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 . . .