Part 44

In other cases the nephritis is evidently a result of the irritation caused by toxins in process of elimination by the kidneys, as there is no evidence of a nephritic infection.

In some instances minute emboli originating in the lungs or heart, become the starting point of the nephritis, which slowly extends by reason of infection or low condition and special susceptibility. Disease of the aorta or renal artery may lead to this condition as noticed by Cadeac and Lustig. Cadeac has also noticed its association with aneurism of the mesenteric arteries so that the strongylus (sclerostoma) armatus may be considered as a factor. Again in old horses and dogs it has been associated with atheroma of the aorta and renal vessels (Trasbot).

Overfeeding is not without its influence, especially when on animal food, which charges the kidneys with excreting an excess of the irritating urea and uric acid, and this is one reason why it is far more frequent in house dogs than in other domestic animals. When the meat is already decomposing and putrid there is the added evil of a quantity of toxins and even of microbes to be eliminated from the system by the much abused kidneys. Add to these that the dog’s urine is even in the normal condition more dense and contains more irritating ingredients than that of herbivora, and that owing to the slight activity of his perspiratory apparatus he can obtain less relief from the skin, and we find a substantial ground for the prevalence of chronic nephritis in this animal.

Disease of the valves of the right heart or dilatation with insufficiency of the auriculo-ventricular valves is a potent cause of nephritis, the reflux of blood into the veins and the increased venous tension, speedily producing passive congestion and a slow type of inflammation in the kidney. This factor is especially liable to operate in dogs, which are particularly obnoxious to rheumatism and valvular ulceration, and are very subject to nervous cardiac disorders; in horses that have contracted heaves; and in beef breeds of cattle which suffer from fatty degeneration of the heart with dilatation.

The influence of calculi must not be overlooked, whether they are lodged in the pelvis, the chalices, or the uriniferous tubules. Their tendency is to induce local irritation and exudation, with fibroid degeneration and thickening of the walls of the tubules or pelvis and of the adjacent tissue.

When to one or more of the above conditions there are added overfeeding or what is worse a low condition from starvation or unwholesome food (permeated by bacteria or cryptogams or containing vegetable acids), and when to crown all there are frequent exposures to cold or wet, we have a vicious combination especially conducive to kidney trouble.

Habitual retention of urine in mares in harness, in house dogs, or in horses in railway cars, and violent exertion, or sprains of the back are among the remaining accessory causes.

Symptoms. These are often slight or obscure, so that not only owners and attendants but even veterinarians are liable to overlook them. Loss of flesh, flabbiness of the muscles and a lack of spirit and energy are among the first symptoms. The horse appears stiff, especially in his loins and hind limbs, and fails to advance the hind feet as far under the belly as formerly, and straddles more. When put to work he is early fatigued and appears unfit for sustained exertion. His movements are slow and if urged to a trot he may even groan with every step and quickly settles back to his sluggish pace. If turned sharply round on himself he does so with difficulty and often groans. When he is mounted or when the loins are pinched he may droop to excess. If you come on him lying down, and urge him to rise he may rise on his fore limbs and sit on his haunches until urged before he makes any attempt to raise himself on his hind. The dog may spend most of his time in the kennel, and show little disposition to run, play or hunt. On the contrary the owner may have to call him several times before he will come out and then he moves listlessly, wearily and even weakly.

In all animals the appetite is poor or capricious, and the patient gradually loses condition, at first slowly and later, after a few weeks or months, more rapidly. The advance of anæmia is also steadily progressive.

Dropsical effusion is not uncommon. It is often prominent in the horse as stocked limbs, but may be absent for a length of time. In other animals it is more likely to appear later in the disease and under the chest or abdomen or in one of the internal serous cavities. Trasbot has found it absent for months in the nephritic dog.

The exploration of the kidney through the flaccid abdominal walls in small animals, and through the rectum in small horses and cattle, may reveal renal tenderness and even swelling. If there is a tendency to frequent passage of urine in small quantities, or to straining without micturition, the indication is of value.

There may be little or no fever, and, when left at rest, little evidence of discomfort.

