Abstract
BackgroundInfluenza A infections have been described to cause secondary hemolytic uremic syndrome and to trigger atypical hemolytic uremic syndrome (aHUS) in individuals with an underlying genetic complement dysregulation. To date, influenza B has not been reported to trigger aHUS.Case presentationA 6-month-old boy presented with hemolytic uremic syndrome triggered by influenza B infection. Initially the child recovered spontaneously. When he relapsed Eculizumab treatment was initiated, resulting in complete and sustained remission. A pathogenic mutation in membrane cofactor protein (MCP) was detected.ConclusionInfluenza B is a trigger for aHUS and might be underreported as such. Influenza vaccination may protect patients at risk.
Highlights
Influenza A infections have been described to cause secondary hemolytic uremic syndrome and to trigger atypical hemolytic uremic syndrome in individuals with an underlying genetic complement dysregulation
Most cases of Hemolytic uremic syndrome (HUS) in industrialized countries are due to infections with pathogenic Shiga toxin-producing Escherichia coli (STEC) with 0157:H7 being the most common serotype, while in some tropical regions Shigella dysenteriae type I is the leading HUS-causing pathogen [2, 3]
Beside this HUS may be due to inborn defects of the alternative pathway regulation of the complement system, denominated atypical HUS
Summary
Hemolytic uremic syndrome (HUS) is a thrombotic microangiopathic disease characterised by thrombocytopenia, hemolytical anemia, and renal impairment [1]. Most cases of HUS in industrialized countries are due to infections with pathogenic Shiga toxin-producing Escherichia coli (STEC) with 0157:H7 being the most common serotype, while in some tropical regions Shigella dysenteriae type I is the leading HUS-causing pathogen [2, 3] Beside this HUS may be due to inborn defects of the alternative pathway regulation of the complement system, denominated atypical HUS (aHUS). Influenza A, predominantly pandemic H1N1 Influenza A, and seasonal influenza A, sometimes in combination with pneumococcal co-infection, have both clearly been described to trigger aHUS [5] These reports included patients with aHUS after H1N1-infections who carry mutations in the gene for the complement regulator membrane cofactor protein (MCP), known as CD46 [6]. Not immunized, the patient will be vaccinated against influenza with quadrivalent vaccines for maximum protection before each start of the upcoming seasons
Sign-in/Register to view highlights & summary Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a callDisclaimer: All third-party content on this website/platform is and will remain the property of their respective owners and is provided on "as is" basis without any warranties, express or implied. Use of third-party content does not indicate any affiliation, sponsorship with or endorsement by them. Any references to third-party content is to identify the corresponding services and shall be considered fair use under The CopyrightLaw.
