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Lecithinized superoxide dismutase reduces cold ischemia-induced chronic allograft dysfunction
Ken Nakagawa1, Dicken D H Koo, David R Davies
1Nuffield Department of Surgery, University of Oxford, John Radcliffe Hospital, Headington, Oxford, OX3 9DU, United Kingdom.
Kidney International
|February 19, 2002
Summary
Lecithinized superoxide dismutase (lec-SOD) reduced early inflammation and cell death from cold ischemia in rat kidney transplants. However, it did not prevent later allo-immune responses contributing to chronic renal allograft failure.
Area of Science:
- Nephrology
- Transplantation immunology
- Biochemistry
Background:
- Chronic renal allograft failure (CAF) is a primary cause of graft loss.
- Ischemia/reperfusion (I/R) injury significantly contributes to CAF.
- Lecithinized superoxide dismutase (lec-SOD) is a novel free radical scavenger evaluated for I/R injury mitigation.
Purpose of the Study:
- To assess the protective effects of lec-SOD against I/R injury in renal transplantation.
- To evaluate lec-SOD's impact on early inflammatory responses and long-term graft outcomes.
Main Methods:
- Fisher rat kidneys were preserved with or without lec-SOD for 1 or 18 hours.
- Kidneys were transplanted into Lewis recipients.
- Early inflammatory markers and long-term outcomes (proteinuria, apoptosis, immune cell infiltration) were assessed.
Main Results:
- Preservation with lec-SOD significantly reduced early granulocyte and macrophage infiltration after 18 hours of cold ischemia.
- lec-SOD attenuated elevated proteinuria and apoptotic cell death at 24 weeks post-transplantation.
- lec-SOD did not prevent the upregulation of ICAM-1, MHC Class II, or T lymphocyte infiltration at 24 weeks.
Conclusions:
- Cold ischemia exacerbates I/R injury, apoptotic cell death, and allo-immune responses, accelerating CAF.
- Preservation with lec-SOD offers protection against early I/R damage.
- Further strategies are needed to address the allo-immune component of CAF.