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Vasopressin-Resistant Nephrogenic Diabetes InsipidusA Result of Amphotericin B Therapy
Galen L. Barbour, MD;
Karl D. Straub, MD, PhD;
Barry L. O'Neal, MD;
James W. Leatherman, MD
Arch Intern Med. 1979;139(1):86-88.
Abstract
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.
(Arch Intern Med 139:86-88, 1979)
Author Affiliations
From the Renal Disease (Drs Barbour and Leatherman) and Pulmonary Disease (Drs Straub and O'Neal) Sections, Department of Medicine, Veterans Administration Hospital, Little Rock, Ark.
Footnotes
Accepted for publication Sept 12, 1978.
Reprint requests to the Veterans Administration Hospital, 300 E Roosevelt Rd, Little Rock, AR 72206 (Dr Barbour).
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