{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,1,16]],"date-time":"2026-01-16T10:59:41Z","timestamp":1768561181428,"version":"3.49.0"},"reference-count":31,"publisher":"Wiley","issue":"1","license":[{"start":{"date-parts":[[2022,1,10]],"date-time":"2022-01-10T00:00:00Z","timestamp":1641772800000},"content-version":"vor","delay-in-days":9,"URL":"http:\/\/creativecommons.org\/licenses\/by\/4.0\/"}],"content-domain":{"domain":["onlinelibrary.wiley.com"],"crossmark-restriction":true},"short-container-title":["Xenotransplantation"],"published-print":{"date-parts":[[2022,1]]},"abstract":"<jats:title>Abstract<\/jats:title><jats:p>Antibody\u2010mediated rejection (AMR) is a major barrier preventing successful discordant organ xenotransplantation, but it also occurs in allotransplantation due to anti\u2010HLA antibodies. Symptomatic acute AMR is rare after heart allograft but carries a high risk of mortality, especially\u00a0&gt;1 year after transplant. As complement activation may play a major role in mediating tissue injury in acute AMR, drugs blocking the terminal complement cascade like eculizumab may be useful, particularly since \u201cstandards of care\u201d like plasmapheresis are not based on strong evidence. Eculizumab was successfully used to treat early acute kidney AMR, a typical condition of \u201cactive AMR,\u201d but showed mitigated results in late AMR, where \u201cchronic active\u201d lesions are more prevalent. Here, we report the case of a heart recipient who presented with acute heart failure due to late acute AMR with eight de novo donor\u2010specific anti\u2010HLA antibodies (DSA), and who fully recovered allograft function and completely cleared DSA following plasmapheresis\u2010free upfront eculizumab administration in addition to thymoglobulin, intravenous immunoglobulins (IVIG), and rituximab. Several clinical (acute onset, abrupt and severe loss of graft function), biological (sudden high\u2010level production of DSA), and pathological features (microvascular injury, C4d deposits) of this cardiac recipient are shared with early kidney AMR and may indicate a strong role of complement in the pathogenesis of acute graft injury that may respond to drugs like eculizumab. Terminal complement blockade should be further explored to treat acute AMR in recipients of heart allografts and possibly also in recipients of discordant xenografts in the future.<\/jats:p>","DOI":"10.1111\/xen.12726","type":"journal-article","created":{"date-parts":[[2022,1,10]],"date-time":"2022-01-10T08:34:19Z","timestamp":1641803659000},"update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":10,"title":["Complement blockade with eculizumab to treat acute symptomatic humoral rejection after heart transplantation"],"prefix":"10.1111","volume":"29","author":[{"ORCID":"https:\/\/orcid.org\/0000-0001-8163-722X","authenticated-orcid":false,"given":"Patrick","family":"Yerly","sequence":"first","affiliation":[{"name":"Service of Cardiology Lausanne University Hospital (CHUV) and Lausanne University  Lausanne 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