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BACKGROUND: The renin–angiotensin system (RAS) is essential in renal physiology; however, disturbance of the RAS is one of the chief pathways involved in renal injury. Dysregulation of RAS may result in both glomerular and tubulointerstitial injuries through direct effects of angiotensin II (Ang II) type 1 receptor. Irbesartan and other Ang II blockers have renoprotective effect through reduction of on renal inflammations. Therefore, the aim of the present study was to demonstrate the renoprotective effect of irbesartan on gentamicin-induced nephrotoxicity in rats concerning the oxidative stress.  MATERIALS AND METHODS: Thirty Sprague-Dawley Male rats divided into three groups, Group I (10 rats) treated with distilled water, Group II (10 rats) treated with gentamicin, and Group III (10 rats) treated with gentamicin plus irbesartan for 12 days. Blood urea, serum creatinine, serum malondialdehyde (MDA), superoxide dismutase (SOD), glutathione reductase (GSH), neutrophil gelatinase-associated lipocalin (NGAL), kidney injury molecules (KIM-1), and cystatin-c were measured in each group.  RESULTS: Irbesartan significantly reduced blood urea, serum creatinine, serum MDA, NGAL, KIM-1, and cystatin-c P &lt; 0.05. Irbesartan significantly increases SOD P &lt; 0.05 without significant effect in elevation of GSH serum levels.  CONCLUSION: Irbesartan has renoprotective effect in attenuation of acute nephrotoxicity through modulation of oxidative stress and antioxidant capacity in rats.

Renoprotective effect of irbesartan in a rat model of gentamicin-induced nephrotoxicity: Role of oxidative stress