Journal
IMMUNOBIOLOGY
Volume 217, Issue 2, Pages 235-243Publisher
ELSEVIER GMBH, URBAN & FISCHER VERLAG
DOI: 10.1016/j.imbio.2011.07.022
Keywords
Complement dysregulation; Endothelium; Haemolytic uraemic syndrome; Shiga toxin; Streptococcus pneumoniae; Thrombotic microangiopathy
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Funding
- Medical Research Council [G0802138] Funding Source: Medline
- Medical Research Council [G0802138] Funding Source: researchfish
- MRC [G0802138] Funding Source: UKRI
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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. (C) 2011 Elsevier GmbH. All rights reserved.
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