Experience with antibody-mediated rejection in kidney allograft recipients.

In our case series, AMR occurred in patients who had DSA. Twelve of the 21 patients (57%) who developed de novo antibodies post-transplant had biopsy-proven episodes of either rejection (of any Banff classification) and/or chronic allograft nephropathy. Only one-third of these 12 patients with rejection episodes were classified as AMR. It is unclear when and how often measurements for DSA should be performed after transplantation. When AMR is suspected, the detection of anti-HLA antibodies should be done using very sensitive assays. An increase in PRA and/or the detection of anti-HLA antibodies specific to previous sensitization events may precede an episode of AMR, even in the absence of DSA. Prospective clinical trials are needed to assess the predictive value of the presence of DSA after transplant. It is uncertain which therapeutic response should follow after the detection of these antibody responses in the absence of clinical symptoms. AMR requires intensive therapy, but no standard treatment has been established. Three patients who had AMR at our center were treated with rituximab in addition to various combinations of plasmapheresis, methylprednisolone, OKT3, and intravenous immune globulin. Only one patient responded to this treatment. Well-controlled clinical trials would help to evaluate the efficacy and benefit of B-cell depletion in combination with other immunosuppressive agents.