Acute Renal Failure in Kidney Transplant Recipients

Acute kidney injury (AKI) is a common clinical problem. Similar to native kidneys, transplanted kidneys are prone to all forms of AKI. Transplanted organs also are predisposed to a number of additional and specific acute insults related to immunologic injury, toxicity of immunosuppressive agents, ischemia–reperfusion injury, and surgical complications. Fig. 213.1 lists common causes of AKI specifically important to allografts along with the time frame posttransplantation that these causes commonly are encountered in clinical practice. Importantly, the timing of the initial AKI that occurs in most allografts is preset and known ahead of time, serving as an excellent platform to study mechanisms that may be common to all forms of acute renal dysfunction. Delayed graft function (DGF) represents a stereotypic form of AKI after kidney transplantation that results in posttransplantation oliguria, increased allograft immunogenicity, and risk of acute rejection. Rarely, a graft never functions (primary nonfunction). Experimental studies have shown that ischemia and reinstitution of blood flow in ischemically damaged kidneys after hypothermic preservation activate a complex sequence of events that sustain renal injury and play a pivotal role in the development of DGF.

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Timing and cause of allograft acute kidney injury (AKI): the common causes of allograft AKI by the usual time frames of their occurrence after transplantation. The thickness of the lines depicts frequency of occurrence in the respective time frames, which are plotted on the X-axis. ABMR, Antibody-mediated rejection; BKN, BK nephropathy; CNI, calcineurin inhibitors; TCMR, T cell–mediated rejection; UTI, urinary tract infection.

The incidence of DGF has been reported variously to occur in 8% to 50% of primary cadaveric renal transplants in the United States and in 35% of cadaveric transplants in a European multicenter study report. According to the United Network for Organ Sharing (UNOS) Renal Transplant Registry, the frequency of DGF in cadaver transplants declined only slightly, from about 29% to 23% during the 1990s, despite improvements in donor and recipient management and in diagnostic and therapeutic tools. In recent unpublished data from Mount Sinai Hospital, New York, including 96,236 transplants from 1995 to 2012, DGF rate was still 21.9% for recipients of cadaveric kidney transplants. These data showing minimal reduction in DGF rates can be explained partly by the expansion of criteria for acceptable donors, including use of marginal and older donors, as well as recipients that may be more predisposed to develop DGF.