Literature DB >> 30012629

COL4A3 Gene Variants and Diabetic Kidney Disease in MODY.

Yiting Wang1, Junlin Zhang1, Yingwang Zhao1, Shanshan Wang1, Jie Zhang2, Qianqian Han1, Rui Zhang1, Ruikun Guo1, Hanyu Li1, Li Li1, Tingli Wang1, Xi Tang1, Changzheng He3, Geer Teng4, Weiyue Gu5, Fang Liu6.   

Abstract

BACKGROUND AND OBJECTIVES: Despite advances in identifying genetic factors of diabetic kidney disease (DKD), much of the heritability remains unexplained. Nine maturity-onset diabetes in young (MODY) probands with kidney biopsy-proven DKD were selected and included in this study. The probands had more severe DKD compared with their parents with MODY, with overt proteinuria or rapid progression to ESKD. We aimed to explore the contribution of the variants in susceptibility genes of DKD to the severity of kidney phenotype between the probands and their parents. DESIGN, SETTING, PARTICIPANTS, & MEASUREMENTS: Whole-exome sequencing was performed to identify suspected MODY probands and their families. Known DKD susceptibility genes were reviewed. Variants reported to be associated with DKD, or those with minor allele frequency <0.05 and predicted to be pathogenic, were selected and analyzed. Immunofluorescence staining of COL4α3 was performed in kidney specimens of patients with DKD with or without R408H and M1209I of COL4A3 variants.
RESULTS: HNF1B-MODY, CEL-MODY, PAX4-MODY, and WFS1-MODY were diagnosed among nine families. We identified 196 selected variants of 25 DKD susceptibility genes among the participants. Analysis of phenotype between probands and parents, gene function, and protein-protein interaction networks revealed that COL4A3 variants were involved in the progression of DKD. Weak granular staining of COL4α3 was observed in the glomerular basement membrane of patients with the R408H and M1209I variants, whereas strong consecutive staining was observed in patients without these variants. Moreover, more number of DKD variants were identified in probands than in their parents with MODY.
CONCLUSIONS: The genetic effect of more pathogenic variants in various DKD susceptibility genes, especially variants in the COL4A3 gene, partially explained the more severe kidney phenotype in probands with kidney biopsy-proven DKD.
Copyright © 2018 by the American Society of Nephrology.

Entities:  

Keywords:  Biopsy; COL4A3 gene; Diabetes Mellitus, Type 2; Diabetic Nephropathies; Fluorescent Antibody Technique; Gene Frequency; Glomerular Basement Membrane; Humans; Kidney Failure, Chronic; Maturity-onset diabetes of the young; Parents; Phenotype; Protein Interaction Maps; Staining and Labeling; Susceptibility gene; Whole Exome Sequencing; diabetic nephropathy; gene expression; kidney; proteinuria

Year:  2018        PMID: 30012629      PMCID: PMC6086715          DOI: 10.2215/CJN.09100817

Source DB:  PubMed          Journal:  Clin J Am Soc Nephrol        ISSN: 1555-9041            Impact factor:   8.237


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