Delayed graft function in renal transplantation

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Abstract
Delayed graft function is an important determinant of patient and graft survival. A complex of pathologic mechanisms intervenes in the pathophysiology of this outcome. This paper reviews the main processes involved in delayed graft function as they relate to five chronologically related stages: donor tissue quality, brain death and related stress, preservation variables, immune factors, and recipient variables. Dialyzed delayed graft function and nondialyzed slow graft function both have a negative impact on graft survival and on the incidence of acute rejection. Expanded-criteria donors, older donors, and non-heart-beating donors are more frequently used. The long-term results of the use of well-selected non-heart-beating donors are surprisingly good. The process of ischemia/reperfusion injury is already initiated in the brain-death donor and continues during preservation of the graft. Graft-infiltrating T cells, heat shock proteins, and heme oxygenase-1 are implicated in the process. Modifications in immunosuppressive therapy and pharmacologic modulations have an effect on delayed graft function. Delayed graft function plays a part in the incidence of acute rejection, impaired graft function, and survival of patients and grafts. This review discusses the current literature on several recent findings of pathophysiologic mechanisms of, and possible therapeutic interventions in, delayed graft function.