{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,9,8]],"date-time":"2026-09-08T23:51:54Z","timestamp":1788911514655,"version":"build-2803163510"},"reference-count":34,"publisher":"Wiley","issue":"1","license":[{"start":{"date-parts":[[2016,9,5]],"date-time":"2016-09-05T00:00:00Z","timestamp":1473033600000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/onlinelibrary.wiley.com\/termsAndConditions#vor"}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["Pediatric Transplantation"],"published-print":{"date-parts":[[2017,2]]},"abstract":"<jats:title>Abstract<\/jats:title><jats:p>Acute<jats:styled-content style=\"fixed-case\">AMR<\/jats:styled-content>is well reported following<jats:styled-content style=\"fixed-case\">ABO<\/jats:styled-content>\u2010incompatible<jats:styled-content style=\"fixed-case\">LT<\/jats:styled-content>x. However, it remains uncommon in<jats:styled-content style=\"fixed-case\">ABO<\/jats:styled-content>\u2010compatible<jats:styled-content style=\"fixed-case\">LT<\/jats:styled-content>x. It typically presents with graft dysfunction \u22642\u00a0weeks post\u2010<jats:styled-content style=\"fixed-case\">LT<\/jats:styled-content>x and is often associated with graft loss. We report the clinical presentation, treatment regimen, and outcome of six pediatric<jats:styled-content style=\"fixed-case\">LT<\/jats:styled-content>x recipients diagnosed with early acute<jats:styled-content style=\"fixed-case\">AMR<\/jats:styled-content>based on (i) clinical signs of graft dysfunction, (ii) histopathology indicative of acute injury\u00a0\u00b1\u00a0C4d staining, and (iii) presence of<jats:styled-content style=\"fixed-case\">HLA DSA<\/jats:styled-content>. All patients developed elevated<jats:styled-content style=\"fixed-case\">ALT<\/jats:styled-content>and<jats:styled-content style=\"fixed-case\">GGT<\/jats:styled-content>\u00a0\u2264\u00a045\u00a0days post\u2010<jats:styled-content style=\"fixed-case\">LT<\/jats:styled-content>x. All showed<jats:styled-content style=\"fixed-case\">HLA<\/jats:styled-content>class I (n=4) and\/or<jats:styled-content style=\"fixed-case\">II<\/jats:styled-content>(n=6)<jats:styled-content style=\"fixed-case\">DSA<\/jats:styled-content>(peak<jats:styled-content style=\"fixed-case\">MFI<\/jats:styled-content>6153\u201311\u00a0910). Four had de novo<jats:styled-content style=\"fixed-case\">DSA<\/jats:styled-content>, and two had preformed<jats:styled-content style=\"fixed-case\">DSA<\/jats:styled-content>. Five were initially diagnosed with ACR refractory to steroid therapy. Four exhibited resolution of graft dysfunction with<jats:styled-content style=\"fixed-case\">AMR<\/jats:styled-content>therapy. Two had refractory<jats:styled-content style=\"fixed-case\">AMR<\/jats:styled-content>\u2014one was re\u2010transplanted; the other was treated with eculizumab and showed improvement in graft function but later died due to a tracheostomy complication. Our case series suggests that<jats:styled-content style=\"fixed-case\">AMR<\/jats:styled-content>following<jats:styled-content style=\"fixed-case\">ABO<\/jats:styled-content>\u2010compatible<jats:styled-content style=\"fixed-case\">LT<\/jats:styled-content>x may be under\u2010diagnosed. The presentation can be variable, and treatment should be individualized. Eculizumab may be an option for refractory<jats:styled-content style=\"fixed-case\">AMR<\/jats:styled-content>. Ultimately, future multicenter studies are needed to better define diagnostic criteria, characterize optimal treatment, and assess long\u2010term outcomes following liver<jats:styled-content style=\"fixed-case\">AMR<\/jats:styled-content>.<\/jats:p>","DOI":"10.1111\/petr.12791","type":"journal-article","created":{"date-parts":[[2016,9,6]],"date-time":"2016-09-06T04:34:26Z","timestamp":1473136466000},"source":"Crossref","is-referenced-by-count":42,"title":["Acute antibody\u2010mediated rejection in<scp>ABO<\/scp>\u2010compatible pediatric liver transplant recipients: case series and review of the literature"],"prefix":"10.1111","volume":"21","author":[{"given":"Laura J.","family":"Wozniak","sequence":"first","affiliation":[{"name":"Pediatric Gastroenterology, Hepatology, and Nutrition David Geffen School of Medicine at UCLA Los Angeles CA USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Bita V.","family":"Naini","sequence":"additional","affiliation":[{"name":"Department of Pathology and Laboratory Medicine David Geffen School of Medicine at UCLA Los Angeles CA USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Michelle J.","family":"Hickey","sequence":"additional","affiliation":[{"name":"Department of Pathology and Laboratory Medicine David Geffen School of Medicine at UCLA Los Angeles CA USA"},{"name":"Immunogenetics Center UCLA Los Angeles CA USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Sarathi","family":"Bhattacharyya","sequence":"additional","affiliation":[{"name":"Medical Student Research Program David Geffen School of Medicine at UCLA Los Angeles CA USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Elaine F.","family":"Reed","sequence":"additional","affiliation":[{"name":"Department of Pathology and Laboratory Medicine David Geffen School of Medicine at UCLA Los Angeles CA USA"},{"name":"Immunogenetics 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