Journal article
HLA-DQA1 and PLCG2 are candidate risk loci for childhood-onset steroid-sensitive nephrotic syndrome
RA Gbadegesin, A Adeyemo, NJA Webb, LA Greenbaum, A Abeyagunawardena, S Thalgahagoda, A Kale, D Gipson, T Srivastava, JJ Lin, D Chand, TE Hunley, PD Brophy, A Bagga, A Sinha, MN Rheault, J Ghali, K Nicholls, E Abraham, HS Janjua Show all
Journal of the American Society of Nephrology | Published : 2015
Abstract
Steroid-sensitive nephrotic syndrome(SSNS) accounts for.80%of cases of nephrotic syndrome in childhood. However, the etiology and pathogenesis of SSNS remain obscure. Hypothesizing that coding variation may underlie SSNS risk, we conducted an exome array association study of SSNS.We enrolled a discovery set of 363 persons (214 South Asian children with SSNS and 149 controls) and genotyped them using the Illumina HumanExome Beadchip. Four common single nucleotide polymorphisms (SNPs) in HLA-DQA1 and HLA-DQB1 (rs1129740, rs9273349, rs1071630, and rs1140343) were significantly associated with SSNS at or near the Bonferroni-adjusted P value for the number of single variants thatwere tested (odds..
View full abstractGrants
Awarded by National Human Genome Research Institute
Funding Acknowledgements
This work was supported by the Doris Duke Charitable Foundation. R.G. is the recipient of a Doris Duke Clinical Scientist Development Award and National Institutes of Health (NIH), National Institute of Diabetes and Digestive and Kidney Disease (NIDDK) K08-DK082495-05 award. R.G. is also the recipient of a P&F grant from Duke O'Brien Center for Kidney research supported by NIH NIDDK P30-DK096493 award. A.A. is supported by the Intramural Research Program of the Center for Research on Genomics and Global Health (CRGGH). The CRGGH is supported by funds from the Office of the Director, NIDDK and National Human Genome Research Institute at the NIH (Z01-HG200362). The funding sources have no role in the writing of the manuscript or the decision to submit it for publication.