Objective: To investigate the changes in kidney and its mechanism during the development of acute phosgene exposure in rats. Methods: Rats were randomized into 2 groups: control and phosgene group (including 1, 3, 6, 12 and 24 h after exposed to phosgene) , 6 rats in each group. Rats in control group were exposed to air for 5 min, while rats in phosgene group were exposed to 8.33 mg/L phosgene for 5 min. The blood samples were collected at 1, 3, 6, 12 and 24 h after phosgene exposure. The blood creatinine (Cr) , urea nitrogen (BUN) and blood gas analysis were detected. HE staining and immunohistochemical staining were performed to observe the expression levels of 8-hydroxy deoxyguanosine and myeloperoxidase. Results: The arterial partial pressure of oxygen and oxygenation index of rats in the phosgene group were significantly lower than those in the control group at 3, 6 and 12 h after exposure (P<0.01) . The lowest points were reached at 6 h, which were (58.67±7.89) mmHg and (202.30±27.20) mmHg, respectively. The Cr and BUN of rats in the phosgene group were significantly higher than those in the control group at 3, 6, 12, and 24 h, and the renal organ coefficients were significantly higher than those in the control group at 3, 6 and 12 h (P<0.01) . HE staining showed that there were more erythrocytes in the glomeruli of rats in the phosgene group, the volume of renal tubular epithelial cells increased, and the cytoplasm was loose and lightly stained. The damage was most obvious at 6 h. The results of immunohistochemical staining showed that the positive expressions of 8-hydroxy deoxyguanosine and myeloperoxidase in the kidney tissue of the phosgene group increased. Conclusion: Hypoxemia and oxidative stress caused by phosgene poisoning may be the cause of renal damage in rats.