The Changing Pattern of Humoral Rejection in Cardiac Transplant Recipients

Abstract

Humoral rejection occurs now more frequently in patients with remote transplants and is commonly associated with the presence of malignancy or infection.

Antibody-Mediated Rejection in Cardiac Transplantation: Emerging Knowledge in Diagnosis and Management

“…[25][26][27][28][29][30][31][32] C4d positivity is also used in combination with histological features-with circulating DSA, or clinical graft dysfunction. 23,[33][34][35][36] Depending on how restrictive the pathological definition of AMR is (ie, number of criteria required), the reported incidence varies, with lower reported incidence with more criteria required. Early estimates using C4d alone ranged from 35% to 71%, whereas those using C4d in combination with other immunopathology markers, clinical graft dysfunction, and DSA reported AMR frequencies of 10%, 27%, and 12.5%, respectively.…”

Successful Treatment of Cardiogenic Shock Caused by Humoral Cardiac Allograft Rejection

“…1 Reported risk factors in heart transplant patients for developing humoral rejection include high levels of PRA, positive pre-or post-transplant crossmatch, induction therapy with OKT3, female gender, malignancy, and preceding infection. 2,4 The present patient had received a transfusion of packed red blood cells and platelets at the time of left ventricular assist device implantation, and this may have caused sensitization to human leukocyte antigens. Current options for treatment of humoral rejection include plasmapheresis, immunoadsorption, intravenous immunoglobulin and cyclophosphamide administration, increasing doses of immunosupression, and rituximab.…”

“…[1][2][3][4][5] In previous case reports in which humoral rejection accompanying hemodynamic compromise was successfully treated, [6][7][8][9][10] the EF of the cardiac allografts was 20-40% at the time of diagnosis of humoral rejection. Cardiogenic shock so profound as to necessitate mechanical circulatory support with ECMO and IABP is rare, but many cases of early graft loss that were previously diagnosed as primary graft failure with unknown cause would have been the consequence of humoral rejection.…”

“…Current options for treatment of humoral rejection include plasmapheresis, immunoadsorption, intravenous immunoglobulin and cyclophosphamide administration, increasing doses of immunosupression, and rituximab. 1,4,6 Rituximab is a genetically engineered monoclonal antibody directed against the pan-B cell surface molecule CD20, inhibiting B-cell proliferation and inducing apoptosis by antibody and complement-dependent cellular toxicity. 6 Tcells are unaffected by rituximab, and consequently, opportunistic infections rarely occur in association with its administration.…”

“…1 Humoral rejection is mediated by antibody and complement deposition in the vasculature of the transplanted heart, and it is associated with decreased graft and patient survival, as well as an increased and earlier risk of cardiac allograft vasculopathy. [1][2][3][4] Although cellular rejection has significantly decreased during the past 2 decades because of improved immunosuppressive therapies, the incidence of humoral rejection is reportedly unchanged. 5 In the most cases of humoral rejection, the characteristic findings in the endomyocardial biopsy and routine staining are interstitial edema and capillary endothelial swelling only, which represent a marked influx of macrophages into the injured capillaries.…”