Inhibition of gentamicin–induced renal tubular cell necrosis

Gentamicin nephrotoxicity limit its usage against gram negative bacteria. Most researches showed that antioxidant agents improved gentamicin nephrotoxicity. According to these investigations oxidative stress play a central role in the mechanism of gentamicin induced nephrotoxicity. Recently Rafieian-Kopaei and colleagues showed that erythropoietin significantly ameliorated serum creatinine, blood urea nitrogen and tubal necrosis in gentamicin induced nephrotoxicity in rat. One of the advantages of this study is treatment of rats for 10 days by erythropoietin after inducing gentamicin nephrotoxicity and besides co- treatment of gentamicin and erythropoietin at 10 days simultaneously. They showed that erythropoietin improved significantly serum creatinine and blood urea nitrogen in gentamicin injected rats simultaneously and even after gentamicin nephrotoxicity induction. This study also showed that erythropoietin ameliorates histopathological injuries especially tubular cell necrosis that induced by gentamicin. Although the detailed renoprotective mechanisms of erythropoietin cannot be fully explained by this study but histological and biochemical results are satisfactory.