Amphotericin B nephrotoxicity in humans decreased by salt repletion.
A major limitation in the use of amphotericin B is its potential to cause nephrotoxicity. In animals, increased dietary sodium reduces renal toxicity. Experience with five patients in whom impaired renal function developed early during amphotericin B therapy is reported. In four of the patients, there was evidence of sodium depletion due to low sodium intake, diuretic administration, or vomiting. In all five patients, sodium loading was associated with improved renal function, which permitted amphotericin B therapy to be continued in fully effective doses to the completion of elective courses of treatment without evidence of residual impaired renal function. These observations are consistent with the hypothesis that intrarenal regulatory mechanisms contribute to changes in renal function due to amphotericin B therapy.
D000368:Aged; D000666:Amphotericin B / Q000009:adverse effects*; D003404:Creatinine / Q000097:blood; D004032:Diet; D005260:Female; D006801:Humans; D007674:Kidney Diseases / Q000139:chemically induced* / Q000188:drug therapy; D008297:Male; D008875:Middle Aged; D012964:Sodium / Q000172:deficiency*; D012965:Sodium Chloride / Q000627:therapeutic use*; D014508:Urea / Q000097:blood
D012965:Sodium Chloride; D000666:Amphotericin B; D014508:Urea; D012964:Sodium; D003404:Creatinine