organs, it is also met with in old and overfed individuals of meat producing breeds of animals, in which the tendency to early maturity and rapid and excessive fattening has been fostered from generation to generation. In man small, granular, fatty kidney is a common result of chronic parenchymatous nephritis, and often coincides with fatty liver. Chronic poisoning by arsenic or phosphorus is another cause, as it is of fatty degeneration in other organs.
Vulpain has attributed it to a lack of active exertion and of general tone, associated with excessive amylaceous feeding, sluggish, shallow breathing and tardy elimination. Goubaux and Trasbot attach great importance to the compulsory retention of urine in house dogs, cats and horses. The damming back of the urine in the convoluted tubes and glomeruli, temporarily arrests secretion, and the inactive and compressed cells tend at once to granular and fatty degeneration.
Lesions. The gland is sensibly increased in size, and pale, yellowish or straw yellow. The capsule is easily detached from the cortical substance, contrary to what is the case in chronic productive inflammation. The cortical substance is increased in thickness, and pale, the pallor being largely in ratio with the duration or extent of the fatty degeneration. The cut surface may be glistening and unctuous to the touch. It is softer than usual, rather friable, and if scraped, furnishes a serous or grayish pulp in which oil globules are prominent features, together with granular epithelium and free granules that dissolve readily in ether. Tubules are varicose and unequal at different parts. The medullary portion has undergone little change. It may be paler at certain points, with some shrinking of its substance and increase of firmness.
Symptoms. As a rule the disease occurs in pampered, overfed and obese animals, and in those of the improved breeds which have great power of digestion, assimilation and fattening. It is especially to be looked for after close confinement on full, stimulating, amylaceous diet. Symptoms are not usually recognized during life. There is, however, a lessening of the urinary secretion, and, as the disease advances, albuminuria. When examined microscopically this is found to contain characteristic elements, such as granular epithelial cells, the granules soluble in ether, oil globules, and at times crystals of cholesterine (Beale). A diagnosis based on the mere presence of oil globules may, however, be fallacious, as these may be present in animals that have just been heavily fed on oleaginous food, and again the oil used to smear the catheter may float in the urine and prove misleading. Under such circumstances vaseline or glycerine may be substituted on the catheter. Scriba induced fatty urine by injecting fat or oil emulsion into the blood, and Chabrie by ligating the large intestine. Trasbot says that cylindroid casts may be present. As in other grave kidney affections, dropsies supervene as the disease advances. These may show in the limbs, in the abdomen, or in other serous cavities. A steadily advancing anæmia with pallor of the mucosæ, listlessness, weakness, debility and sluggishness are to be noted.
Prognosis. Since the disease is rarely diagnosed until it has reached an advanced stage, it usually progresses steadily to a fatal issue. If, however, it can be detected at an earlier stage, it may be palliated, or held in abeyance, for a length of time varying with the extent of the lesions. As it is very largely a disease of meat producing animals and as the subject is at first in a condition of marked obesity, it can usually be turned over to the butcher without material loss.
Treatment. If the disease has resulted from the inbred propensity to fattening, the family that shows the disposition must be subjected to a somewhat different regimen, open air exercise must take the place of confinement in warm stables, a rather bare pasturage is valuable for herbivora, and a restricted diet in which the oleaginous, saccharine, and amylaceous constituents do not predominate, is strongly indicated. Crossing with a strange male having many of the desirable qualities of the herd, but which is more vigorous may be resorted to. When the secretion of urine becomes scanty an abundance of pure water, or a diet of succulent grass or roots or ensilage or even small doses of alkaline diuretics may be resorted to. Any source of arsenic or phosphorus poisoning should be cut off, and as an antidote to phosphorus, oil of turpentine may be given in small doses. This agent may, indeed, replace the alkalies as a diuretic, bringing in an element of tone for the mucosa which is not to be despised. Or balsam of copaiba or buchu leaves may be substituted.
When the small white kidney (granular, fatty) results from chronic nephritis, the prevention and treatment would be as for that disease. Little hope is to be entertained of entire restoration to health.
AMYLOID KIDNEY. LARDACEOUS OR WAXY KIDNEY.
This condition of the kidney has been found in the ox (Gerlach) and dog (Rabe, etc.). There are usually similar degenerative lesions in the liver, pancreas, intestines and other organs. It is usually a concomitant of some chronic wasting disease (chronic nephritis, tuberculosis, etc.).
Morbid Anatomy. The kidney is usually enlarged, pale and on section waxy or glistening. Soaked in dilute compound tincture of iodine it shows spots of a walnut or mahogany brown color. The glomeruli are well marked and show the earlier changes, later the tubes do so excepting the epithelium. The latter is swollen, granular, fatty.
Symptoms. There may have been those of chronic nephritis. Rabe has noticed in dogs dropsy of the limbs, ascites, emaciation, anorexia, followed by uræmia, coma, weakness, vomiting, and if the kidney alone was affected great lowering of temperature (35.9°C). With hepatic complication there was greater weakness, giddiness, and higher temperature (39.6°C). Urine is usually increased (in man albuminous) and the casts have shown the anyloid reaction. They tend to be fatty or finely granular. Casts may, however, show anyloid reaction when the kidney, post mortem, does not (Jaksch).
Diagnosis from Bright’s disease is often impossible.
Treatment is essentially the same as in chronic nephritis, and is not hopeful.
Trasbot recommends KI 3 to 7 grs., or tinct of iodine 3 drops for shepherd dog. Ol. terebinth and alkaline diuretics are also commended.
RENAL CALCULUS.
This is much more common than is supposed. Small calculi formed in the tubuli uriniferi of cattle on dry winter feeding often pass without recognition, and habitually disappear on rich spring and summer grass.
If retained in the pelvis until increasing size forbids their passage through the ureter they form pelvic calculi.
If retained in the bladder so that they cannot enter the urethra they form cystic calculi.
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