Antibody-mediated rejection (AMR) is a major cause of late kidney transplant failure. Although hyperacute (i.e., preformed antibody-mediated) rejection has been recognized since the 1960s, the role of antibodies in other forms of rejection was not clear until new diagnostic methods became available. The knowledge about the role of antibodies in allograft rejection, particularly in some forms of chronic allograft rejection, has been evolving rapidly over the last decade.
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AMR is characterized by circulating DSAs or non-HLA antibodies, evidence of complement deposition, microvascular inflammation with leukocyte infiltration, and endothelial injury. The cellular and molecular pathways that regulate ABMR are still under investigation. Treatment protocols for AMR use permutations of a multiple-prong approach that include: the suppression of the T-cell dependent antibody response, the removal of donor reactive antibody, the blockade of the residual alloantibody, and the depletion of naive and memory B-cells.
Because of current immunosuppressive medications, the rates of acute rejection and 1-year graft survival have substantially improved. Current strategies for the treatment of AMR include antibody depletion with plasmapheresis (PLEX), immunoadsorption (IA), immunomodulation with intravenous immunoglobulin (IVIG), and T cell– or B cell–depleting agents.
Some treatment benefits have been found in using PLEX and IA, and some small nonrandomized trials have identified some benefits in using rituximab and the proteasome inhibitor-based therapy bortezomib. To target antibody-producing plasma cells, several centers have advocated the use of bortezomib, a Takeda Oncology Company product. It is proteasome inhibitor that is already approved for the treatment of multiple myelom
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