The Excretion of Acid in Unilateral Renal Disease in Man.

In chronic forms of renal disease the capacity to excrete acid, and in particular ammonia, is reduced (1-5). The mechanisms involved in this reduction, however, are not well understood. The excretion of acid might be decreased by a specific tubular defect in the secretion of hydrogen ions or the formation of ammonia or alternatively by total loss of function in groups of nephrons with normal tubular function in the remaining nephrons. Since the excretion of hydrogen ions is influenced to a considerable extent by extrarenal factors, it is difficult to make comparisons between normal subjects and patients with renal disease, who often have alterations in systemic acid-base equilibrium, solute load, and salt excretion. To overcome such limitations, Morrin, Bricker, Kime, and Klein (6) employed an experimental model of unilateral disease in the dog that allowed examination of the diseased kidney in the same milieu as the normal kidney. In man, except for a few observations in renal arterial stenosis (7-10), the acidifying capacity of the diseased kidney has not been studied in a comparable way. The present investigation was undertaken to examine the mechanism of acid excretion in forms of human renal disease confined to one kidney or involving one kidney to a greater extent than the other. Patients with predominantly