Dexmedetomidine mitigation of renal ischaemia-reperfusion injury: comprehensive insights from cellular mechanisms to clinical application.

Abstract

Renal ischaemia-reperfusion injury (IRI) is a critical cause of acute kidney injury (AKI) after major surgery, leading to elevated morbidity, mortality, and long-term renal dysfunction. Despite advances in perioperative care, the occurrence of IRI remains high. The renoprotective properties of dexmedetomidine (DEX), a selective α2-adrenergic receptor agonist, have been demonstrated, reducing oxidative stress, inflammation, apoptosis, ferroptosis, cellular senescence, and renal fibrosis while enhancing mitochondrial function and autophagy. From cellular studies to clinical applications, DEX has been effective in mitigating renal IRI, enhancing postoperative renal outcomes, and lowering the incidence of AKI in various surgical settings. This review comprehensively discusses and summarises the renoprotective effects and the underlying mechanisms of DEX, with a focus on its application across various surgical and clinical scenarios. In conclusion, DEX effectively mitigates renal IRI, as evidenced by robust in vitro, in vivo, and clinical studies. It significantly reduces kidney damage and improves surgical outcomes. However, its efficacy is less pronounced in kidney transplantation, suggesting that its renoprotective effects vary depending on the clinical context.