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Statistical Validation of Rare Complement Variants Provides Insights into the Molecular Basis of Atypical Hemolytic Uremic Syndrome and C3 Glomerulopathy
Journal article   Open access   Peer reviewed

Statistical Validation of Rare Complement Variants Provides Insights into the Molecular Basis of Atypical Hemolytic Uremic Syndrome and C3 Glomerulopathy

Amy J Osborne, Matteo Breno, Nicolo Ghiringhelli Borsa, Fengxiao Bu, Véronique Frémeaux-Bacchi, Daniel P Gale, Lambertus P van den Heuvel, David Kavanagh, Marina Noris, Sheila Pinto, …
The Journal of immunology (1950), Vol.200(7), pp.2464-2478
04/01/2018
DOI: 10.4049/jimmunol.1701695
PMCID: PMC6324840
PMID: 29500241
url
https://doi.org/10.4049/jimmunol.1701695View
Published (Version of record) Open Access

Abstract

Atypical hemolytic uremic syndrome (aHUS) and C3 glomerulopathy (C3G) are associated with dysregulation and overactivation of the complement alternative pathway. Typically, gene analysis for aHUS and C3G is undertaken in small patient numbers, yet it is unclear which genes most frequently predispose to aHUS or C3G. Accordingly, we performed a six-center analysis of 610 rare genetic variants in 13 mostly complement genes ( , , , , , , , , , , , , and ) from >3500 patients with aHUS and C3G. We report 371 novel rare variants (RVs) for aHUS and 82 for C3G. Our new interactive Database of Complement Gene Variants was used to extract allele frequency data for these 13 genes using the Exome Aggregation Consortium server as the reference genome. For aHUS, significantly more protein-altering rare variation was found in five genes , , , , and than in the Exome Aggregation Consortium (allele frequency < 0.01%), thus correlating these with aHUS. For C3G, an association was only found for RVs in and the N-terminal C3b-binding or C-terminal nonsurface-associated regions of In conclusion, the RV analyses showed nonrandom distributions over the affected proteins, and different distributions were observed between aHUS and C3G that clarify their phenotypes.
Glomerulonephritis, Membranoproliferative - pathology Gene Frequency - genetics Genetic Predisposition to Disease - genetics Complement C3 - metabolism Humans Male Mutation, Missense - genetics Atypical Hemolytic Uremic Syndrome - pathology Glomerulonephritis, Membranoproliferative - genetics Complement Pathway, Alternative - physiology Female Complement Pathway, Alternative - genetics Complement Factor H - genetics Atypical Hemolytic Uremic Syndrome - genetics Complement C3 - genetics

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