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Hyperacute graft dysfunction in an orthotopic heart transplant in the presence of non‐ HLA antibodies
Author(s) -
Villa Cecelia,
Mesa Kelly,
Cristy Smith Mary,
Mooney Deirdre M.,
Coletti Andrew,
Klohe Ellen
Publication year - 2020
Publication title -
american journal of transplantation
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.89
H-Index - 188
eISSN - 1600-6143
pISSN - 1600-6135
DOI - 10.1111/ajt.15564
Subject(s) - medicine , coagulopathy , plasmapheresis , extracorporeal membrane oxygenation , panel reactive antibody , antibody , heart transplantation , cardiogenic shock , immunology , pathology , transplantation , human leukocyte antigen , myocardial infarction , antigen
Antibody‐mediated rejection ( AMR ) in heart transplants in the absence of anti‐ HLA donor‐specific antibody ( DSA ) is not well studied or documented. This case reviews hyperacute fulminant graft dysfunction suspected to be mediated by non‐ HLA antibodies. After cross clamp removal, the patient developed severe pulmonary edema, profound coagulopathy, and biventricular failure. The patient's presumed AMR , cardiogenic shock, and coagulopathy were treated with extracorporeal membrane oxygenation ( ECMO ), plasmapheresis, intravenous immunoglobulin ( IVIG ), multiple blood products, and prothrombin complex concentrate. The recipient was 0% panel‐reactive antibody ( PRA ), ABO , and crossmatch compatible. Intraoperative biopsy sample revealed a thrombotic process suggestive of a coagulation pathway activated by AMR ; however, no C4d deposition was detected. Postmortem biopsies also suggested AMR . Retrospective testing of the patient's pretransplant serum revealed strong antiangiotensin II type 1 receptor ( AT 1R) antibodies and a strongly positive endothelial cell crossmatch. Anti‐ AT 1R antibodies are known to be AT 1 receptor agonists and may trigger inflammation and activate the extrinsic coagulation pathway. Given the potential effects of signaling through the AT 1R, the patient's preexisting anti‐ AT 1R antibodies and procoagulant therapy may have adversely affected the patient's clinical course.