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Nephrol Dial Transplant (2001) 16: 1982-1985
© 2001 European Renal Association-European Dialysis and Transplant Association

Editorial Comments

To what extent can limiting cold ischaemia/reperfusion injury prevent delayed graft function?

Thierry Hauet1, Jean Michel Goujon1 and Alain Vandewalle2,

1 Unité de Transplantation Expérimentale, INRA, Domaine du Magneraud, Surgères and Faculté de Médecine, Centre Hospitalo, Universitaire, La Milétrie, Poitiers and 2 Unité 478 INSERM, Institut Fédératif de Recherche 02, Faculté de Médecine Xavier Bichat, Paris, France

Introduction

Renal injury may be caused by numerous factors, including ischaemia, toxins and autoimmune diseases. In recent years, chronic allograft nephropathy has become one of the main causes of late organ loss following transplantation. Several clinical and experimental studies have suggested that, in addition to alloantigen-dependent factors, several alloantigen-independent factors may be also involved in this process [1]. The most commonly accepted alloantigen-independent risk factors for chronic allograft nephropathy are cytomegalovirus infection, drug cytotoxicity, patient noncompliance, donor age, hyperlipidaemia and hypertension. These non-immunological factors certainly play an important part in the onset of chronic allograft nephropathy by directly damaging the transplanted kidney and also through their interaction with a variety of immune factors such as histo-incompatibility and acute rejection episodes. Non-immune renal injury of the kidney to be transplanted may also begin before the brain death of the donor and continue after transplantation [2].

Until recently, the . . . [Full Text of this Article]

Strategies for attenuating ischaemia/reperfusion injury

The consequences of cold storage on reperfused kidneys

Is there a link between ischaemia/reperfusion injury and the onset of interstitial fibrosis?

Conclusions and perspectives

Acknowledgments

Notes

References


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