Background: L-carnosine can suppress increased renal sympathetic nerve activity (SNA) during the renal ischemia by its action on the central nervous system and that this suppressive effect is probably responsible for the renoprotection against ischemic/reperfusion induced renal injury. In addition, the renoprotective effect of L-carnosine on ischemic acute renal failure seems to be induced by its conversion to L-histidine and L-histamine, and it is mediated through the activation of histamine H3 receptors in the central nervous system. Objective: Studying the effect of carnosine as a potential antioxidant agent on cadmium–induced lipid peroxidation and renal oxidative stress in aged rats. Materials and Methods: The present study was performed on 45 aged female Wistar rats, weighing at the start of the study between 280-380 g. Animals were randomly divided into the following equal groups: Control group, Cadmium group, and Carnosine treated group. Blood samples were collected and were subjected to measurement of serum urea, creatinine, albumin, malondialdehyde (MDA), superoxide dismutase (SOD), nitric oxide (NO) levels, tumor necrosis factor-α (TNF-α), interleukin10 (IL-10) levels, renal tissue tumor necrosis factor-α (TNF-α), superoxide dismutase (SOD), nitric oxide (NO) levels and measurement of cadmium (Cd) level in blood and renal tissue. Also, histopathological study of rat kidneys was performed. Results: Significant increases in serum urea and creatinine, MDA, IL10, serum and renal tissue NO, TNF -α, blood and renal tissue cadmium levels were encountered in cadmium group compared to control group. Carnosine treatment significantly decreased serum urea, creatinine, MDA, IL10, serum and renal tissue NO, TNF -α, blood and renal tissue cadmium levels compared to cadmium group though the levels were still significantly higher than control group. Serum albumin, serum and renal tissue SOD levels significantly decreased in cadmium group compared to control group. By treatment with carnosine, significant increases were observed compared to cadmium group though still significantly less compared to control group.                                          Conclusion: Increased lipid peroxides induced by cadmium toxicity in aged rats may implicate the renal oxidative stress. Moreover, pretreatment with carnosine successively boosted the antioxidant system through several mechanisms such as scavenging/neutralizing free radicals, regulating enzymatic/non enzymatic antioxidants. However, future work is needed to confirm our results.