Cyclosporine A (CsA) is the most widely used immunosuppressive drug for preventing graft rejection and autoimmune disease. However, the therapeutic treatment induces several side effects such as nephrotoxicity, cardiotoxicity and hepatotoxicity. This study aimed to assess the protective role of lipoic acid (LA) on kidney and liver toxicity of male albino rats induced by CsA. Forty adult male rats were allocated into four groups. Group (I) served as a control group. Group (II), received orally CsA (25 mg/kg body weight), daily for 3 week. Group III (recovery CsA group), treated orally with CsA (25 mg/kg body weight), daily for 3 weeks, then recovered for other 3 weeks. Group IV (LA and CsA group), received LA (100 mg/kg body weight) orally 1 hour before treatment by CsA (25 mg/kg body weight) daily for 3 weeks. The results indicated that treatment of CsA caused a significant elevation of serum urea, creatinine, uric acid and glucose concentrations. Also, a significant elevation of serum alanine and aspartate aminotransferases (ALT & AST), gamma glutamate transferase (GGT) activities was recorded in comparison with the control group. On the other hand, serum of total protein, albumin and globulin contents showed a highly significant decrease. Renal and hepatic malondialdehyde (MDA) concentration was markedly increased, reflecting increased lipid peroxidation, whereas reduced glutathione (GSH) level and superoxide dismutase (SOD) activity were significantly decreased. On the other hand, LA plus CsA dose-dependently inhibited levels of serum urea, creatinine and uric acid, in addition to AST, ALT and GGT activities. Serum total protein, albumin, globulin and glucose restored in group (IV). The administration of LA plus CsA exhibited a significant reduction of lipid peroxidation (LPO), while GSH content and SOD activity were enhanced significantly, reflecting allevaiation in kindney and liver toxicity. In conclusion, the results demonstrate that lipoic acid has the potential to ameliorate cyclosporine A-induced kidney and liver toxicity by improving lipid peroxidation, GSH content and restoring SOD activity.