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Article

A haplotype in CFH family genes confers high risk of rare glomerular nephropathies.

Scientific reports - 20 Jul 2017

Ding Yin, Zhao Weiwei, Zhang Tao, Qiang Hao, Lu Jianping, Su Xin, Wen Shuzhen, Xu Feng, Zhang Mingchao, Zhang Haitao, Zeng Caihong, Liu Zhihong, Chen Huimei

Abstract excerpt

Despite distinct renal lesions, a series of rare glomerular nephropathies are reportedly mediated by complement overactivation. Genetic variations in complement genes contribute to disease risk, but the relationship of genotype to phenotype has not been straightforward. Here, we screened 11 complement genes from 91 patients with atypical hemolytic uremic syndrome (aHUS), C3 glomerulopathy (C3G) and...

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Topics

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Share to Atypical Hemolytic Uremic Syndrome
Share to Complement Activation

Methodology Data sources Editorial policy Privacy About Contact Helena Bioinformatics

Share to Complement C3

Share to Complement Factor H

Share to Glomerulonephritis, Membranoproliferative

Share to Linkage Disequilibrium

Share to Multigene Family

Share to Structure-Activity Relationship

Source

Open in PubMed Open full text

Identifiers

PMID: 28729648
DOI: 10.1038/s41598-017-05173-8
PMCID: PMC5519609

Genes

CFH
CFHR3
SPR

Provenance

PubMed metadata and Literature Corpus relationships. Corpus snapshot updated 6 Sept 2026. Manifest publication-graph-cohort-2026-09-06.1.

Source receipt: pubmed, retrieved 6 Sept 2026.

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