Role of Inflammatory Cytokine Adsorption on VA‐ECMO‐Induced Acute Kidney Injury of Rats

ABSTRACT Extracorporeal membrane oxygenation (ECMO) is a high‐risk, invasive therapy that sustains life through an external system. However, it often leads to complications such as bleeding, thrombosis, infection, and acute kidney injury (AKI). While up to 70% of ECMO patients develop AKI, the mechanisms driving this injury remain unclear, and effective treatments are limited. To address this, we developed a rat model of AKI induced by veno‐arterial ECMO (VA‐ECMO) and tested the protective effects of a multi‐targeted inflammatory factor adsorption technology. Rats undergoing 3‐h VA‐ECMO exhibited hallmark renal dysfunction, including elevated levels of serum creatinine (Scr) and increased blood urea nitrogen (BUN), accompanied by upregulated renal inflammatory cytokines and tubular apoptosis. Incorporating a cytokine‐targeted hemoperfusion device normalized Scr/BUN levels, reduced histopathological damage, and suppressed apoptosis. Mechanistically, adsorption therapy downregulated pro‐inflammatory mediators and rebalanced apoptotic regulators, favoring anti‐apoptotic Bcl‐2 over pro‐apoptotic Bax and cleaved caspase‐3. These results demonstrate that cytokine adsorption alleviates VA‐ECMO‐induced AKI through dual suppression of systemic inflammation and intrinsic apoptosis. This study provides a mechanistic basis for clinical translation of adsorption‐based strategies to preserve renal function in ECMO patients, addressing a critical unmet need in critical care.