CASE REPORT article

Front. Nephrol.

Sec. Kidney Transplantation

Volume 5 - 2025 | doi: 10.3389/fneph.2025.1572641

This article is part of the Research TopicCase reports in kidney transplantationView all articles

Failure of Eculizumab to block complement to prevent relapse of anti-phospholipid syndrome in kidney transplant recipient

Provisionally accepted
Thibault  LabanThibault LabanFredéric  PigneurFredéric PigneurConstance  GuillaudConstance GuillaudMarie-Agnes  DRAGON-DUREYMarie-Agnes DRAGON-DUREYHoucine  HamidiHoucine HamidiMarc  MichelMarc MichelHamza  SakhiHamza SakhiNizar  JOHERNizar JOHERPhilippe  GrimbertPhilippe GrimbertAntoine  MORELAntoine MORELMarie  MatignonMarie Matignon*
  • Assistance Publique Hopitaux De Paris, Paris, France

The final, formatted version of the article will be published soon.

Catastrophic antiphospholipid syndrome (CAPS) leads to organ dysfunction due to thrombotic microangiopathy (TMA). Complement may play a role in CAPS and its blockade could prevent antiphospholipid syndrome (APS) complications after kidney transplantation (KT).We report here a recurrence of APS after KT in a 38-year-old woman with early acute cortical kidney allograft necrosis despite preventive eculizumab treatment probably due to insufficient complement blockade.The patient had a recurrent but controlled CAPS for years with renal dysfunction leading to a preemptive KT. Anticoagulation and eculizumab were used to prevent thrombosis and TMA after KT. She developed acute kidney injury (AKI) with incomplete biological TMA. Imaging showed renal allograft cortical necrosis. In the absence of donor-specific anti-HLA antibodies, we concluded a relapse of APS. Additional doses of eculizumab and plasma exchange allowed normalisation of biological tests and improvement of kidney allograft function. Retrospective complement analysis showed incomplete blockade at the time of AKI. One year after KT, renal allograft function remained impaired.

Keywords: kidney tranplantation, Anti phospholipid syndrome, Eculizumab, thrombotic micro angiopathy, Cortical necrosis

Received: 07 Feb 2025; Accepted: 21 Apr 2025.

Copyright: © 2025 Laban, Pigneur, Guillaud, DRAGON-DUREY, Hamidi, Michel, Sakhi, JOHER, Grimbert, MOREL and Matignon. This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) or licensor are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.

* Correspondence: Marie Matignon, Assistance Publique Hopitaux De Paris, Paris, France

Disclaimer: All claims expressed in this article are solely those of the authors and do not necessarily represent those of their affiliated organizations, or those of the publisher, the editors and the reviewers. Any product that may be evaluated in this article or claim that may be made by its manufacturer is not guaranteed or endorsed by the publisher.