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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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Autores principales: Zhao, Hailin, Alam, Azeem, Soo, Aurelie Pac, George, Andrew J.T., Ma, Daqing
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Elsevier 2018
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5835570/
https://www.ncbi.nlm.nih.gov/pubmed/29398595
http://dx.doi.org/10.1016/j.ebiom.2018.01.025
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author Zhao, Hailin
Alam, Azeem
Soo, Aurelie Pac
George, Andrew J.T.
Ma, Daqing
author_facet Zhao, Hailin
Alam, Azeem
Soo, Aurelie Pac
George, Andrew J.T.
Ma, Daqing
author_sort Zhao, Hailin
collection PubMed
description 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.
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spelling pubmed-58355702018-03-06 Ischemia-Reperfusion Injury Reduces Long Term Renal Graft Survival: Mechanism and Beyond Zhao, Hailin Alam, Azeem Soo, Aurelie Pac George, Andrew J.T. Ma, Daqing EBioMedicine Review 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. Elsevier 2018-02-02 /pmc/articles/PMC5835570/ /pubmed/29398595 http://dx.doi.org/10.1016/j.ebiom.2018.01.025 Text en © 2018 The Authors http://creativecommons.org/licenses/by-nc-nd/4.0/ This is an open access article under the CC BY-NC-ND license (http://creativecommons.org/licenses/by-nc-nd/4.0/).
spellingShingle Review
Zhao, Hailin
Alam, Azeem
Soo, Aurelie Pac
George, Andrew J.T.
Ma, Daqing
Ischemia-Reperfusion Injury Reduces Long Term Renal Graft Survival: Mechanism and Beyond
title Ischemia-Reperfusion Injury Reduces Long Term Renal Graft Survival: Mechanism and Beyond
title_full Ischemia-Reperfusion Injury Reduces Long Term Renal Graft Survival: Mechanism and Beyond
title_fullStr Ischemia-Reperfusion Injury Reduces Long Term Renal Graft Survival: Mechanism and Beyond
title_full_unstemmed Ischemia-Reperfusion Injury Reduces Long Term Renal Graft Survival: Mechanism and Beyond
title_short Ischemia-Reperfusion Injury Reduces Long Term Renal Graft Survival: Mechanism and Beyond
title_sort ischemia-reperfusion injury reduces long term renal graft survival: mechanism and beyond
topic Review
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5835570/
https://www.ncbi.nlm.nih.gov/pubmed/29398595
http://dx.doi.org/10.1016/j.ebiom.2018.01.025
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