scholarly journals Antibody Mediated Rejection of the Cardiac Allograft

10.5772/26456 ◽  
2012 ◽  
Author(s):  
Christopher R. ◽  
Christina T.
Keyword(s):  
Cardiac Allograft ◽  
Antibody Mediated Rejection

scholarly journals Antibody-mediated rejection with detection of de novo donor-specific anti-human leucocyte antigen Class II antibodies 3 years after heart transplantation: a case report

2020 ◽  
Vol 4 (1) ◽  
pp. 1-4
Author(s):  
Bernd Ludwig ◽  
Johanna Schneider ◽  
Daniela Föll ◽  
Qian Zhou
Keyword(s):  
Heart Transplantation ◽  
De Novo ◽  
Survival Rates ◽  
Graft Function ◽  
Left Ventricular ◽  
Cardiac Allograft ◽  
Left Ventricular Ejection ◽  
High Dose ◽  
Ventricular Ejection Fraction ◽  
Antibody Mediated Rejection

Abstract Background Antibody-mediated rejection (AMR) in cardiac transplantation may manifest early within the first weeks after transplantation but also late after months to years following transplantation resulting in mild heart failure to cardiogenic shock. While patients with early cardiac AMR are less affected and seem to have survival rates comparable to transplant recipients without AMR, late cardiac AMR is frequently associated with graft dysfunction, fulminant forms of cardiac allograft vasculopathy, and a high mortality rate. Nevertheless, AMR of cardiac allografts remains difficult to diagnose and to treat. Case summary We report the case of a 47-year-old male patient with late AMR of the cardiac allograft 3 years after heart transplantation. Antibody-mediated rejection was confirmed by endomyocardial biopsy and the presence of donor-specific antibodies (DSA). The patient was treated with high dose of prednisolone, plasmapheresis, intravenous Gamma Globulin, rituximab, immunoadsorption, and bortezomib. Under this treatment regimen left ventricular ejection fraction and pro B-type natriuretic peptide recovered, and the patient improved to New York Heart Association Class I. Currently, 3 years after the diagnosis of cardiac AMR, graft function continues to be nearly normal, and there is no evidence for transplant vasculopathy. Discussion This case illustrates that AMR can occur at any time after transplantation. Although graft function fully recovered after treatment in our patient, the level of DSA remained high, suggesting that DSA may not be a reliable parameter to determine the intensity and duration of the therapy.

94: Phosphoproteomic Analysis of Cardiac Allograft Biopsies Reveals Novel Markers of Antibody Mediated Rejection

2010 ◽  
Vol 29 (2) ◽  
pp. S37-S37
Author(s):  
C. Lai ◽  
J. Wei ◽  
F. Li ◽  
Q. Zhang ◽  
D. Gjertson ◽  
...  
Keyword(s):  
Cardiac Allograft ◽  
Antibody Mediated Rejection

Characterization of a Specific Mechanism for Late Loss of Cardiac Allograft: The Role of Antibody-Mediated Rejection.

2014 ◽  
Vol 98 ◽  
pp. 55
Author(s):  
A. Loupy ◽  
C. Toquet ◽  
D. Vernerey ◽  
P. Rouvier ◽  
S. Varnous ◽  
...  
Keyword(s):  
Cardiac Allograft ◽  
Specific Mechanism ◽  
Antibody Mediated Rejection ◽  
Late Loss

100 Intracapillary Macrophages in Cardiac Allograft Biopsies for Diagnosis of Antibody-Mediated Rejection (AMR)

2012 ◽  
Vol 31 (4) ◽  
pp. S42
Author(s):  
M. Fedrigo ◽  
G. Feltrin ◽  
E. Benazzi ◽  
F. Poli ◽  
A. Frigo ◽  
...  
Keyword(s):  
Cardiac Allograft ◽  
Antibody Mediated Rejection

38: Endothelialitis in Cardiac Allograft Biopsies: Expanding the Spectrum of Antibody Mediated Rejection

