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<p>Kidney transplant rejection is still a&#xa0;main reason for premature graft loss. Currently, a differentiation is made between antibody-mediated rejection (AMR) and T&#xa0;cell-mediated rejection (TCMR) and histopathologically differentiated by the Banff 2022 classification. Treatment recommendations for the different forms of rejection were recently updated. For the treatment of TCMR steroid pulse therapy and/or antithymocyte globulin (ATG) remain standard, depending on the severity. In acute AMR elimination of circulating antibodies should be carried out in the early phase after transplantation by plasmapheresis (PP) or immunoadsorption (IA), but in chronically active AMR there is too little evidence for PP or IA. In both forms of AMR high-dose intravenous administration of immunoglobulins (IVIG) can be useful. Severe treatment-refractory cases of early acute AMR can be treated with a&#xa0;complement inhibitor such as eculizumab, especially in the presence of signs of thrombotic microangiopathy. In cases of chronic AMR adherence should be evaluated, and the immunosuppressive regimen should be optimized as, so far, there was no good evidence for treatment escalation. Recently, anti-CD38 (cluster of differentiation) therapy with felzartamab, a&#xa0;monoclonal antibody directed against natural killer cells and plasma cells, has shown promising results in a&#xa0;phase 2 trial in patients with later active AMR. Isolated case reports and case series with daratumumab provide additional evidence for the inclusion of anti-CD38 treatment in AMR.</p>

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Update Therapie Nierentransplantation und Rejektion

  • 期刊论文

  • 发表日期：

    2025年12月4日

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  • Christine Kurschat,
  • Klemens Budde

摘要

Kidney transplant rejection is still a main reason for premature graft loss. Currently, a differentiation is made between antibody-mediated rejection (AMR) and T cell-mediated rejection (TCMR) and histopathologically differentiated by the Banff 2022 classification. Treatment recommendations for the different forms of rejection were recently updated. For the treatment of TCMR steroid pulse therapy and/or antithymocyte globulin (ATG) remain standard, depending on the severity. In acute AMR elimination of circulating antibodies should be carried out in the early phase after transplantation by plasmapheresis (PP) or immunoadsorption (IA), but in chronically active AMR there is too little evidence for PP or IA. In both forms of AMR high-dose intravenous administration of immunoglobulins (IVIG) can be useful. Severe treatment-refractory cases of early acute AMR can be treated with a complement inhibitor such as eculizumab, especially in the presence of signs of thrombotic microangiopathy. In cases of chronic AMR adherence should be evaluated, and the immunosuppressive regimen should be optimized as, so far, there was no good evidence for treatment escalation. Recently, anti-CD38 (cluster of differentiation) therapy with felzartamab, a monoclonal antibody directed against natural killer cells and plasma cells, has shown promising results in a phase 2 trial in patients with later active AMR. Isolated case reports and case series with daratumumab provide additional evidence for the inclusion of anti-CD38 treatment in AMR.