N-acetylcysteine ameliorates amphotericin-induced nephropathy in rats

Leonid Feldman*, Shai Efrati, Victor Dishy, Leonid Katchko, Sylvia Berman, Michael Averbukh, Mordechai Aladjem, Zhan Averbukh, Joshua Weissgarten

*Corresponding author for this work

Research output: Contribution to journalArticlepeer-review


Background: Amphotericin B may cause acute reduction in renal function. N-acetylcysteine (NAC) has a renoprotective activity in several nephrotoxic renal insults, but its effect on amphotericin-induced renal failure has not been investigated yet. Methods: Acute renal failure was induced in 30 Sprague-Dawley rats by a single intraperitoneal injection of amphotericin B (50 mg/kg). NAC (10 mg/kg) in isotonic saline or isotonic saline alone were administered daily for 4 days, starting 1 day before the amphotericin B injection. Glomerular filtration rate (GFR) was assessed using 99m-technetium diethylene triaminepentaacetic acid. Before and following amphotericin B administration, a 24-hour urine collection was performed for sodium, potassium and magnesium determination. The kidneys were preserved for pathologic examination. Results: Amphotericin B induced a significant decrease of GFR in both groups. Four days after amphotericin injection the GFR in the NAC-treated group was significantly higher than in the control group (0.62 ± 0.20 vs. 0.46 ± 0.14 ml/min, p = 0.042). Histologic signs of acute tubular necrosis were attenuated in the NAC-treated group. There were no significant differences between the groups in sodium, potassium and magnesium urine excretion after amphotericin injection. Conclusions: NAC treatment exerted a renoprotective effect on deterioration of GFR in a rat model of amphotericin-induced renal failure. No functional protection on tubular function, as obviated by similar polyuria and urine losses of potassium and magnesium in both groups, was observed.

Original languageEnglish
Pages (from-to)p23-p27
JournalNephron - Physiology
Issue number1
StatePublished - 2005
Externally publishedYes


  • Acute renal failure
  • Amphotericin B
  • N-acetylcysteine
  • Nephrotoxicity


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