Oxygenation of the Transplanted Kidney.

Although kidney oxygen tensions are heterogenous, and mostly below renal vein level, the nephron is highly dependent on aerobic metabolism for active tubular transport. This renders the kidney particularly susceptible to hypoxia, which is considered a main characteristic and driver of acute and chronic kidney injury, albeit the evidence supporting this assumption is not entirely conclusive. Kidney transplants are exposed to several conditions that may interfere with the balance between oxygen supply and consumption, and enhance hypoxia and hypoxic injury. These include conditions leading to and resulting from brain death of kidney donors, ischemia and reperfusion during organ donation, storage and transplantation, postoperative vascular complications, vasoconstriction induced by immunosuppression, and impaired perfusion resulting from interstitial edema, inflammation, and fibrosis. Acute graft injury, the immediate consequence of hypoxia and reperfusion, results in delayed graft function and increased risk of chronic graft failure. Although current strategies to alleviate hypoxic/ischemic graft injury focus on limiting injury (eg, by reducing cold and warm ischemia times), experimental evidence suggests that preconditioning through local or remote ischemia, or activation of the hypoxia-inducible factor pathway, can decrease hypoxic injury. In combination with ex vivo machine perfusion such approaches hold significant promise for improving transplantation outcomes.