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Chronic Allograft Nephropathy

  • Pankaj Baluja
    Affiliations
    Department of Medicine, University of Oklahoma, Oklahoma City, OK

    Department of Pathology, University of Oklahoma, Oklahoma City, OK
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  • Lukas Haragsim
    Correspondence
    Address Correspondence to Lukas Haragsim, MD, Associate Professor of Medicine, University of Oklahoma Health Science Center, Oklahoma City, OK 73104.
    Affiliations
    Department of Medicine, University of Oklahoma, Oklahoma City, OK

    Department of Pathology, University of Oklahoma, Oklahoma City, OK
    Search for articles by this author
  • Zoltan Laszik
    Affiliations
    Department of Medicine, University of Oklahoma, Oklahoma City, OK

    Department of Pathology, University of Oklahoma, Oklahoma City, OK
    Search for articles by this author
      With the advent of calcineurin inhibitors, the success of kidney and other solid-organ transplants has improved significantly from the standpoint of reducing the incidence of acute rejection. Over the past 2 decades, both short-term allograft survival and acute rejection rates have dramatically improved with improved diagnostic and therapeutic techniques such as standardized pathology scoring; potent antirejection drugs such as anti–thymocyte globulin, interleukin-2 receptor antibodies, cyclosporine, tacrolimus, sirolimus, and mycophenolate mofetil; and improved infection control such as valganciclovir and antifungal therapy. However, long-term graft loss has remained at nearly constant levels over the same period of time, with the average half-life of a deceased-donor kidney transplant in the United States remaining approximately 1 decade. In addition to death with a functioning allograft and calcineurin toxicity, a chronic fibrotic process—known at various times as chronic rejection, chronic allograft dysfunction, and chronic allograft nephropathy (CAN)—account for the leading causes of transplant failure.

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