2009 ◽  
Vol 28 (2) ◽  
pp. S78
Author(s):  
C.J. Sailey ◽  
F. Tavora ◽  
J.C. Papadimitriou ◽  
C. Drachenberg ◽  
A. Burke
Keyword(s):  
Cardiac Allograft ◽  
Antibody Mediated Rejection

Management of children undergoing cardiac transplantation with high Panel Reactive Antibodies

2011 ◽  
Vol 21 (S2) ◽  
pp. 124-132 ◽  
Author(s):  
Alfred Asante-Korang ◽  
Jeffrey P. Jacobs ◽  
Jeremy Ringewald ◽  
Jennifer Carapellucci ◽  
Kristin Rosenberg ◽  
...  
Keyword(s):  
Human Leukocyte Antigen ◽  
Cardiac Transplantation ◽  
Human Leukocyte ◽  
Cardiac Allograft Vasculopathy ◽  
Cardiac Allograft ◽  
Allograft Vasculopathy ◽  
Leukocyte Antigen ◽  
Antibody Mediated Rejection ◽  
Frequent Use ◽  
Reactive Antibody

AbstractHighly sensitised children in need of cardiac transplantation have overall poor outcomes because of increased risk for dysfunction of the cardiac allograft, acute cellular and antibody-mediated rejection, and vasculopathy of the cardiac allograft. Cardiopulmonary bypass and the frequent use of blood products in the operating room and cardiac intensive care unit, as well as the frequent use of homografts, have predisposed potential recipients of transplants to allosensitisation. The expansion in the use of ventricular assist devices and extracorporeal membrane oxygenation has also contributed to increasing rates of allosensitisation in candidates for cardiac transplantation. Antibodies to Human Leukocyte Antigen can be detected before transplantation using several different techniques, the most common being the “complement-dependent lymphocytotoxicity assays”. “Solid-phase assays”, particularly the “Luminex®single antigen bead method”, offer improved specificity and more detailed information regarding specificities of antibodies, leading to improved matching of donors with recipients. Allosensitisation prolongs the time on the waiting list for potential recipients of transplantation and increases the risk of complications and death after transplantation. Aggressive reduction of antibodies to Human Leukocyte Antigen in these high-risk patients is therefore of vital importance for long-term survival of the patient and cardiac allograft. Strategies to decrease Panel Reactive Antibody or percent reactive antibody before transplantation include plasmapheresis, intravenous administration of immunoglobulin, and specific treatment to reduce B-cells, particularly Rituximab. These strategies have resulted in varying degrees of success. Antibody-mediated rejection and cardiac allograft vasculopathy are two of the most important complications of transplantation in patients with high Panel Reactive Antibody. The treatment of antibody-mediated rejection in recipients of cardiac transplants is largely empirical and includes the use of high-dose corticosteroids, plasmapheresis, intravenous administration of immunoglobulins, anti-thymocyte globulin, and Rituximab. Cardiac allograft vasculopathy is believed to be secondary to chronic complement-mediated endothelial injury and chronic vascular rejection. The use of proliferation signal inhibitors, such as sirolimus and everolimus, has been shown to delay the progression of cardiac allograft vasculopathy. In some non-sensitised recipients of cardiac transplants, thede novoformation of antibodies to Human Leukocyte Antigen after transplantation may increase the likelihood of adverse clinical outcomes. The use of serial testing for donor-specific antibodies after cardiac transplantation may be advisable in patients with frequent episodes of rejection and patients with history of sensitisation. Allosensitisation before transplantation can negatively influence outcomes after transplantation. A high incidence of antibody-mediated rejection and graft vasculopathy can result in graft failure and decreased survival. Current strategies to decrease allosensitisation have helped to expand the pool of donors, improve times on the waiting list, and decrease mortality. Centres of transplantation offering desensitisation are currently using plasmapheresis to remove circulating antibodies; intravenous immunoglobulin to inactivate antibodies; cyclophosphamide to suppress B-cell proliferation; and Rituximab to deplete B-lymphocytes. Similar approaches are also used to treat antibody-mediated rejection after transplantation with promising results.

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