Abstract
Studies of 47 patients with intravenous amphotericin B revealed some impairment of renal function in all cases. Azotemia developed in 46 cases. Microscopic examination in eight cases showed damage to the distal renal tubule. Profound hypokalemia was recognized in two cases; and symptoms suggesting hypokalemia, which were generally ameliorated by potassium administration, were noted in most cases. It is postulated that the initial potassium loss is due to a “tubular leak” and that subsequent potassium depletion leads to further tubular damage.
Mild to severe anemia developed in all cases during therapy. Serial red cell indices, bone marrow examinations and red cell survival studies indicated that hemolysis, rather than bone marrow depression, was responsible.
The decision to treat, to modify therapy or to terminate treatment must be made on the basis of severity of disease, probability of progression, and renal status.
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