Abstract：
:Several mutations in the CFH gene have been described in non-Shiga-toxin-associated haemolytic uraemic syndrome (non-Stx-HUS), a rare syndrome characterized by haemolytic anaemia, thrombocytopenia and acute renal failure. Mutations in genes encoding other complement regulatory proteins, membrane cofactor protein (CD46) and complement factor I (CFI), were also involved in the pathogenesis of the disease. Anyway, mutations in the three genes account for no more than 50% of cases of non-Stx-HUS. Human complement factor H related 5 (CFHR5) is a recently characterised member of the human complement factor H (CFH) family that has been found as a component of immune deposits in human kidney with sclerotic lesions from different causes. CFHR5 possesses cofactor activity and has been proposed to play a role in complement regulation in the glomerulus. We screened CFHR5 gene for variations potentially involved in the aetiology of HUS. Forty-five patients with HUS and 80 controls were analysed. Altogether, 5 genetic variants in CFHR5 were found in overall 9/45 HUS patients and in 4/80 controls. Statistical analysis showed that allelic variants in CFHR5 were prefentially associated with HUS. Based on these data, we conclude that, though not causative, CFHR5 genetic alterations may play a secondary role in the pathogenesis of HUS.
journal_name
Mol Immunoljournal_title
Molecular immunologyauthors
Monteferrante G,Brioschi S,Caprioli J,Pianetti G,Bettinaglio P,Bresin E,Remuzzi G,Noris Mdoi
10.1016/j.molimm.2006.08.004subject
Has Abstractpub_date
2007-03-01 00:00:00pages
1704-8issue
7eissn
0161-5890issn
1872-9142pii
S0161-5890(06)00556-6journal_volume
44pub_type
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pub_type： 杂志文章
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pub_type： 杂志文章
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