Thrombotic microangiopathy induced by interferon beta in patients with multiple sclerosis: three cases treated with

Marco Allinovi1, Calogero Lino Cirami1, Leonardo Caroti1

  • 1Nephrology Unit, Careggi University Hospital, Florence, Italy.

Clinical Kidney Journal
|October 6, 2017
PubMed
Abstract

Insights

Interferon-beta (IFN-beta) can cause thrombotic microangiopathy (TMA) in multiple sclerosis patients. Eculizumab shows promise in treating this severe kidney complication when conventional therapies fail.

Area of Science:

  • Nephrology
  • Neurology
  • Immunology

Background:

  • Interferon-beta (IFN-beta) is a common treatment for relapsing-remitting multiple sclerosis (RRMS).
  • IFN-beta-associated thrombotic microangiopathy (TMA) is a rare but serious complication, potentially leading to kidney failure.
  • TMA can occur years after initiating IFN-beta therapy, even if well-tolerated initially.

Purpose of the Study:

  • To analyze cases of TMA in RRMS patients treated with IFN-beta.
  • To review the literature on IFN-beta-induced TMA.
  • To evaluate the efficacy of eculizumab in treating IFN-beta-induced TMA.

Main Methods:

  • Retrospective analysis of TMA cases from 2010-2015.
  • Literature review of IFN-beta-induced TMA.
  • Evaluation of treatment outcomes, including eculizumab therapy.

Main Results:

  • Three RRMS patients with IFN-beta-induced TMA were identified.
  • Conventional therapies (IFN withdrawal, plasma exchange) were ineffective in improving renal outcomes.
  • All three patients showed significant renal recovery with eculizumab, discontinuing dialysis without recurrence.

Conclusions:

  • IFN-beta-induced TMA is a severe complication in RRMS patients with poor prognosis under conventional treatment.
  • Eculizumab demonstrated a favorable effect on renal recovery in these cases.
  • Vigilance by neurologists and nephrologists is crucial for early detection and prevention of irreversible kidney damage.