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. 2024 Dec 30;10(3):828-837.
doi: 10.1016/j.ekir.2024.12.031. eCollection 2025 Mar.

Early Thrombotic Microangiopathy After ABO-Incompatible Living Donor Kidney Transplantation

Dominique Bertrand  1 , Arnaud Del Bello  2 , Rebecca Sberro Soussan  3 , Sophie Caillard  4 , Guillaume Claisse  5 , Lionel Couzi  6 , Sophie Girerd  7 , Alexandre Hertig  8 , Yannick Le Meur  9 , Vincent Pernin  10 , Coralie Poulain  11 , Cédric Rafat  12 , Marie Matignon  13 , Arnaud Buteux  14 , Arnaud François  15 , Mathilde Lemoine  1 , Charlotte Laurent  1 , Nassim Kamar  2 , Tristan de Nattes  16 , Dominique Guerrot  17
Affiliations

Early Thrombotic Microangiopathy After ABO-Incompatible Living Donor Kidney Transplantation

Dominique Bertrand et al. Kidney Int Rep. .

Abstract

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.

Keywords: ABO-incompatible; antibody-mediated rejection; eculizumab; kidney transplantation; thrombotic microangiopathy.

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Figures

None
Graphical abstract
Figure 1
Figure 1
Flow chart. ABOi, ABO-incompatible, DGF, delayed graft function; DSA, donor-specific antibodies; HLA, human leukocyte antigen; KT, kidney transplantation; SGF, slow graft function TMA, thrombotic microangiopathy.
Figure 2
Figure 2
Anti–blood group antibodies titter (IgG and IgM) (a) before desensitization and (b) at time of KT. KT, kidney transplantation; TMA, thrombotic microangiopathy.
Figure 3
Figure 3
Death-censored graft survival in the TMA group and control. TMA, thrombotic microangiopathy.
See this image and copyright information in PMC

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