Abstract
Humoral or vascular rejection results from a B cell-mediated production of immunoglobulin (Ig) G antibody against a transplanted organ, producing immune complex deposition on the vascular endothelium, activation of the complement cascade, generation of endothelial dysfunction, and regional ischemic injury. Antibody-mediated rejection, which may be accompanied by hemodynamic compromise, is associated with reduced long-term graft survival. 1 Patients believed to be at an increased risk of developing humoral rejection include women, 2 particularly those with high levels of panel reactive antibodies, 3 cytomegalovirus seropositivity, 4,5 and positive cross matches, 3,6 and subjects with prior sensitization to OKT3. 7 Treatment options for humoral rejection include plasmapheresis to lower the circulating immunoglobulin levels followed by high-dose cyclophosphamide to reduce the B-cell population. Other modalities include total lymphoid irradiation, photophoresis, splenectomy, and, for treatment failures, retransplantation. 8 Rituximab is a chimeric humanized monoclonal antibody directed against the pan B-cell surface molecule, CD20. It is approved for the treatment of low-grade B-cell non-Hodgkin’s lymphoma. It has also been used successfully for the treatment of posttransplant B-cell lymphoproliferative disease. 9 We report a case of late humoral rejection successfully treated with rituximab.
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