Renal Effects of Acute Carbon Monoxide Poisoning: The Role of HIF-2α as a Biomarker of Tubular Injury.

Introduction: Carbon monoxide (CO) poisoning is a serious public health concern that induces acute hypoxia, leading to organ damage. The effects of CO exposure on renal function remain insufficiently studied. This study aimed to investigate the impact of CO poisoning on kidney function and structure in an experimental rat model and to evaluate the role of hypoxia-inducible factor-2 alpha (HIF-2α) in this process. Methods: A total of 69 female Wistar Albino rats were used in the study. The rats were divided into a control group (n=9) and experimental groups exposed to CO poisoning and sacrificed at one hour (n=12), six hours (n=12), 12 hours (n=12), 24 hours (n=12), and 48 hours (n=12) post-exposure. CO exposure was administered at a concentration of 5000 ppm for 60 minutes. Blood gas analysis was performed, histopathological changes were evaluated using hematoxylin and eosin (H&E) staining, and HIF-2α expression was assessed via immunohistochemistry. Results: Significant histopathological changes were observed in kidney tissue following CO poisoning, including tubular degeneration, epithelial necrosis, and necrotic debris accumulation (p<0.001). Blood gas analysis showed a significantly elevated carboxyhemoglobin (COHb) level at one hour post-exposure (p<0.001), which returned to normal after six hours. Immunohistochemical analysis revealed a significant increase in HIF-2α expression following CO exposure (p<0.001), with a positive correlation between HIF-2α expression and tubular damage. Discussion: CO poisoning induces renal tubular injury and increases HIF-2α expression as a hypoxic response. These findings suggest that HIF-2α could serve as a potential biomarker for assessing renal damage due to CO exposure. Further studies are needed to evaluate the diagnostic and therapeutic implications of these findings in CO poisoning.