Abstract
Background: Acute kidney injury (AKI) is associated with increased morbidity and mortality in patients with acute myocardial infarction (AMI). Use of trans-valvular pumps and veno-arterial extracorporeal membrane oxygenation (VA-ECMO) for patients with AMI is growing. Trans-valvular pumps transfer rotational kinetic energy to blood and generate flow from the left ventricle into the ascending aorta. VA-ECMO drains blood from the venous system and returns oxygenated blood into the descending aorta, thereby increasing systemic perfusion. The impact of these support strategies on renal blood flow and function remains poorly understood. We hypothesized that compared to a trans-valvular pump, VA-ECMO is associated with increased renal injury in AMI. Methods and Results: Adult male swine were subjected to left anterior descending artery occlusion for 90 minutes followed by either immediate reperfusion (IRI), trans-valvular pumping (Impella CP) or VA-ECMO starting 30 minutes before reperfusion, or sham-operated controls (n=4/group). Compared to IRI, urinary levels of the biomarker kidney injury molecular 1 (KIM-1) were increased by VA-ECMO, not Impella. Inflammatory factors IL6 and IL1beta were increased by VA-ECMO, not Impella in both plasma and cortex tissue by ELISA analysis. KIM-1 protein expression for precursor KIM-1 and the extracellular domain (soluble) of KIM-1, as well as STAT3, HIF1alpha were analyzed by Western blot. Compared to sham, IRI and VA-ECMO reduced levels of soluble KIM-1 and increased levels of the KIM-1 protein precursor, pSTAT3 and HIF1a in the renal cortex. Impella had no impact on these protein levels. Conclusion: This is first study to identify that VA-ECMO, not Impella, increases urinary levels of KIM-1 , a highly sensitive biomarker of acute kidney injury. The shedding of KIM-1 extracellular domain from the renal cortex is associated with systemic inflammatory response. These findings may identity novel approaches to limit renal injury in AMI patients requiring mechanical circulatory support.
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