Ischemia-reperfusion injury: Pathophysiology and clinical approach

Significant ischemia-reperfusion injury (IRI) occurs in every deceased donor organ transplant and in some live donor ones. In renal transplants, it remains the leading contributor to delayed graft function (DGF), which in turn predisposes to increased acute rejection and worse long-term allograft function. Donor organ quality, modalities and time of organ preservation and recipient risk factors can all contribute to the generation of IRI in the graft. IRI pathogenesis involves a complex interplay between microvascular, cellular and systemic factors. Activation of inflammatory and immune responses is considered a major factor in the generation and amplification of damage. Activation of T-cells, not only by antigen binding but also by antigen-independent mechanisms, can play an important role in this process. As a result ofbetter understanding of IRI pathogenesis, improved diagnostics and therapeutics have been developed to reduce the extent of the ischemic insult in the graft. This has enabled a safer expansion of the donor pool in order to better cope with the always increasing demand for organs for transplantation.