Abstract
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.
| Original language | English |
|---|---|
| Pages (from-to) | 235-243 |
| Number of pages | 9 |
| Journal | Immunobiology |
| Volume | 217 |
| Issue number | 2 |
| DOIs | |
| Publication status | Published - Feb 2012 |
| Externally published | Yes |
UN SDGs
This output contributes to the following UN Sustainable Development Goals (SDGs)
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SDG 3 Good Health and Well-being
Keywords
- Complement dysregulation
- Endothelium
- Haemolytic uraemic syndrome
- Shiga toxin
- Streptococcus pneumoniae
- Thrombotic microangiopathy
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