Atypical hemolytic uremic syndrome (aHUS) is characterized by uncontrolled complement activation leading to thrombotic microangiopathy and severe end-organ damage. The most common trigger for an episode of aHUS in the background of genetic deregulation of the alternative complement pathway is systemic infection. There are only 4 reported cases of aHUS triggered by influenza B thus far. Current accepted therapies for aHUS include plasma exchange and eculizumab. We describe a unique patient with aHUS with a rare membrane cofactor protein mutation triggered by influenza B infection, who achieved complete remission with treatment with high-dose corticosteroids after failure of plasmapheresis.
*Department of Pediatrics, Division of Pediatric Hematology Oncology
†Department of Pediatrics, Division of Pediatric Nephrology, Rush University Children’s Hospital , Chicago, IL
The authors declare that they have nothing to disclose.
Reprints: Nupur Mittal, MD, Rush University Children’s Hospital, 1725 West Harrison St, Suite 710, Chicago, IL 60612 (e-mail: Nupur_mittal@rush.edu).
Received September 8, 2017
Accepted February 28, 2018