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Renal transplant (RT) is the definitive treatment for end-stage renal disease, which is known as a high prevalence pathology with strong economic repercussion both for patients and health systems. Solid organ transplantation is a classically described clinical setting in which massive amounts of reactive oxygen species (ROS) are produced due to ischaemia-reperfusion, thus becoming an essential pathophysiological element involved in delayed graft function in the context of RT. Nevertheless, no clinical protocol yet exists to counteract the damage mediated by ROS intensively produced throughout the transplant process. The available evidence shows a number of successful experiences in the use of antioxidant supplementation and reinforcement over other oxidative stress-related pathologies. This article addresses the pathophysiological role of oxidative stress in RT and its known consequences in function and structure of the allograft, with the objective of gathering consistent information that demonstrates the central role of oxidative stress in this pathology, and to consider it as a possible therapeutic approach in the future. *Correspondence to: Ramón Rodrigo, Laboratory of Oxidative Stress and Nephrotoxicity, Molecular and Clinical Pharmacology Program, Institute of Biomedical Sciences, Faculty of Medicine, University of Chile, P.O.B. 70058, Chile, E-mail: rrodrigo@med.uchile.cl

Role of ischemia-reperfusion in oxidative stress-mediated injury during kidney transplantation