To the Editor: Atypical hemolytic–uremic syndrome is a disease of uncontrolled complement activation associated with a high mortality rate, and most cases progress to end-stage renal disease.1 About 50% of patients with this syndrome carry mutations in genes encoding complement proteins.2 Complement inhibition has been suggested for the treatment of atypical hemolytic–uremic syndrome,3 but currently no data on this treatment option are available. We report on a case of atypical hemolytic–uremic syndrome that was successfully treated with eculizumab, a humanized monoclonal antibody that blocks complement activity by cleavage of the complement protein C5, thereby preventing the generation of the inflammatory . . .
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Nürnberger et al. (2009) studied this question.
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