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Tytuł pozycji:

Hyperacute graft dysfunction in an orthotopic heart transplant in the presence of non-HLA antibodies.

Tytuł:
Hyperacute graft dysfunction in an orthotopic heart transplant in the presence of non-HLA antibodies.
Autorzy:
Villa C; HLA Lab, Vitalant, Spokane, Washington.
Mesa K; Mechanical Heart Program, Providence Sacred Heart Medical Center & Children's Hospital, Spokane, Washington.
Cristy Smith M; Center for Advanced Heart Disease and Transplantation, Providence Sacred Heart Medical Center & Children's Hospital, Spokane, Washington.
Mooney DM; Center for Advanced Heart Disease and Transplantation, Providence Sacred Heart Medical Center & Children's Hospital, Spokane, Washington.
Coletti A; Center for Advanced Heart Disease and Transplantation, Providence Sacred Heart Medical Center & Children's Hospital, Spokane, Washington.
Klohe E; HLA Lab, Vitalant, Spokane, Washington.
Źródło:
American journal of transplantation : official journal of the American Society of Transplantation and the American Society of Transplant Surgeons [Am J Transplant] 2020 Feb; Vol. 20 (2), pp. 593-599. Date of Electronic Publication: 2019 Sep 09.
Typ publikacji:
Case Reports; Journal Article; Research Support, Non-U.S. Gov't
Język:
English
Imprint Name(s):
Publication: 2023- : [New York] : Elsevier
Original Publication: Copenhagen : Munksgaard International Publishers, 2001-
MeSH Terms:
Heart Transplantation*
Graft Rejection/*etiology
Receptor, Angiotensin, Type 1/*agonists
Adult ; Aged ; Blood Grouping and Crossmatching ; Extracorporeal Membrane Oxygenation ; Graft Rejection/immunology ; HLA Antigens/immunology ; Histocompatibility Testing ; Humans ; Male ; Primary Graft Dysfunction/etiology ; Receptor, Angiotensin, Type 1/immunology
References:
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Colvin M, Cook J, Zeevi A, et al. Antibody-mediated rejection in cardiac transplantation: emerging knowledge in diagnosis and management. A scientific statement from the American Heart Association. Circulation. 2015;131:1608-1639.
Banan B, Mohanakumar T. Increased sensitization to HLA and to cardiac self-antigens (myosin and Vimentin) in patients waiting for cardiac transplantation with left ventricular assisting Device (LVAD) [Abstract]. J Heart Lung Transplant. 2014;S25:47.
von Salisch S, Markus J. Identification of non-HLA antibodies in ventricular assist device recipients. J Heart Lung Transplant. 2012;S46:82-99.
Hickey M, Reed E. Antibodies to angiotensin type II receptor I are associated with primary graft dysfunction after orthotopic heart transplant in patients with ventricular assist device as bridge to transplant. In: Proceedings from the 2017 American Transplant Congress; April 29-May 3, 2017; Chicago, IL. Abstract 225.
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Hiemann NE, Meyer R, Dragun D, et al. Non-HLA antibodies targeting vascular receptors enhance alloimmune response and microvasculopathy after Heart Transplantation. Transplantation. 2012;94(9):919-924.
Reinsmoen N, Lai CH, Kobashigawa J, et al. Increased negative impact of donor HLA-specific together with non-HLA-specific antibodies’ on graft outcome. Transplantation. 2014;97:595-601.
Dragun D, Wallukat G. Angiotensin II type 1-recetor activating antibodies in renal-allograft rejection. N Engl J Med. 2005;352:558-569.
Senchenkova E, Granger D. Angiotensin II-mediated microvascular thrombosis hypertension. Hypertension. 2010;56(6):1089-1095.
Dragun D, Catar R, Philippe A. Non-HLA-antibodies targeting angiotensin type 1 receptor and antibody mediated rejection. Clinic for Nephrology and Intensive Care Medicine, Campus Virchow-Klinikum and Center for Cardiovascular Research, Medical Facility of the Charite, Berlin Germany. Hum Immunol.2012;73:1282-1286.
Butler C, Valenzuela N, Reed E, et al. Not all antibodies are created equal: factors that influence antibody mediated rejection. J Immunol Res. 2017;2017:7903471.
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Contributed Indexing:
Keywords: autoantibody; clinical research/practice; health services and outcomes research; heart transplantation/cardiology; patient characteristics; patient survival; rejection; risk assessment/risk stratification
Substance Nomenclature:
0 (HLA Antigens)
0 (Receptor, Angiotensin, Type 1)
Entry Date(s):
Date Created: 20190811 Date Completed: 20210219 Latest Revision: 20230124
Update Code:
20240104
DOI:
10.1111/ajt.15564
PMID:
31400258
Czasopismo naukowe
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 (AT1R) antibodies and a strongly positive endothelial cell crossmatch. Anti-AT1R antibodies are known to be AT1 receptor agonists and may trigger inflammation and activate the extrinsic coagulation pathway. Given the potential effects of signaling through the AT1R, the patient's preexisting anti-AT1R antibodies and procoagulant therapy may have adversely affected the patient's clinical course.
(© 2019 The American Society of Transplantation and the American Society of Transplant Surgeons.)

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