Vasopressin-resistant nephrogenic diabetes insipidus. A result of amphotericin B therapy
G. L. Barbour, K. D. Straub, B. L. O'Neal and J. W. Leatherman
Polyuria and polydipsia developed in two cases during amphotericin B
therapy for deep mycoses. Neither patient could concentrate his urine in
response to water deprivation or exogenous vasopressin. Other causes of
vasopressin-resistant nephrogenic diabetes insipidus were not present.
Three months after amphotericin B therapy had been discontinued,
concentrating ability improved toward normal. A third patient was further
observed and demonstrated normal diluting capacity but impaired free-water
reabsorption, suggesting a distal tubular defect consistent with
nephrogenic diabetes insipidus. Four months after discontinuing therapy,
renal concentrating ability was normal. Amphotericin B can induce a
reversible form of nephrogenic diabetes insipidus.
