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CFH and CFHR Copy Number Variations in C3 Glomerulopathy and Immune Complex-Mediated Membranoproliferative Glomerulonephritis
Journal article   Open access   Peer reviewed

CFH and CFHR Copy Number Variations in C3 Glomerulopathy and Immune Complex-Mediated Membranoproliferative Glomerulonephritis

Rossella Piras, Matteo Breno, Elisabetta Valoti, Marta Alberti, Paraskevas Iatropoulos, Caterina Mele, Elena Bresin, Roberta Donadelli, Paola Cuccarolo, Richard J. H Smith, …
Frontiers in genetics, Vol.12, pp.670727-670727
06/11/2021
DOI: 10.3389/fgene.2021.670727
PMCID: PMC8240960
PMID: 34211499
url
https://doi.org/10.3389/fgene.2021.670727View
Published (Version of record) Open Access

Abstract

C3 Glomerulopathy (C3G) and Immune Complex-Mediated Membranoproliferative glomerulonephritis (IC-MPGN) are rare diseases characterized by glomerular deposition of C3 caused by dysregulation of the alternative pathway (AP) of complement. In approximately 20% of affected patients, dysregulation is driven by pathogenic variants in the two components of the AP C3 convertase, complement C3 ( C3 ) and Factor B ( CFB ), or in complement Factor H ( CFH ) and Factor I ( CFI ), two genes that encode complement regulators. Copy number variations (CNVs) involving the CFH -related genes ( CFHRs ) that give rise to hybrid FHR proteins also have been described in a few C3G patients but not in IC-MPGN patients. In this study, we used multiplex ligation-dependent probe amplification (MLPA) to study the genomic architecture of the CFH-CFHR region and characterize CNVs in a large cohort of patients with C3G ( n = 103) and IC-MPGN ( n = 96) compared to healthy controls ( n = 100). We identified new/rare CNVs resulting in structural variants (SVs) in 5 C3G and 2 IC-MPGN patients. Using long-read single molecule real-time sequencing (SMRT), we detected the breakpoints of three SVs. The identified SVs included: 1) a deletion of the entire CFH in one patient with IC-MPGN; 2) an increased number of CFHR4 copies in one IC-MPGN and three C3G patients; 3) a deletion from CFHR3 -intron 3 to CFHR3-3 ′ UTR ( CFHR3 4 – 6 Δ) that results in a FHR3-FHR1 hybrid protein in a C3G patient; and 4) a CFHR3 1 – 5 -CFHR4 10 hybrid gene in a C3G patient. This work highlights the contribution of CFH-CFHR CNVs to the pathogenesis of both C3G and IC-MPGN.
C3 glomerulopathy (C3G) complement copy number variations (CNVs) factor H (FH) factor H-related proteins (FHRs) Genetics immune complex-mediated membranoproliferative glomerulonephritis (IC-MPGN) single molecule real-time (SMRT) structural variants (SVs)

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