Morphologic and immunohistochemical findings in antibody-mediated rejection of the cardiac allograft.
The recognition and acceptance of the entity of antibody-mediated rejection (AMR) of solid organs has been slow to develop. Greatest acceptance and most information relates to cardiac transplantation. AMR is thought to represent antibody/complement mediated injury to the microvasculature of the graft that can result in allograft dysfunction, allograft loss, accelerated graft vasculopathy, and increased mortality. The morphologic hallmark is microvascular injury with immunoglobulin and complement deposition in capillaries, accumulation of intravascular macrophages, and in more severe cases, microvascular hemorrhage and thrombosis, with inflammation and edema of the affected organ. Understanding of the pathogenesis of AMR, criteria and methods for diagnosis, and treatment strategies are still in evolution, and will be addressed in this review.
Department of Pathology and Laboratory Medicine, David Geffen School of Medicine at UCLA, Los Angeles, CA, USA. gfishbein@mednet.ucla.edu
Gregory A
GA
Fishbein
Michael C
MC
Fishbein
D000906:Antibodies / Q000276:immunology* / Q000378:metabolism; D000920:Antibody-Dependent Cell Cytotoxicity; D015415:Biomarkers / Q000378:metabolism; D003181:Complement C4 / Q000276:immunology / Q000378:metabolism; D006084:Graft Rejection / Q000175:diagnosis / Q000453:epidemiology / Q000276:immunology* / Q000473:pathology*; D006680:HLA Antigens / Q000276:immunology / Q000378:metabolism; D016027:Heart Transplantation / Q000276:immunology* / Q000473:pathology*; D006801:Humans; D015995:Prevalence; D012307:Risk Factors; D014184:Transplantation, Homologous
D000906:Antibodies; D015415:Biomarkers; D003181:Complement C4; D006680:HLA Antigens