Chronic Parenchymatous Nephritis.
Synonyms.—Chronic Desquamative Nephritis; Chronic Tubal Nephritis; Chronic Diffuse Nephritis with Exudation.
Definition.—A chronic inflammation of the kidney, in which there is degeneration of the renal epithelium, connective tissue changes in the stroma, permanent changes in the glomeruli, and an exudation from the blood-vessels.
Etiology.—This is mostly a disease of early and middle life, though no age is exempt. Males are more often affected than females, the greater exposure, mode of life, and drink habits of the former, no doubt, accounting for the difference in the two sexes.
It may follow the acute nephritis of cold, scarlet fever, or pregnancy, or chronic congestion of the kidney, though usually it begins insidiously and seemingly independent of any acute disease.
Occurring in children, however, there is usually a history of scarlatinal nephritis.
Indulgence in alcoholic and malt beverages is no doubt responsible for the disease, the frequency with which it appears in beer-drinkers being evidence. Malaria is regarded by many authors as being a cause of chronic nephritis. Workmen exposed to cold and damp, and who live in damp, poorly ventilated apartments, are subject to Bright's disease.
Tuberculosis, syphilis, and suppurative diseases are also associated with chronic nephritis. In all probability, toxins either from a perverted metabolism or introduced from without, so influence the nutrition of the kidney as to give rise to chronic diffuse nephritis.
Pathology.—Although there are several pathological types of chronic nephritis, one form may merge into another, so that the line of demarcation may be very difficulty if not impossible, to detect. Three principal forms, however, are easily recognized.
(1) The large white kidney; (2) The small white kidney; (3) The red or variegated kidney of chronic hemorrhagic nephritis.
The large white kidney, the most common type, is usually smooth and pale, or yellowish in color, and the capsule loosely attached, so that it readily strips off. The cortex is broader than normal, owing to an extensive growth of connective tissue, and a put section reveals a yellowish-white or mottled appearance. The pyramids are highly congested and of a deep-red color. The microscope reveals the renal epithelium swollen, with fatty and granular degeneration, and the tubules of the cortex are distended with tube-casts, coagulated matter, and blood-corpuscles. Hyaline changes are also found in the epthelial cells.
The glomeruli are enlarged, the capsule cells increasing in such numbers as to compress the tufts. The interstitial tissue is increased and shows polynuclear leukocytes, red-blood cells, and round cells throughout certain areas, and some thickening of the arterial walls.
The small white kidney, or secondary cirrhotic kidney, results from the gradual increase in the connective tissue, followed by a shrinkage due probably to advanced degeneration of the epithelium. Some observers believe that this variety may be independent of the first form. The capsule is thick, rough, or granular, and not so easily detached. On section, the structures are found dense and resisting, and present numerous yellowish-white foci, due to fatty degeneration of the epithelium of the glomeruli and convoluted tubes. As the interstitial tissue increases, the parenchyma atrophies.
As the interstitial changes progress, many of the glomeruli are destroyed, while the degeneration of the epithelium of the Convoluted tubes is extensive; there is also thickening of the arteries.
The chronic hemorrhagic kidney is enlarged, congested, and of a dark-red color or mottled appearance, closely resembling acute diffuse nephritis. The capsule is adherent to the roughened surface. A cut section reveals the cortex thickened in places, while contracted at other points, due to the interstitial alteration. The reddish-brown or mottled areas are due to hemorrhage in and about the tubes. The further changes are the same as found in the large white kidney.
Symptoms.—When it comes to the clinical phase of Bright's disease, we are unable to differentiate the various types just mentioned, the symptoms of one being more or less common to all. If the disease follows an acute nephritic, it will be difficult to draw the dividing line that separates the one from the other, so insidiously does the one merge into the other. In a large proportion of cases, it comes on insidiously, with but few. if any, characteristic symptoms of nephritis.
The patient notices that he is losing flesh and strength, that he tires on the slightest exertion, that his appetite is failing, and that nausea is often present. He may have a sense of weight and uneasiness in the loins and frequent desire to micturate, though the secretion is not normal in quantity. It will now be noticed that his color is bad, he is pale, or the skin has a muddy hue, there is puffiness of the eyelids and face, soon followed by swelling of the ankles and in time by general anasarca.
