Molecular Mechanisms and Potential Therapeutic Targets of Ischemia–Reperfusion Injury in Kidney Transplantation

End-stage renal disease (ESRD) is a serious and lethal disease that carries with it a high morbidity and mortality rate if left untreated. Treating ESRD is conducted via renal replacement therapy and/or kidney transplantation, with the latter being the preferred option given the better outcomes and quality of life for the patients. However, as ESRD rises in prevalence, kidney transplantation rates remain largely unchanged. In every kidney transplantation, ischemia–reperfusion injury (IRI) is inevitable and the effect this has on the kidney depends based on donor type. IRI works through a variety of molecular mechanisms, primarily mitochondrial oxidative stress and programmed cell death mechanisms. Given the urgency to ensure the best outcomes for these limited kidney transplants, there has been a continued effort to find various potential therapeutic mechanisms to counteract IRI preoperatively, intraoperatively, and postoperatively. These include hypothermic machine perfusion, ischemic conditioning, nanoparticle removal of free radicals, peptide-based therapies, microRNA, and more. There is an ongoing effort to find the best way to mitigate IRI in kidney transplantation and this is being achieved through a better understanding of the molecular mechanisms of IRI.