Any indication of urinary trouble, and especially with dropsy, weakness, flabbiness and anæmia and a subnormal temperature, should lead to examination of the urine, as a crucial test. A high density is good ground for suspicion. But this is not constant. In advanced cases (chronic interstitial nephritis, small white kidney, atrophic nephritis) it may be 1015 to 1025, in exceptional advanced cases with polyuria, it may be 1010, 1005, or even 1001. With such a condition, however, there is great anæmia, pallor of the mucosæ, and prostration. Tested with nitric acid and heat, the urine throws down an abundant precipitate of albumen. Under the microscope it shows a profusion of granular, degenerating epithelial cells, and casts of the uriniferous tubes.

Progress. The course of the disease is usually slow, extending over several months, but with a tendency to constant advance. The thirst increases and the urine increases in amount, clearness and levity. There may supervene extreme sluggishness, dropsies, anæmia, and weakness, irritability of the heart, and palpitations on slight exertion. So long as the heart’s action is strong, elimination may be maintained and life prolonged for months (in cow, Dickinson), or years (Friedberger and Fröhner). When the heart’s action becomes weak, elimination is rendered imperfect and the animal shows catarrh of the lungs or bowels (common in dogs), local inflammation of the lungs, pleura or pericardium, or œdemas, or hæmorrhages. The toxic effect on the nerve centres is shown by stupor or lethargy, or vertigo. When an abscess forms it is associated with a temporary rise of temperature (Trasbot). The patient may die in convulsions, in a state of coma, or by gradually advancing debility and failure of the heart.

Lesions. In cases of comparatively =short standing= the kidney is usually of full size, or somewhat enlarged, with firmly adherent capsule and rough or even nodular surface. The surface of the cortex may be red or grayish or parti-colored, pink and gray. The cortical portion is firm and it may even be attenuated somewhat, while the medullary portion, naturally lighter, has often grayish streaks converging toward the hilus. When the gray streaks are scraped with the knife a serous fluid, mixed with fatty granules or globules, is obtained. The glomeruli may be still about the normal size with some increase of the epithelial tuft cells. The tubules contain casts (colloid, hyaline, granular), and their epithelium normally columnar, are flattened down to cubes and are swollen, granular or fatty.

In cases of =older standing= the connective tissue has usually undergone a marked increase. The capsule is thick, dense and adherent. The cortical substance is shrunken with a great increase of the fibrous elements, and the same holds true of the medullary portion. In consequence of this, even in the cortical substance the white or gray color predominates. The parenchymatous tissue (glomeruli, tubules) have greatly shrunken. In connection with the contraction of the forming fibrous hyperplasia, there is a general shrinkage of the kidney in size, it may be to one-half its original volume. Trasbot reports a case of nephritis, of 8 months standing, in the dog, with a kidney half the normal size. In the end the parenchyma may have practically disappeared, and the kidney may have shrunken to a small, firm, white, fibrous mass. Abscess of the kidney is exceptionally met with (Laurent, Lafosse).

Lesions of distant organs are not uncommon. Bronchitis, pneumonia, pleurisy, insufficiency of the tricuspid or mitral valves, dilated heart, hypertrophied or fatty heart, congested or fibroid liver, arteritis, and dropsies are among such morbid conditions.

Prognosis. This is almost always unfavorable. Death may be delayed for months or years, and partial transient recoveries may take place but a restoration to normal structure and function is not to be looked for.

