439 Renal ischemic reperfusion injury (IRI) can lead to delayed graft function and likely decreased long term graft survival as well. Increasing evidence supports an important role for adhesion molecules, cytokines and apoptosis in the pathogenesis of renal IRI. Interleukin-1 receptor knockout mice have accelerated recovery from IRI (J Am Soc Neph, in press), suggesting a deleterious role for IL-1 in IRI. Interleukin-1 converting enzyme (ICE) is a cysteine protease important in IL-1 processing as well as Fas- and TNF-mediated apoptosis. We hypothesized that the ICE pathway could mediate renal IRI. We therefore evaluated renal IRI in mice genetically deficient in ICE. ICE knockout (KO) mice and C57BL controls (c) underwent 30 min of warm renal ischemia followed by various times of reperfusion. Serum creatinine(SCr) mg/dl, renal neutrophils/10 high power fields (PMN) and tubular necrosis scores were assessed. n≥3 per group, mean±se, *P<0.05 vs controlTableThese data demonstrate that, contrary to predicted, ICE deficient mice had delayed recovery from renal ischemia, with increased PMNs in renal tissue and more severe tubular necrosis. ICE may play an important protective role during renal IRI.