NEPHROTOXIC EFFECTS OF AMPHOTERICIN B INCLUDING RENAL TUBULAR ACIDOSIS

A detailed study of the effects of amphotericin B on renal function in a patient receiving this drug revealed that inulin clearance (CIN), p-aminohippurate clearance (CPAH) and the maximal tubular secretory capacity for p-aminohippurate (TmPAH) decreased during therapy to about one third of their pretreatment values. Concentrating ability was impaired. Urinary potassium losses became excessive, with severe hypokalemia. Urinary calcium and magnesium excretion rates were depressed. Of special interest was the development of a syndrome of renal tubular acidosis. After twenty days of amphotericin B administration, the minimum urinary pH achieved in response to an ammonium chloride load was 6.7, and the excretion of titratable acid was severely impaired. This represents the second occasion on which a syndrome of renal tubular acidosis has been detected in patients receiving amphotericin B. Two months after amphotericin B therapy was stopped, acid excretion, concentrating ability and electrolyte excretion had returned to normal, and TmPAH was 89 per cent of its pretreatment value, but CIN and CPAH were still moderately impaired. The findings of the study emphasize the severity of the renal damage and electrolyte changes that can be produced by amphotericin B therapy, and the need to assess renal function during and after the period of treatment. Prevention of dehydration and also of hypokalemia, by early oral administration of potassium supplements, are suggested as ways to help reduce the nephrotoxic effects of this drug. In view of the development of a renal tubular acidosis syndrome, concurrent alkali (citrate) therapy may be useful. © 1969.