Is complement a culprit in infection-induced forms of haemolytic uraemic syndrome?

Sally Johnson1, Aoife Waters

  • 1Department of Paediatric Nephrology, Great North Children's Hospital, Newcastle Upon Tyne Hospitals NHS Foundation Trust, Queen Victoria Road, Newcastle Upon Tyne, UK. sally.johnson@lineone.net

Immunobiology
|August 20, 2011
PubMed

Haemolytic uraemic syndrome (HUS) accounts for the most common cause of childhood acute renal failure. Characterized by the classical triad of a microangiopathic haemolytic anaemia, thrombocytopaenia and acute renal failure, HUS occurs as a result of Shiga-toxin producing microbes in 90% of cases. The remaining 10% of cases represent a heterogeneous subgroup in which inherited and acquired forms of complement dysregulation have been described in up to 60%. Emerging evidence suggests that microbes associated with HUS exhibit interaction with the complement system. With the advent of improved genetic diagnosis, it is likely that certain cases of infection-induced HUS may be attributed to underlying defects in complement components. This review summarises the interplay between complement and infection in the pathogenesis of HUS.

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