DIFFERENTIAL DIAGNOSIS OF TERMINAL GLOMERULONEPHRITIS AND MALIGNANT HYPERTENSION. I. RENAL ASPECTS

Abstract

The distinction between patients who show renal failure which has not progressed to uremia and is due respectively to terminal glomerulonephritis and malignant hypertension, is difficult. Because it is left for the pathologist to make the differentiation, the concept has grown that it is not clinically possible to establish it by study of renal function. That this is not the case is shown by studies based on the excretions of diadrast and inulin, or urea and urinary protein, on the concentrating power of the kidneys, the urinary sediment, arterial pressure, hematocrit index and serum protein content. The studies were done in 10 patients from each group, selected because they presented the lowest levels of renal function observed in each series in the absence of the clinical syndrome of uremia. Terminal glomerulonephritis is distinguished by a low rate of glomerular filtration, of tubular secretory capacity, and, usually, a higher rate of proteinuria than appear in malignant hypertension with renal failure. In spite of the lower level of renal excretory function in terminal glomerulonephritis, such patients survive more than four times as long as do patients with malignant hypertension in renal failure. The changes of renal function usually demonstrable in the terminal nephritic are in accord with the structural changes in the kidneys of such patients, in that they indicate lesions glomerular and capillary in locus, associated with great parenchymal destruction and fibrous replacement and suggest the frequent occurrence of large inequalities of function in the remaining nephrons. In malignant hyper-tensives with renal failure, intraglomerular hydrostatic pressure seems often to be increased above the normal and the flow of blood through the residue of intact tubular tissue is diminished, the latter presumably as the result of ar-teriolar constriction and (afferent) arteriolar sclerosis. A subsequent communication in this series will establish the cooperation of severe arteriolar and arterial disease with renal failure as the cause of death in patients of this group. In some of these patients, in spite of greatly increased arterial pressure and presumptive constriction of glomerular efferent arterioles, intraglomerular hydrostatic pressure seems not to be increased above the normal or is even low. This observation testifies to the severity of afferent arteriolar sclerosis or constriction in these patients. The conclusion is drawn that in these, as in the terminal glomerulonephritics, the implications of functional study agree with what is known of the structural changes caused by the disease. Evidence is obtained which suggests that the hypoproteinemia of Bright''s disease, whether it occurs "hiring chronic glomerulonephritis or in malignant hypertension with renal failure, apparently serves as a means of maintaining glomerular filtration when, in the absence of hypoproteinemia, the proportion of water filtered through the glomeruli would be grossly deficient or nil.