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1 Department of Medicine, Johns Hopkins University School of Medicine, Baltimore, MD, USA
2 Department of Anesthesiology and Critical Care Medicine, Johns Hopkins University School of Medicine, Baltimore, MD, USA
* To whom correspondence should be addressed. E-mail: hrabb1{at}jhmi.edu.
Acute renal failure (ARF) commonly occurs after whole body ischemia. Most experimental models of ARF have relied on the isolated renal artery clamping model, however there is a pressing need to develop and understand the pathogenesis of new models with more "clinical relevance". We evaluated a new murine model of ARF after whole body ischemia reperfusion injury (WBIRI). WBIRI was induced by a infusion of potassium chloride and a cardiac arrest period of 10 minutes. Resuscitation was achieved by cardiac compressions, ventilation, epinephrine and fluids. WBIRI lead to a significant increase in serum creatinine (SCr) and renal tubular injury by 24 hours. Renal myeloperoxidase (MPO) levels increased at 24 hours after WBIRI. Increased expression of the pro-inflammatory genes, ICAM-1 and IL-6, were also observed in the kidney following WBIRI. Based on recent data that T cells are important mediators of isolated renal IRI, WBIRI was evaluated in T cell deficient, nu/nu mice. T cell deficient mice had a significantly reduced rise in SCr and decreased tubular injury compared to wild type mice. T cell deficient mice had a decrease in ICAM-1 expression after WBIRI, but no decrease in renal MPO. This study describes a new clinically relevant model of ARF after WBIRI in mice, and identifies the T cell as an important mediator of renal injury following WBIRI. Reduced ICAM-1 expression may provide a mechanism for this involvement.
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