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Ischaemia reperfusion injury: mechanisms of progression to chronic graft dysfunction

Lookup NU author(s): Dr Aldi Situmorang, Professor Neil SheerinORCiD



This work is licensed under a Creative Commons Attribution 4.0 International License (CC BY 4.0).


© 2018 The Author(s) The increasing use of extended criteria organs to meet the demand for kidney transplantation raises an important question of how the severity of early ischaemic injury influences long-term outcomes. Significant acute ischaemic kidney injury is associated with delayed graft function, increased immune-associated events and, ultimately, earlier deterioration of graft function. A comprehensive understanding of immediate molecular events that ensue post-ischaemia and their potential long-term consequences are key to the discovery of novel therapeutic targets. Acute ischaemic injury primarily affects tubular structure and function. Depending on the severity and persistence of the insult, this may resolve completely, leading to restoration of normal function, or be sustained, resulting in persistent renal impairment and progressive functional loss. Long-term effects of acute renal ischaemia are mediated by several mechanisms including hypoxia, HIF-1 activation, endothelial dysfunction leading to vascular rarefaction, sustained pro-inflammatory stimuli involving innate and adaptive immune responses, failure of tubular cells to recover and epigenetic changes. This review describes the biological relevance and interaction of these mechanisms based on currently available evidence.

Publication metadata

Author(s): Situmorang GR, Sheerin NS

Publication type: Article

Publication status: Published

Journal: Pediatric Nephrology

Year: 2019

Volume: 34

Issue: 6

Pages: 951-963

Print publication date: 01/06/2019

Online publication date: 30/03/2018

Acceptance date: 02/03/2018

Date deposited: 12/04/2018

ISSN (print): 0931-041X

ISSN (electronic): 1432-198X

Publisher: Springer Verlag


DOI: 10.1007/s00467-018-3940-4


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