It is now generally recognized that we must separate from the other forms of kidney disease the condition of chronic congestion. Since Traube first called attention to the causation and characters of this lesion, all authors have recognized its special character, although there are still minor differences of opinion concerning it.
ETIOLOGY.—Chronic congestion of the kidney may be produced by any mechanical cause which interferes with the escape of the blood from the renal veins. Thrombi of the veins, tumors pressing on the veins, emphysema of the lungs, hydro-pneumothorax, pericarditis,—all may produce this lesion. As to how often it is produced by the pregnant uterus is still a question. But the most common cause of all is organic disease of the heart. Practically, the lesion comes under consideration as a complication of heart disease, of aneurism of the arch of the aorta, and of emphysema of the lungs.
LESIONS.—If the congestion has not existed for a long time, we find the kidneys increased in size and their weight great in proportion to their size. They are of an unnatural hardness—a hardness which can be imitated by injecting the blood-vessels of a normal kidney with water. The capsules are not adherent, the surfaces of the kidneys are smooth. Both the cortical and pyramidal portions are congested, and this congestion gives the entire organs a peculiar reddish, livid color. No lesions are found in the Malpighian bodies, tubes, stroma, or blood-vessels, except that the epithelium of the convoluted tubes may be a little swollen.
If the congestion has lasted for a longer time, the kidneys may continue to be large or they may be somewhat reduced in size; the weight remains out of proportion to the size. There are the same unnatural color and consistence. The capsules are now often slightly adherent and the surfaces of the kidneys finely nodular. In the cortex there may be patches of new connective tissue enclosing atrophied tubules, or there may be a more diffuse growth of connective tissue separating the tubes from each other. In the convoluted tubules the epithelial cells may be swollen and finely granular, or very much swollen and coarsely granular, so as to nearly fill the tubes, or flattened so that the cavities of the tubes are unnaturally large. The tubes may also contain cast-matter and detached and broken epithelial cells. The capsules of the Malpighian bodies may be a little thickened and the capsular endothelium swollen. In the pyramids the epithelium of the straight tubes may be granular and detached, and there is often cast-matter in the looped tubes. It is difficult to tell whether there is any real change in the veins of the kidney.
As a result of the same interference with the venous circulation, similar changes are found in other parts of the body—in the lungs, liver, spleen, stomach, small intestine, and pia mater. In all these organs there is, first, simply a venous congestion, then after a time structural changes are added. Formation of new connective tissue and of new functional cells of the particular organ, degeneration of these cells, dilatation and tortuousness of the small veins and capillaries, are regularly present. The kidney lesion, therefore, is only one of a number of lesions, all dependent on a common mechanical cause.
SYMPTOMS.—Of the persons who die with chronic congestion of the kidney, a large number present marked symptoms during life, but it is difficult to determine how largely these symptoms are due to the congestion of the kidney.
A congestion of the kidney of only a few days' duration does not seem usually to give rise to any symptoms. Even if such a congestion is prolonged to two or three weeks, as we see in some cases of hydro-pneumothorax from perforation of the lung, there may be no renal symptoms and no changes in the urine. On the other hand, it is extremely rare for organic heart disease or emphysema of the lungs to prove fatal without some disease of the kidneys.
The question is still further complicated by the fact that both in cardiac disease and emphysema there may be either chronic congestion of the kidney or chronic diffuse nephritis with the same symptoms.
After excluding the cases of cardiac hypertrophy secondary to kidney disease and the cardiac diseases with complications, I find in my casebooks 137 cases in which the patients died simply from heart disease, changes in the viscera due to the disturbance of the venous circulation, and kidney disease. Of these cases, 84 presented the lesions of chronic diffuse nephritis; 53 were in the state of chronic congestion. Of the cases of chronic diffuse nephritis, 27 were large white kidneys, 29 atrophied kidneys, 28 could not be classed as either large white or atrophied. In these cases there existed during life certain regular symptoms. There were changes in the urine, dropsy, headache, delirium, convulsions, coma, dyspnoea, vomiting, cough, hæmoptysis, loss of flesh and strength.
As regards the quantity of the urine, there was a very great variety until shortly before the patient's death; then the urine was usually diminished in amount, sometimes suppressed. A very marked decrease in the amount of urine was more constant in the cases of chronic diffuse nephritis than in those of chronic congestion. But in several cases both of chronic diffuse nephritis and of chronic congestion the patients passed from thirty to forty ounces of urine up to the time of their deaths.