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HLA class II eplet mismatch load improves prediction of dn DSA development after living donor kidney transplantation
Author(s) -
Tafulo Sandra,
Malheiro Jorge,
Santos Sofia,
Dias Leonídio,
Almeida Manuela,
Martins La Salete,
Pedroso Sofia,
Mendes Cecília,
Lobato Luísa,
CastroHenriques António
Publication year - 2021
Publication title -
international journal of immunogenetics
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.41
H-Index - 47
eISSN - 1744-313X
pISSN - 1744-3121
DOI - 10.1111/iji.12519
Subject(s) - medicine , multivariate analysis , transplantation , cohort , kidney transplantation , urology , gastroenterology , human leukocyte antigen , surgery , immunology , antigen
Abstract HLA donor‐specific antibodies developed de novo after transplant remain a major cause of chronic allograft dysfunction. Our study main purpose was to determine whether HLA MM, assessed traditionally and by HLA total and AbVer eplet mismatch load (EptMM and EpvMM) assessed with HLAMatchMaker, had impact on dn DSA development after living donor kidney transplantation (LDKT). We retrospectively analysed a cohort of 96 LDKT between 2008 and 2017 performed in Hospital Santo António. Seven patients developed dn DSA‐II and EpvMM and EptMM were greater in dn DSA‐II group compared to the no dn DSA‐II (18.0 ± 8.7 versus 9.9 ± 7.9, p = .041 and 41.3 ± 18.9 versus 23.1 ± 16.7, p = .018), which is not observed for AgMM (2.29 versus 1.56; p = .09). In a multivariate analysis, we found that preformed DSA (HR = 7.983; p = .023), living unrelated donors (HR = 8.052; p = .024) and retransplantation (HR = 14.393; p = .009) were predictors for dn DSA‐II (AUC = 0.801; 0.622–0.981). HLA‐II EpvMM (HR = 1.105; p = .028; AUC = 0.856) showed to be a superior predictor of dn DSA‐II, when compared to AgMM (HR = 1.740; p = .113; AUC = 0.783), when adjusted for these clinical variables. Graft survival was significantly lower within dn DSA‐II patient group (36% versus 88%, p < .001). HLA molecular mismatch analysis is extremely important to minimize risk for HLA‐II dn DSA development improving outcome and increasing chance of retransplant lowering allosensitization.