Objective: This study was conducted to investigate the protective effect of L-arginine (L-Arg) on renal damage induced by cadmium (Cd) and lead (Pb) toxicities in rats. Methods: Thirty-six healthy mature male albino rats were allocated into six experimental groups (n=6/group): control group, L-arginine group (L-Arg) administered 200 mg/kg b.wt L-Arg, cadmium chloride group (Cd) received 5 mg/kg b.wt Cd chloride, lead acetate group (Pb) received 25 mg/kg b.wt Pb acetate, L-Arg + Cd chloride

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... (L-Arg + Cd) received L-Arg 30 minutes prior to Cd chloride, and L-Arg + Pb acetate group (L-Arg + Pb) received L-Arg 30 minutes prior to Pb acetate. All treatments were given orally once daily for 15 days. Results: The results revealed that exposure of rats to Cd chloride and Pb acetate resulted in a significant (p < 0.05) increase in serum creatinine, urea, uric acid, and renal malondialdehyde (MDA) levels and a significant (p < 0.05) decrease in superoxide dismutase (SOD), catalase (CAT), reduced glutathione (GSH) activities in kidney and induced histopathological alterations in kidney tissue. However, pretreatment with L-Arg attenuated all deleterious effects induced by Pb and Cd. Conclusion: The present results support the hypothesis that the amino acid, L-arginine, is an efficient antioxidant capable of minimizing the hazard effects of cadmium chloride and lead acetate on the kidney.