Conclusion
N-acetylcysteine pretreatment was effective in reducing the incidence and severity of acute kidney injury as well as in increasing survival. However, N-acetylcysteine posttreatment worsened folic acid toxicity. Only pretreatment was effective in increasing glutathione. These data may help explain the variation from clinical studies of N-acetylcysteine use.
Results
Plasma concentrations of creatinine, cystatin C, and reduced glutathione were measured. Survival time was assessed up to 7 days. The survival rates in N-acetylcysteine pretreatment mice were significantly better (73.33% vs. 46.67%, p < .04) and acute kidney injury was significantly less compared with placebo. However, mice with posttreatment exhibited significantly worse survival and more severe acute kidney injury. Histologic findings were consistent with functional parameters. Glutathione levels decreased less in N-acetylcysteine pretreatment but also increased beginning on day 2 compared with placebo (11.5 vs. 8.1 μg/mL, p < .05). Glutathione levels did not increase in N-acetylcysteine posttreatment. However, three different N-acetylcysteine interventions neither significantly improved nor worsened renal function in the milder acute kidney injury model.