| Literature DB >> 23870792 |
Valerie Wilson1, Rebecca Darlay, William Wong, Katrina M Wood, Jeannette McFarlane, Lone Schejbel, Ida M Schmidt, Claire L Harris, James Tellez, Eva-Maria Hunze, Kevin Marchbank, Judith A Goodship, Timothy H J Goodship.
Abstract
We report a male infant who presented at 8 months of age with atypical hemolytic uremic syndrome (aHUS) responsive to plasma therapy. Investigation showed him to have complement factor H (CFH) deficiency associated with a homozygous CFH mutation (c.2880delT [p.Phe960fs]). Mutation screening of the child's parents revealed that the father was heterozygous for this change but that it was not present in his mother. Chromosome 1 uniparental isodisomy of paternal origin was confirmed by genotyping chromosome 1 SNPs. CD46 SNP genotyping was undertaken in this individual and another patient with CFH deficiency associated with chromosome 1 uniparental isodisomy. This showed a homozygous aHUS risk haplotype (CD46GGAAC) in the patient with aHUS and a homozygous glomerulonephritis risk haplotype (CD46AAGGT) in the patient with endocapillary glomerulonephritis. We also showed that FHL-1 (factor H-like protein 1) was present in the patient with aHUS and absent in the patient with glomerulonephritis. This study emphasizes that modifiers such as CD46 and FHL-1 may determine the kidney phenotype of patients who present with homozygous CFH deficiency.Entities:
Keywords: Complement; glomerulonephritis; hemolytic uremic syndrome
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Year: 2013 PMID: 23870792 DOI: 10.1053/j.ajkd.2013.05.020
Source DB: PubMed Journal: Am J Kidney Dis ISSN: 0272-6386 Impact factor: 8.860