The cardiac response in acute difeuse glomerulonephritis

Abstract

The recognition of the presence of acute circulatory decompensation is extremely important in the diagnosis and treatment of acute diffuse glomerulonephritis. The cardinal symptoms, namely, hypertension, edema, hematuria and renal insufficiency as shown by nitrogen retention in the blood, may be absent. The pathology in the kidney consequently may not be detected. Cases of this description are reported in this series. The only clue to the diagnosis is obtained by a proper interpretation of the circulatory symptoms. The sudden advent of circulatory decompensation as evidenced by dilatation of the right side of the heart, pulmonary congestion, and an enlarged and tender liver should lead one to suspect the presence of acute nephritis. This applies particularly in cases in which valvular or coronary artery lesions are absent and no other cause for decompensation can be found. Although it is generally believed that the edema in acute diffuse glomerulonephritis is a “tissue disturbance”, caused by some derangement of general metabolism, the fact must not be overlooked that water retention may also be due to the circulatory disturbance. The determination of this point is of extreme importance in deciding upon the form of therapy to be pursued. Pulmonary edema may be the cause of death in acute nephritis. It may occur even though the structural changes in the kidney are not sufficient to produce complete renal insufficiency. The early recognition of the etiology of the circulatory symptoms may be the means of saving life. In addition to dietetic measures, proper cardiac supportive treatment should be undertaken. Often, rest in bed will suffice. The liberal use of caffein products such as diuretin, theocalcin and caffein sodium benzoate, and digitalis are indicated.