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Ischemia-Reperfusion Injury Reduces Long Term Renal Graft Survival: Mechanism and Beyond
Ischemia-reperfusion injury (IRI) during renal transplantation often initiates non-specific inflammatory responses that can result in the loss of kidney graft viability. However, the long-term consequence of IRI on renal grafts survival is uncertain. Here we review clinical evidence and laboratory s...
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Published in: | EBioMedicine 2018-02, Vol.28 (C), p.31-42 |
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Main Authors: | , , , , |
Format: | Article |
Language: | English |
Subjects: | |
Citations: | Items that this one cites Items that cite this one |
Online Access: | Get full text |
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Summary: | Ischemia-reperfusion injury (IRI) during renal transplantation often initiates non-specific inflammatory responses that can result in the loss of kidney graft viability. However, the long-term consequence of IRI on renal grafts survival is uncertain. Here we review clinical evidence and laboratory studies, and elucidate the association between early IRI and later graft loss. Our critical analysis of previous publications indicates that early IRI does contribute to later graft loss through reduction of renal functional mass, graft vascular injury, and chronic hypoxia, as well as subsequent fibrosis. IRI is also known to induce kidney allograft dysfunction and acute rejection, reducing graft survival. Therefore, attempts have been made to substitute traditional preserving solutions with novel agents, yielding promising results.
•Ischaemia reperfusion injury (IRI) potentiates delayed renal graft function and causes reduction in renal graft survival•IRI causes innate immune system activation, hypoxic injury, inflammation and graft vascular disease•Reducing prolonged cold ischaemic time improves graft survival•Novel protective strategies include mesenchymal stem cells, machine perfusion, and ex vivo preservation solution saturated with gas.•Further studies are needed to investigate the long-term effects of novel ex vivo preservation agents |
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ISSN: | 2352-3964 2352-3964 |
DOI: | 10.1016/j.ebiom.2018.01.025 |