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

Interferon-beta, the most widely prescribed medication for multiple sclerosis, is generally considered safe. Nevertheless, rarely serious and/or life-threatening side effects have been reported such as thrombotic microangiopathy. A few mechanisms have been proposed to explain how interferon causes thrombotic microangiopathy, but insufficient immunological studies have been unable to pin this phenomenon down to a single pathophysiologic pathway. We report thrombotic microangiopathy due to acquired complement factor I deficiency in a male receiving interferon-beta treatment for multiple sclerosis. After three years of starting the therapy, the 28-year-old patient presented with malignant hypertension causing seizures, rapidly progressive renal failure requiring hemodialysis, and hemolytic anemia. Corticosteroid and plasma exchange sessions permitted hemolysis control. Nonetheless, the patient remained hemodialysis-dependent. Exploration of the complement system found a complement factor I deficiency whose activity normalized at the control carried out after two years. We concluded that IFNβ treatment may cause complement factor I deficit, which can lead to thrombotic microangiopathy and severe renal failure.