title: Biological modulation of renal ischemia-reperfusion injury.
abstract: OBJECTIVE
  Biological modulation of renal ischemia-reperfusion injury holds the potential to reduce the incidence of early graft dysfunction and to safely expand the donor pool with kidneys that have suffered prolonged ischemic injury before organ recovery.
  
  
  RESULTS
  In the current review, we will discuss clinical studies that compare kidney transplant recipients with and without early graft dysfunction in order to elucidate the pathophysiology of ischemic acute allograft injury. We will specifically review the mechanisms leading to depression of the glomerular filtration rate and activation of the innate immune system in response to tissue injury.
  
  
  CONCLUSIONS
  We conclude that the pathophysiology of delayed graft function after kidney transplantation is complex and shares broad similarity with rodent models of ischemic acute kidney injury. Given the lack of specific therapies to prevent delayed graft function in transplant recipients, comprehensive efforts should be initiated to translate the promising findings obtained in small animal models into clinical interventions that attenuate ischemic acute kidney injury after transplantation.
authors.affiliation: Department of Surgery, Maastricht University Medical Center, Maastricht, The Netherlands. m.snoeijs@mumc.nl
authors.forename: Maarten G J
authors.initials: MG
authors.lastname: Snoeijs
authors.forename: L W Ernest
authors.initials: LW
authors.lastname: van Heurn
authors.forename: Wim A
authors.initials: WA
authors.lastname: Buurman
mesh_terms: D000208:Acute Disease; D000818:Animals; D019610:Cytoprotection; D006801:Humans; D016030:Kidney Transplantation / Q000009:adverse effects / Q000379:methods*; D009926:Organ Preservation / Q000009:adverse effects / Q000379:methods*; D019188:Organ Preservation Solutions / Q000627:therapeutic use; D010477:Perfusion; D055031:Primary Graft Dysfunction / Q000209:etiology / Q000503:physiopathology / Q000517:prevention & control*; D020011:Protective Agents / Q000627:therapeutic use; D015427:Reperfusion Injury / Q000209:etiology / Q000503:physiopathology / Q000517:prevention & control*; D018570:Risk Assessment; D012307:Risk Factors; D014019:Tissue Donors / Q000600:supply & distribution*; D014184:Transplantation, Homologous; D016896:Treatment Outcome
chemical_list: D019188:Organ Preservation Solutions; D020011:Protective Agents