Treatment. This cannot be expected to be much more than palliative. The avoidance of overwork, and of the exposure to cold and wet, and the securing of a free action of the skin by warm buildings and clothing, are essential. The diet should be easily digested and non-stimulating, for herbivora green food, carrots, roots, apples, silage, with a moderate allowance of oats to counteract weakness and anæmia; and for carnivora, milk, buttermilk, mush made of oat, wheat or barley meal, with, if necessary, a slight allowance of tender raw meat. Tonics fill a similar need. Iron and bitters may be combined. Or hydrochloric acid or nitromuriatic acid with bitters (nux, calumba, salicin, quassia) may be tried. These acids are especially valuable when the case has originated in or is maintained by calculi, indigestion or hepatic disorder. When the heart is defective in tone, it may be stimulated by small doses of digitalis, strophanthus, sparteine, caffein, or nitro-glycerine, or to a certain extent by strychnia or nux. These, however, must be used with judgment, if it is found that they aggravate the case by increasing the arterial tension. In those cases in which there is an excessive secretion of watery urine, the possible source of this in musty aliment should be avoided, and the flow checked by nux vomica, in moderate doses, and bromide or iodide of potassium in full doses. When, on the other hand, the urine becomes scanty and dense, the great danger of a toxic action must be met by agents that favor excretion. Pure water at will is perhaps the least objectionable of such agents, but potassium or sodium acetate or citrate, or even sodium chloride, in weak solution, may be given. In some cases benefit will come from a moderate use of the balsam of copiaba, or the leaves of buchu, which may improve the tone of the secretory elements. The most promptly effective of these agents is pilocarpin (Friedberger and Fröhner), but it has the serious drawback of inducing profuse and dangerous depletion and debility. Yet in careful hands, and with good cardiac tone, it may often be used to advantage.

Fomentations over the loins, warm baths and mustard embrocations, may at times be beneficial. Attempts have been made to check the hyperplasia by the use of arsenic, mercury or the compounds of iodine, but their use in such cases is based on theory rather than accomplished results.

HYPERTROPHY OF THE KIDNEY.

Hypertrophy of both kidneys has not been recorded in domestic animals. On the other hand the extraordinary development of one in compensation for the loss or atrophy of the other is not uncommon. In this the organ follows the general law of adaptation, seen in the double symmetrical organs (testicle, etc.) and the more so that its functional activity is indispensable to life. Among causes are: blocking of an ureter by calculus, worms, neoplasm, nephritic abscess, gangrene, etc. The enlargement of the remaining kidney is a vicarious act and essentially a physiological one.

If compensation is perfect, it may be impossible to detect symptoms apart from those of the primary disease.

Prognosis. Life is endangered in case of any subsequent kidney disease.

ATROPHY OF THE KIDNEY.

Result of hyperplasia of connective tissues and compression and absorption of parenchyma. Unilateral or partial. Causes: chronic productive inflammation, calculus in tubes, ureter, or pelvis, tumor, retention cyst, embolism. Lesions: sclerosis of kidney, firmness, pallor, anæmia, lack of glomeruli and tubules, cysts, congenital, urinous retention, colloid. Symptoms: reduced secretion, palpation of kidney. Treatment: Prevention: arrest conditions, abundance of water, succulent food, parasiticides, operation on cysts, counteract nephritis.

Unlike hypertrophy, this is constantly the result of a pathological process. So long as a normal functional activity of the secreting elements is carried on, such parts must maintain their size and healthy characters. But with the compression of such secreting elements (glomeruli and convoluted tubes) by a hyperplasia of connective tissue, by pressure from without or from the damming back of the urine in the pelvis and tubes, the secretory elements are absorbed and removed, and the final result is a general atrophy. If such atrophy appears in both kidneys at once it can only be very partial in extent, as extreme atrophy of both, with loss of their secretory function, would entail poisoning and death from the retained urinary products. The comparative frequency of the disease may be inferred from the reports of the numbers of specimens found by Barrier and Moussu in old horses in the dissecting rooms. The latter observed a dozen cases in a single winter, other examples are recorded by Cadeac (horse), Soula (swine) and Trasbot (in various animals).

Causes. The most common source of the condition is the occurrence of chronic productive inflammation. The new product in such cases, if not pus, or a growth that rapidly passes into fatty or granular degeneration, or into gangrene, tends to form tissue of a low organization, especially fibrous. The resulting increase of the fibrous trabeculæ, in undergoing subsequent contraction necessarily compresses the secretory tissue and the final result is a visible and, it may be, extreme wasting. Hence any slowly advancing productive inflammation is liable to result in absorption and removal of the kidney parenchyma, and distinct atrophy of the gland.