Renal Warm Ischemia in Organ Donors After Circulatory Death

Chronic kidney disease is the most common type of organ failure worldwide, with a prevalence of 13.4% for all stages. Organ transplant is the only curative option for end-stage kidney failure. However, the shortage of organ donors remains a major obstacle in organ transplant, with donation after circulatory death being the most viable path to increasing the donor pool. The circumstances that surround this type of donation are different from donation after brain death, namely concerning warm ischemia times, which are longer and may preclude a successful transplant. This article describes the pathophysiology of warm ischemia and summarizes recent developments in technological and methodological practices that mitigate the mechanisms of warm ischemia. Anoxia, mitochondrial dysfunction, calcium overload, oxidative and nitrosative stress, immune response, and no reflow are the main mechanisms by which ischemia leads to cell death and organ dysfunction. In situ oxygenated recirculation, abdominal normothermic organ recirculation, abdominal hypothermic organ recirculation, and ex vivo machine perfusion ensure continued organ perfusion and prevent prolonged warm ischemia in organ donation. These practices, coupled with optimizations in the identification and assessment of potential donors after circulatory death, may lead to a significant increase in the number and success rates of organ transplant worldwide.