Dialyzed delayed graft function (DGF) and nondialyzed slow graft function (SGF) both determine a large portion of the negative impact on patient and graft survival, on early acute rejection incidence, on tubulointerstitial fibrosis/tubular atrophy, and on graft function. In an era where expanded-criteria donors, including older donors, and non-heart beating donors are used to overcome organ shortage, the long-term results of kidney transplantation are influenced by the events occurring within the first 24 hr before and after the transplantation procedure. The ischemia-reperfusion injury is initiated in the brain-death donor and continues during preservation and engraftment of the transplant. The determinants of this DGF/SGF complex intervene in five chronologically related stages--donor tissue quality, brain death and related stress, preservation variables, immune factors, and recipient variables. For each of these five stages, therapeutic interventions or preventive measures are capable of partially reversing the expected dismal outcome of DGF/SGF; these measures are discussed in this article. Donor selection and pharmacologic modulations do have an effect on DGF/SGF.
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