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

Johnson S., Waters A.

IMMUNOBIOLOGY, cilt.217, sa.2, ss.235-243, 2012 (SCI-Expanded) identifier identifier identifier

  • Yayın Türü: Makale / Tam Makale
  • Cilt numarası: 217 Sayı: 2
  • Basım Tarihi: 2012
  • Doi Numarası: 10.1016/j.imbio.2011.07.022
  • Dergi Adı: IMMUNOBIOLOGY
  • Derginin Tarandığı İndeksler: Science Citation Index Expanded (SCI-EXPANDED), Scopus
  • Sayfa Sayıları: ss.235-243
  • Anahtar Kelimeler: Complement dysregulation, Endothelium, Haemolytic uraemic syndrome, Shiga toxin, Streptococcus pneumoniae, Thrombotic microangiopathy, THROMBOTIC THROMBOCYTOPENIC PURPURA, FACTOR-H-AUTOANTIBODIES, STREPTOCOCCUS-PNEUMONIAE INFECTION, INVASIVE PNEUMOCOCCAL DISEASE, COFACTOR PROTEIN CD46, COXSACKIE-VIRUS GROUP, ENDOTHELIAL-CELLS, SHIGA-TOXIN, FACTOR-I, ESCHERICHIA-COLI
  • Dokuz Eylül Üniversitesi Adresli: Hayır

Özet

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.