Vasopressin-resistant nephrogenic diabetes insipidus. A result of amphotericin B therapy.
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.
D000666:Amphotericin B / Q000009:adverse effects*; D003919:Diabetes Insipidus / Q000139:chemically induced*; D006801:Humans; D007671:Kidney Concentrating Ability / Q000187:drug effects*; D007674:Kidney Diseases / Q000139:chemically induced*; D008297:Male; D008875:Middle Aged; D009994:Osmolar Concentration; D014556:Urine / Q000032:analysis; D014667:Vasopressins; D014868:Water Deprivation
D014667:Vasopressins; D000666:Amphotericin B