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Thrombotic microangiopathy due to acquired complement factor I deficiency in a male receiving interferon-beta

Sanda Mrabet1, Rihem Dahmane1, Boukadida Raja1

  • 1Department of Nephrology, Dialysis, and Transplantation, Université de Sousse, Faculté de Médecine de Sousse, Hôpital Sahloul, Sousse, Tunisia.

British Journal of Clinical Pharmacology
|December 8, 2022
PubMed
Abstract

Insights

Interferon beta treatment for multiple sclerosis can cause a rare complication called thrombotic microangiopathy. This condition may stem from a deficiency in complement factor I, leading to severe kidney damage.

Area of Science:

  • Neurology
  • Immunology
  • Nephrology

Background:

  • Interferon-beta (IFNβ) is a primary treatment for multiple sclerosis.
  • While generally safe, rare side effects like thrombotic microangiopathy (TMA) can occur.
  • The exact mechanism of IFNβ-induced TMA remains unclear.

Observation:

  • A 28-year-old male on IFNβ therapy developed TMA.
  • Symptoms included severe hypertension, seizures, renal failure requiring dialysis, and hemolytic anemia.
  • Complement factor I deficiency was identified, normalizing after 2 years.

Findings:

  • IFNβ treatment can induce complement factor I deficiency.
  • This deficiency is a potential mechanism for IFNβ-related TMA.
  • The condition can lead to significant renal impairment.

Implications:

  • Highlights a novel pathway for IFNβ-induced TMA.
  • Suggests monitoring complement factor I in patients on IFNβ.
  • Informs potential therapeutic strategies for managing this rare side effect.
Keywords:
alternative complement pathwayatypical haemolytic uremic syndromecomplement factor Iinterferon-betamultiple sclerosisthrombotic microangiopathy

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