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Effect of N-acetylcysteine against Vancomycin-Induced Nephrotoxicity: A Randomized Controlled Clinical Trial
Shirinsadat Badri1,2, Rasool Soltani1, Mina Sayadi3
1Department of Clinical Pharmacy and Pharmacy Practice, Faculty of Pharmacy, Isfahan University of Medical Sciences, Isfahan, Iran.
Background:
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.
Methods:
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.
Results:
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).
Conclusion:
NAC has the potential for reduction of VIN. However, more studies are necessary to confirm this effect.
Insights
N-acetylcysteine (NAC) may help prevent vancomycin-induced nephrotoxicity (VIN) by reducing kidney damage. Further research is needed to confirm NAC's protective effects against VIN.
Area of Science:
- Nephrology
- Pharmacology
- Toxicology
Background:
- Vancomycin-induced nephrotoxicity (VIN) is a significant clinical concern.
- The mechanism of VIN is thought to involve indirect reactive oxygen species production in kidney tissue.
- N-acetylcysteine (NAC), an antioxidant, was investigated for its potential to prevent VIN.
Purpose of the Study:
- To evaluate the efficacy of N-acetylcysteine (NAC) in preventing vancomycin-induced nephrotoxicity (VIN).
Main Methods:
- A randomized controlled trial comparing NAC (600 mg every 12 hours for 10 days) with a placebo in patients receiving vancomycin.
- Monitoring of serum creatinine, blood urea nitrogen, creatinine clearance, and urine volume.
- Assessment of acute kidney injury (AKI) incidence in both groups.
Main Results:
- Patients receiving NAC showed significantly lower serum creatinine and higher creatinine clearance compared to the control group.
- While not statistically significant, the incidence of vancomycin-induced AKI was lower in the NAC group (4.76%) versus the control group (12.63%).
Conclusions:
- N-acetylcysteine (NAC) demonstrates potential in reducing vancomycin-induced nephrotoxicity.
- Additional studies are required to definitively establish NAC's role in preventing VIN.
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