Extracorporeal Membrane Oxygenation (ECMO) Does Not Restore Renal Autoregulation in Endotoxin‐Induced Acute Renal Failure

Abstract

Endotoxin‐induced shock may be treated with ECMO for cardiopulmonary support. Renal function during ECMO may be altered due to partial cardiopulmonary bypass and altered regulation of cardiovascular regulating hormones. In anesthetized pigs (n=8), we compared renal function at baseline, after endotoxic shock with acute renal failure was established (via i.v. injection of E coli endotoxin), and after 2 hours of stabilization on venoarterial ECMO. Endotoxin caused a mean arterial pressure (MAP) 33% decrease (p≤0.05) from 88±3 to 59±3 mm Hg. ECMO could maintain blood flow to prevent any further deterioration of MAP, but did not return MAP (56±4 mm Hg) to baseline. Interestingly, the 59% decrease (p≤0.05) in renal microcirculatory blood flow (as measured by microsphere method) caused by endotoxin, was prevented from dropping further with ECMO. However, the endotoxin‐induced 76% decrease in GFR (p≤0.05) continued to decline with ECMO resulting in deterioration of urine flow towards complete renal shut down. The urine flow decrease was due mainly to a decrease in osmotic clearance. Results are consistent with the drop of endogenous vasopressin (VP) levels seen with ECMO that we previously reported. We and others have demonstrated that exogenous VP at high doses is needed to reverse renal shut down. Results suggest that during ECMO, VP replacement therapy may be necessary to restore renal perfusion pressure to maintain urine flow.