Pathological antibody-mediated rejection in pediatric heart transplant recipients: Immunologic risk factors, hemodynamic significance, and outcomes
Corresponding Author
Seth A. Hollander
Department of Pediatrics (Cardiology), Stanford University School of Medicine, Stanford, CA, USA
Correspondence
Seth A. Hollander, Pediatrics (Cardiology), Stanford University, Palo Alto, CA, USA.
Email: [email protected]
Search for more papers by this authorDavid M. Peng
Department of Pediatrics (Cardiology), University of Michigan School of Medicine, Ann Arbor, MI, USA
Search for more papers by this authorMarcos Mills
Department of Pediatrics (Cardiology), Stanford University School of Medicine, Stanford, CA, USA
Search for more papers by this authorGerald J. Berry
Department of Pathology, Stanford University School of Medicine, Stanford, CA, USA
Search for more papers by this authorMarny Fedrigo
Department of Cardiac Thoracic and Vascular Sciences, University of Padua Medical School, Padua, Italy
Search for more papers by this authorDoff B. McElhinney
Department of Cardiothoracic Surgery, LPCH Heart Center Clinical and Translational Research Program, Stanford University, Stanford, CA, USA
Search for more papers by this authorChristopher S. Almond
Department of Pediatrics (Cardiology), Stanford University School of Medicine, Stanford, CA, USA
Search for more papers by this authorDavid N. Rosenthal
Department of Pediatrics (Cardiology), Stanford University School of Medicine, Stanford, CA, USA
Search for more papers by this authorCorresponding Author
Seth A. Hollander
Department of Pediatrics (Cardiology), Stanford University School of Medicine, Stanford, CA, USA
Correspondence
Seth A. Hollander, Pediatrics (Cardiology), Stanford University, Palo Alto, CA, USA.
Email: [email protected]
Search for more papers by this authorDavid M. Peng
Department of Pediatrics (Cardiology), University of Michigan School of Medicine, Ann Arbor, MI, USA
Search for more papers by this authorMarcos Mills
Department of Pediatrics (Cardiology), Stanford University School of Medicine, Stanford, CA, USA
Search for more papers by this authorGerald J. Berry
Department of Pathology, Stanford University School of Medicine, Stanford, CA, USA
Search for more papers by this authorMarny Fedrigo
Department of Cardiac Thoracic and Vascular Sciences, University of Padua Medical School, Padua, Italy
Search for more papers by this authorDoff B. McElhinney
Department of Cardiothoracic Surgery, LPCH Heart Center Clinical and Translational Research Program, Stanford University, Stanford, CA, USA
Search for more papers by this authorChristopher S. Almond
Department of Pediatrics (Cardiology), Stanford University School of Medicine, Stanford, CA, USA
Search for more papers by this authorDavid N. Rosenthal
Department of Pediatrics (Cardiology), Stanford University School of Medicine, Stanford, CA, USA
Search for more papers by this authorAbstract
Biopsy-diagnosed pAMR has been observed in over half of pediatric HT recipients within 6 years of transplantation. We report the incidence and outcomes of pAMR at our center. All endomyocardial biopsies for all HT recipients transplanted between 2010 and 2015 were reviewed and classified using contemporary ISHLT guidelines. Graft dysfunction was defined as a qualitative decrement in systolic function by echocardiogram or an increase of ≥3 mm Hg in atrial filling pressure by direct measurement. Among 96 patients, pAMR2 occurred in 7 (7%) over a median follow-up period of 3.1 years, while no cases of pAMR3 occurred. A history of CHD, DSA at transplant, and elevated filling pressures were associated with pAMR2. Five-sixths (83%) of patients developed new C1q+ DSA at the time of pAMR diagnosis. There was a trend toward reduced survival, with 43% of patients dying within 2.3 years of pAMR diagnosis.
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