Research progress on the pathogenesis of AKI complicated by ECMO.

Abstract

Extracorporeal membrane oxygenation (ECMO) stands as a pivotal intervention for patients grappling with cardiopulmonary insufficiency. However, alongside its therapeutic benefits, ECMO carries the risk of complications, with acute kidney injury (AKI) emerging as a significant concern. The precise pathophysiological underpinnings of AKI in the context of ECMO remain incompletely elucidated. A comprehensive literature review was conducted to explore the epidemiology and pathophysiological mechanisms underlying the utilization of ECMO in the management of AKI. ECMO initiates a multifaceted cascade of inflammatory reactions, encompassing complement activation, endothelial dysfunction, white blood cell activation, and cytokine release. Furthermore, factors such as renal hypoperfusion, ischemia-reperfusion injury, hemolysis, and fluid overload exacerbate AKI. Specifically, veno-arterial ECMO (VA-ECMO) may directly induce renal hypoperfusion, whereas veno-venous ECMO (VV-ECMO) predominantly impacts pulmonary function, indirectly influencing renal function. While ECMO offers significant therapeutic advantages, AKI persists as a potentially fatal complication. A thorough comprehension of the pathogenesis underlying ECMO-associated AKI is imperative for effective prevention and management strategies. Moreover, additional research is warranted to delineate the incidence of AKI secondary to ECMO and to refine clinical approaches accordingly.