Introduction: Renal ischemia–reperfusion injury (IRI) is a major cause of acute kidney injury. Currently, hydrogen sulfide (H2S) as third gasotransmitter, after nitric oxide (NO) and carbon monoxide (CO) has been known to play a role in the treatment of I/R injury. The present study examined the effects of exogenous H2S on renal ischemia reperfusion (IR) injury in male rats. Methods and Materials: In this study, twenty-one male Sprague-Dawley rats were randomly assigned to Sham, IR, and sodium hydrosulfide (NaHS, an H2S donor) groups. To create a model of renal IRI, renal pedicles were occluded for 60 minutes followed by 24 hours of reperfusion. Rats in the NaHS group received intraperitoneal injections of 100 μmol/kg NaHS 30 minutes before the I/R procedure. Sham group underwent operation without clamping of renal pedicles. After 24 hours of reperfusion, plasma and renal tissue samples were collected for functional and histological evaluation. Results: Renal IR led to a significant increase in Plasma creatinine and BUN as markers of renal function. Administration of NaHS decreased serum BUN and Cr levels, as well as histological damage caused by renal IR injury. Conclusion: Our findings demonstrate that exogenous H2S can against renal IRI by improve renal function, less tubular damage and less acut tubular necrosis.