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Updated: Jun 8, 2026

In Vitro Methods for Comparing Target Binding and CDC Induction Between Therapeutic Antibodies: Applications in Biosimilarity Analysis
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Published on: May 4, 2017

New treatment options for atypical hemolytic uremic syndrome with the complement inhibitor eculizumab

Ozlem Köse1, Lothar-Bernd Zimmerhackl, Therese Jungraithmayr

  • 1Department of Nephrology, University Hospital of Essen, University Duisburg-Essen, Essen, Germany.

Seminars in Thrombosis and Hemostasis
|September 25, 2010
PubMed

Hemolytic uremic syndrome (HUS) is a disease characterized by microangiopathic hemolytic anemia, consumptive thrombocytopenia, and renal impairment. Often HUS is triggered by Shiga-like toxin- producing ESCHERICHIA COLI. Less common is atypical HUS (aHUS), which is caused by defective complement control. aHUS is associated with mutations in genes encoding complement regulatory proteins in ~50% of patients with this syndrome. Furthermore, autoantibodies that inactivate to factor H have also been linked to the disease. Initial triggers include infections, use of endothelial-affecting drugs, malignancies, transplantation, and pregnancy. Advances in our understanding of the pathogenesis of atypical HUS suggest that complement inhibition may be used as treatment for the disease. We discuss the potential benefit of the complement inhibitor eculizumab for the treatment of aHUS.

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