Back to Search Start Over

Epistatic role of the MYH9/APOL1 region on familial hematuria genes.

Authors :
Konstantinos Voskarides
Panayiota Demosthenous
Louiza Papazachariou
Maria Arsali
Yiannis Athanasiou
Michalis Zavros
Kostas Stylianou
Dimitris Xydakis
Eugenios Daphnis
Daniel P Gale
Patrick H Maxwell
Avraam Elia
Cristian Pattaro
Alkis Pierides
Constantinos Deltas
Source :
PLoS ONE, Vol 8, Iss 3, p e57925 (2013)
Publication Year :
2013
Publisher :
Public Library of Science (PLoS), 2013.

Abstract

Familial hematuria (FH) is explained by at least four different genes (see below). About 50% of patients develop late proteinuria and chronic kidney disease (CKD). We hypothesized that MYH9/APOL1, two closely linked genes associated with CKD, may be associated with adverse progression in FH. Our study included 102 thin basement membrane nephropathy (TBMN) patients with three known COL4A3/COL4A4 mutations (cohort A), 83 CFHR5/C3 glomerulopathy patients (cohort B) with a single CFHR5 mutation and 15 Alport syndrome patients (cohort C) with two known COL4A5 mild mutations, who were categorized as "Mild" (controls) or "Severe" (cases), based on renal manifestations. E1 and S1 MYH9 haplotypes and variant rs11089788 were analyzed for association with disease phenotype. Evidence for association with "Severe" progression in CFHR5 nephropathy was found with MYH9 variant rs11089788 and was confirmed in an independent FH cohort, D (cumulative p value = 0.001, odds ratio = 3.06, recessive model). No association was found with APOL1 gene. Quantitative Real time PCR did not reveal any functional significance for the rs11089788 risk allele. Our results derive additional evidence supporting previous reports according to which MYH9 is an important gene per se, predisposing to CKD, suggesting its usefulness as a prognostic marker for young hematuric patients.

Subjects

Subjects :
Medicine
Science

Details

Language :
English
ISSN :
19326203
Volume :
8
Issue :
3
Database :
Directory of Open Access Journals
Journal :
PLoS ONE
Publication Type :
Academic Journal
Accession number :
edsdoj.7055c818119043ffaada19dbb738d3b8
Document Type :
article
Full Text :
https://doi.org/10.1371/journal.pone.0057925