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BACKGROUND: Chronic renal allograft failure (CAF) is influenced by both allo-dependent and independent factors and is a major cause of graft loss in clinical renal transplantation. We evaluated a novel membrane-bound free radical scavenger, lecithinized superoxide dismutase (lec-SOD), to determine its potential in limiting the harmful effects of ischemia/reperfusion injury on CAF. METHODS: Fisher rat kidneys were stored for either 1 hour or 18 hours in cold Marshall's preservation solution either with or without lec-SOD and transplanted into Lewis recipients. RESULTS: Within 3 days of transplantation, an early inflammatory response involving granulocytes and macrophages was detected in renal allografts exposed to 18 hours cold ischemia that was significantly reduced by preservation with lec-SOD. By 24 weeks post-transplantation, elevated proteinuria and detection of apoptotic cells was observed in kidneys exposed to 18 hours of cold ischemia, that was attenuated by preservation with lec-SOD (P < 0.05). However, up-regulated expression of intracellular adhesion molecule-1 (ICAM-1) and major histocompatibility complex (MHC) Class II together with a T lymphocyte infiltration were observed at 24 weeks that was not prevented by preservation with lec-SOD. CONCLUSIONS: These results demonstrate that ischemia/reperfusion injury, apoptotic cell death and allo-immune responses may be exacerbated by cold ischemia and accelerate the development of CAF. Preservation with lec-SOD may protect against the early damage induced by cold ischemia and reperfusion injury.

Original publication

DOI

10.1046/j.1523-1755.2002.00217.x

Type

Journal article

Journal

Kidney Int

Publication Date

03/2002

Volume

61

Pages

1160 - 1169

Keywords

Animals, Apoptosis, Cryopreservation, Free Radical Scavengers, Histocompatibility Antigens Class I, Humans, Intercellular Adhesion Molecule-1, Ischemia, Kidney, Kidney Transplantation, Leukocytes, Male, Phosphatidylcholines, Rats, Rats, Inbred F344, Rats, Inbred Lew, Recombinant Proteins, Renal Circulation, Reperfusion Injury, Superoxide Dismutase