The urine is characteristic, though the quantity varies at times. When the inflammation is very mild, the quantity may be nearly normal; but with the exacerbations that occur, the urine is very scanty and sometimes almost suppressed. It is dark or of a smoky color, and always contains albumin and tube-casts. On standing-, a heavy sediment is deposited containing tube-casts, hyaline, granular, epithelial, and fatty casts of various sizes and forms, together with leukocytes, red blood-corpuscles, epithelium from the kidneys and pelvis, and a large deposit of albumin.
The specific gravity ranges from 1,020 to 1,030, though in the later stages it may be as low as 1,001 to 1,005. The albumin in severe cases may amount to one-third or one-half of the urine voided.
Dyspnea may occur quite early, and during the later stages is a constant symptom, which may be due to hydrothorax, to edema of the lungs, to contraction of the arteries, or to failure of the heart's action. The dyspnea is more severe at night and early morning, and is always worse on lying down.
Uremic symptoms may occur, though convulsions are not common in chronic exudative nephritis. Headache, with nausea and vomiting and sleeplessness, followed by dullness and coma, with muscular twitchings, would be the symptoms of uremic poisoning, and would be serious. There is generally increased tension of the pulse, and hypertrophy of the heart is quite common. Nephritic retinitis, as shown by dimness of vision, occurs quite often.
Course of the Disease,—This is quite variable, and may be short or of long duration. In some cases the anemia, dropsy, and albumin are present from a very early stage, and continue without interruption till death, which occurs in one or two years.
Other patients will have attacks of dropsy and dyspnea lasting for weeks or months, followed by a seeming return to health. If the urine be examined, however, during these intervals, albumin will be found present.
Other cases only show pallor of the skin, and urine of low specific gravity containing albumin, for years.
Diagnosis.—The diagnosis of Bright's disease is readily made by a chemical and microscopic examination of the urine, though it may be very difficult, if not impossible, to determine the stage and type of the disease. In the large white kidney, there is generally less urine passed, and it has a higher specific gravity than in the other forms, and there is more dropsy present, while the history of alcoholism and the presence of blood-casts and red blood-corpuscles in the urine would suggest the hemorrhagic kidney.
Prognosis.—Albuminuria or Bright's disease is one of the gravest of diseases, and the prognosis is generally unfavorable. Life may be prolonged for years by judicious treatment, though the disease may terminate fatally in three months.
In children, chronic nephritis following scarlet fever may terminate in recovery. If the disease has continued one year, it is nearly always unfavorable. Death is usually the result of uremia, dropsy, cardiac dilatation, or other complications.
Treatment.—This will be along the same lines as indicated in acute Bright's disease. We are not to forget, however, that in chronic nephritis we have a vice of nutrition as well as an inflammation, and that remedies that improve the condition of the digestive apparatus and make a better blood-supply are equally important with agents to correct renal wrongs.
The patient should wear flannels to protect the body from chilling, and, where possible, he should remove to a warm and equable climate. Alcoholic and malt stimulants must be restricted. The diet should consist largely of milk in some form, sweet milk, buttermilk, whey, or malted milk, as the patient may prefer. Rich broths and fruits are to be used as the patient may desire. Pure water may be taken freely, and helps nature flush the uriniferous tubules of their inflammatory products. An infusion of the vegetable diuretics mentioned in acute nephritis will be found useful.
To improve the condition of the skin, jaborandi and pilocarpin will be successfully used. To relieve the dropsical effusion and at the same time improve the tone of the heart, apocynum and digitalis will be among our best agents.
Constipation must be overcome by the use of seidlitz salts, antibilious physic, elaterium, apocynum, and like agents.
Fowler's solution, strychnia, quinine, and iron may be useful as tonics when such agents are required. The old compound tonic mixture, the triple phosphate of iron, quinine, and strychnia, will be found an efficient combination. Howe's acid solution of iron in drop doses will also be found useful where a ferruginous preparation is indicated.
Counter-irritation, though unpleasant, will often prove beneficial, and the old compound tar-plaster, or the more modern thapsia plaster worn over the loins, will be attended with good results.
Berberis aquifolium is a good remedy in controlling inflammation, and also as a tissue-builder, and should not be overlooked. Oversexual indulgence must be strictly enjoined, as it not only aggravates the disease but is regarded by some as an exciting cause.
The Eclectic Practice of Medicine, 1907, was written by Rolla L. Thomas, M. S., M. D.