Renal Tubular Acidosis Due to Amphotericin B

Abstract

Nephrotoxicity, the major complication of long-term therapy with amphotericin B, is attributed to drug-induced renal vasoconstriction plus a direct toxic action on renal tubules. Hypokalemia and hyposthenuria may precede azotemia; biopsy usually shows nephrocalcinosis. Since these features suggest renal tubular acidosis (RTA), urinary acid excretion was studied in seven patients with amphotericin nephropathy. The results were compared with findings in 25 normal controls, six patients with other forms of renal disease and six with RTA. Five of the patients on amphotericin B had defects in acid excretion characteristic of distal RTA. These defects could not be attributed to decreased glomerular filtration. A tubular defect in acid excretion, superimposed on an ischemic kidney, appears to underlie both the hypokalemia and the nephrocalcinosis characteristic of amphotericin nephropathy. Concomitant alkali therapy during prolonged amphotericin B administration might prove prophylactically useful.