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When to intervene for donor-specific antibody after heart transplantation

Njue, Faith; Chih, Sharon

Current Opinion in Organ Transplantation: June 2019 - Volume 24 - Issue 3 - p 271–278
doi: 10.1097/MOT.0000000000000634
HEART TRANSPLANTATION: Edited by Jon A. Kobashigawa

Purpose of review Posttransplant donor-specific human leukocyte antigen (HLA) antibodies (DSA) represent a complex area in heart transplantation with nonstandardized practice and paucity of clinical data to guide optimal management.

Recent findings De novo DSA after heart transplantation is common and associated with rejection, cardiac allograft vasculopathy, allograft failure, and mortality. Advances in methods for HLA antibody detection have enabled identification of DSA with high precision and sensitivity. The detection of HLA antibodies must, however, be interpreted within appropriate laboratory and clinical contexts; it remains unclear which DSA are associated with greatest clinical risk. Increased antibody and clinical surveillance as well as optimization of maintenance immunosuppression are required for all patients with DSA. Antibody-directed therapies are reserved for patients with allograft dysfunction or rejection. Treatment of DSA may also be considered in asymptomatic high-risk patients including those in whom DSA arise de novo posttransplant, is persistent, high titer, or complement activating. The impact of DSA reduction and removal on long-term clinical outcomes remains unknown.

Summary Despite improvements in DSA detection, identification, and characterization, best therapeutic strategies are unclear. Prospective multicenter studies are needed to develop effective standardized approaches for DSA management in heart transplantation.

Heart Failure and Transplantation, Division of Cardiology, Department of Medicine, University of Ottawa Heart Institute, Ottawa, Ontario, Canada

Correspondence to Sharon Chih, MBBS, PhD, Division of Cardiology, University of Ottawa Heart Institute, 40 Ruskin Street, Ottawa, Ontario, K1Y 4W7, Canada. Tel: +1 613 696 7000 ext 67327; fax: +1 613 696 7359; e-mail:

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