Late kidney dysfunction in a kidney transplant recipient

Abstract

Late kidney transplant dysfunction may be a harbinger of graft failure. For many years, calcineurin inhibitor toxicity was felt to be the main cause for graft dysfunction with fibrosis and transplant loss. Recently this idea has come into question. With the observation that peritubular capillary C4d staining in kidney allografts may indicate antibodymediated injury in conjunctionwith biopsy study findings, an appreciation for antibody-mediated rejection as amajor cause of late graft dysfunction and loss has emerged. Twenty percent to 30% of patients develop de novo donorspecific antibodies after kidney transplantation. There are noUS Food andDrugAdministration-approved treatments for antibody-mediated rejection, nor have any randomized controlled trials assessed efficacy. Off-label treatment strategies include some combination of plasma exchange, intravenous immunoglobulin, and rituximab. Other approaches, including splenectomy, bortezomib, and eculizumab, have also been tried. © 2014 by the American Society of Nephrology.