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Scholarly Commons > HCA Healthcare Journal > Vol. 5 > Iss. 4 (2024)

 

Keywords

atypical hemolytic uremic syndrome; aHUS; pediatrics; nephrology; mutation; influenza B virus; genetics; CD46 mutation; complement system proteins; MCP gene

Disciplines

Infectious Disease | Nephrology | Pediatrics

Abstract

Background

Atypical hemolytic uremic syndrome (aHUS) is a thrombotic microangiopathy that presents with a triad of hemolytic anemia, thrombocytopenia, and acute kidney impairment. It can be attributed to mutations in an array of different complement proteins leading to the overactivation of the complement system, the most impacted being the alternative pathway. Though rare, influenza B has been documented as a potential trigger to the development of aHUS.

Case Presentation

We discuss a 10-year-old girl with a history of aHUS who was found to have a repeat episode of aHUS following an influenza B infection. There have only been a few reports of aHUS triggered by influenza B, making this a unique case. Given the recurrence and atypical features present in this case, a genetic workup was obtained, which showed a heterozygous mutation of complement protein CD46. The presence of mutations in CD46 is a known predisposing factor to aHUS, but influenza B infection is rarely implicated as a trigger to aHUS. The prognosis of aHUS varies and is dependent on the complement mutation specific to the individual.

Conclusion

Patients with CD46 mutations have been shown to have high rates of relapse but less long-term kidney damage, as seen in this case. Clinicians should be aware of the association between influenza B and aHUS to improve patient outcomes.

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