Kidney international reports · 2024
Early Thrombotic Microangiopathy After ABO-Incompatible Living Donor Kidney Transplantation.
СтатьяНазвание и аннотация: Перевод в очереди
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Bertrand Dominique, Del Bello Arnaud, Sberro Soussan Rebecca, Caillard Sophie, Claisse Guillaume, Couzi Lionel, Girerd Sophie, Hertig Alexandre, Le Meur Yannick, Pernin Vincent, Poulain Coralie, Rafat Cédric, Matignon Marie, Buteux Arnaud, François Arnaud, Lemoine Mathilde, Laurent Charlotte, Kamar Nassim, de Nattes Tristan, Guerrot Dominique
Аннотация
INTRODUCTION: Although long-term graft survival is comparable with that of ABO-compatible (ABOc) renal transplantation, the risk of antibody-mediated rejection (ABMR) following ABO-incompatible (ABOi) transplantation is higher and can occur as an early thrombotic microangiopathy (TMA).
METHODS: We designed a retrospective multicenter study, including all patients who presented with a TMA (histological and/or biological) after an ABOi transplantation (< 1 month) and compared with matched controls who had a favorable initial course with a normal biopsy.
RESULTS: Between 2013 and 2022, 375 ABOi kidney transplants were performed and 23 patients (6.1%) developed TMA (median: 1 day, interquartile range [IQR]: 0-3 days). Twenty-one patients (91.3%) had biological TMA. Among 23 early graft biopsies, histological evidence of active TMA was found in 17 cases (80.9%). All patients received treatment: 20 of 23 received at least 1 session of plasmapheresis and 19 of 23 received at least 1 injection of eculizumab. Eight early graft losses (30.4%) occurred (median: 7 days, IQR: 3-16 days). IgG and IgM anti-blood group antibody (ABGA) levels (peak and last pregraft assay) were significantly higher in the TMA group (peak: P = 0.01 for IgG and P = 0.0006 for IgM; last assay before kidney transplantation [KT]: P < 0.0001 for IgG and P = 0.0003 for IgM). A level ≥ 1/8 for IgG and ≥ 1/4 or IgM before transplantation were significantly and independently predictive of the occurrence of TMA. No other predictive factors were found.
CONCLUSION: TMA after ABOi transplantation is not a rare phenomenon and is associated with a poor prognosis in nonresponders-to-treatment patients. ABGA titer performed by hemagglutination is an imperfect marker of the occurrence of such a phenomenon.
METHODS: We designed a retrospective multicenter study, including all patients who presented with a TMA (histological and/or biological) after an ABOi transplantation (< 1 month) and compared with matched controls who had a favorable initial course with a normal biopsy.
RESULTS: Between 2013 and 2022, 375 ABOi kidney transplants were performed and 23 patients (6.1%) developed TMA (median: 1 day, interquartile range [IQR]: 0-3 days). Twenty-one patients (91.3%) had biological TMA. Among 23 early graft biopsies, histological evidence of active TMA was found in 17 cases (80.9%). All patients received treatment: 20 of 23 received at least 1 session of plasmapheresis and 19 of 23 received at least 1 injection of eculizumab. Eight early graft losses (30.4%) occurred (median: 7 days, IQR: 3-16 days). IgG and IgM anti-blood group antibody (ABGA) levels (peak and last pregraft assay) were significantly higher in the TMA group (peak: P = 0.01 for IgG and P = 0.0006 for IgM; last assay before kidney transplantation [KT]: P < 0.0001 for IgG and P = 0.0003 for IgM). A level ≥ 1/8 for IgG and ≥ 1/4 or IgM before transplantation were significantly and independently predictive of the occurrence of TMA. No other predictive factors were found.
CONCLUSION: TMA after ABOi transplantation is not a rare phenomenon and is associated with a poor prognosis in nonresponders-to-treatment patients. ABGA titer performed by hemagglutination is an imperfect marker of the occurrence of such a phenomenon.