Urinary ammonia content as a determinant of urinary pH during chronic metabolic acidosis

Abstract

During the course of metabolic acidosis, the urine pH initially falls but then rises to levels that seem inappropriate to the degree of systemic acidosis. We investigated the factors responsible for the reduced urinary acidity during chronic metabolic acidosis, using fasting as the model of acidosis and varying the serum bicarbonate concentration by acid or alkali supplements. The rise in urine pH was found to be greatest in those with the most profound acidosis and least in those with milder degrees. This paradoxical relation-ship could not be related to improvement of systemic acidosis, external potassium deficits, acidification defects, or increases of nonvolatile buffer excretion. The factor which correlated with the rise of urine pH was the urinary content of ammonia. This observation suggests that the urinary ammonia concentration may determine, rather than be determined by, the urinary acidity during chronic metabolic acidosis. Addition of ammonia to segments of the nephron with large secretory reserves for H + should not elevate urine pH. Since the collecting duct is the only segment of the nephron shown to have limited H + secretory capacity, we propose that the alkalinizing effect of ammonia on urine pH during prolonged acidosis is due to augmented addition of basic NH 3 to the collecting duct by diffusion from the loop of Henle. This view is compatible with the concept that ammonia entering the proximal tubule may be excreted by this route.