Effect of N-acetylcysteine against Vancomycin-Induced Nephrotoxicity: A Randomized Controlled Clinical Trial

The proposed mechanism of vancomycin-induced nephrotoxicity (VIN) is indirect production of reactive oxygen species in the kidney tissue. This study aimed to investigate the effectiveness of N-acetylcysteine (NAC), an anti-oxidant agent, in the prevention of VIN.

Patients who received vancomycin for any indication were randomly divided to drug (NAC) and control groups. The patients in the drug group received oral NAC 600 mg every 12 hours for 10 days, starting concurrently with vancomycin. Serum creatinine (SCr) levels and blood urea nitrogen (BUN) as well as creatinine clearance (CrCl) and 12-hour urine volume were recorded at baseline, every other day during the study, and 12 hours after the last dose of vancomycin on the 10th day. Furthermore, the cases of acute kidney injury (AKI; ≥ 0.5 mg/dL or at least 50% increase in serum creatinine from baseline) were recorded in the two groups.

Over the study period, 84 and 95 patients completed the study in drug and control groups, respectively. SCr and CrCl were significantly lower and higher, respectively, at all-time points (except for baseline) in the NAC compared to the control group. Furthermore, although not statistically significant, 12 cases of vancomycin-induced AKI were observed in the control group (12.63%), while 4 cases (4.76%) were reported from drug group (P = 0.066; relative risk [RR] = 0.377, 95% CI: 0.126–1.124).

NAC has the potential for reduction of VIN. However, more studies are necessary to confirm this effect.