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A novel mutation in the Complement Factor B gene (CFB) and atypical hemolytic uremic syndrome
Journal article   Peer reviewed

A novel mutation in the Complement Factor B gene (CFB) and atypical hemolytic uremic syndrome

Hanan Tawadrous, Tara Maga, Josefina Sharma, Juan Kupferman, Richard Smith and Morris Schoeneman
Pediatric nephrology (Berlin, West), Vol.25(5), pp.947-951
05/2010
DOI: 10.1007/s00467-009-1415-3
PMID: 20108004

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Abstract

We report the case of an 8-year-old girl diagnosed with atypical hemolytic uremic syndrome (aHUS) with a complement factor B (CFB) gene mutation. aHUS is a disease of complement dysregulation. In approximately 50% of patients, mutations are identified in genes encoding regulators of complement—complement factor H (CFH), membrane cofactor protein or complement factor I (CFI)—or activators of complement—complement factor B (CFB) or C3. The mutation in this patient was identified in exon 12 of CFB and changes a lysine at amino acid position 533 to an arginine (c.1598A>G p.Lys533Arg). The two other mutations previously reported in CFB associated with aHUS are c.858C>G, p.F286L in exon 6 and c.967A>Gp.K323E in exon 7.
Atypical hemolytic uremic syndrome Pediatrics Complement Medicine & Public Health Factor B

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