Proximal Renal Tubular Acidosis and Hypophosphatemia Induced by Arginine

Abstract

Arginine monohydrochloride is a cationic amino acid widely used to test pituitary function (1). In the recent past, its use for the treatment of severe metabolic alkalosis and hepatic encephalopathy was often recommended (2–4). Recognition of its potential for severe hyperkalemia (5,6) prompted the cautious use of this compound. Its use, however, is bound to continue in view of the widespread administration of amino acids in the course of hyperalimentation. This study was undertaken to systematically examine the effect of arginine, at a dose similar to that commonly used clinically, on urinary acidification and plasma electrolyte composition. Our results are in keeping with previous studies showing the development of metabolic acidosis and hyperkalemia during a brief infusion. They further demonstrate that arginine, like other cationic amino acids (7–9), markedly impairs proximal bicarbonate reabsorption. Of interest, a significant fall in plasma phosphate was uncovered by these studies. This could not be ascribed to renal phosphate wastage because phosphate excretion decreased markedly. Hence, arginine induces proximal renal tubular acidosis associated with hypophosphatemia without a renal phosphate leak.