![]() The eMERGE-III imputed genotype and phenotype data are available through dbGAP, accession number phs001584.v2.p2. The PAGE consortium control genotype data are available on dbGAP under accession number phs000356.v2.p1. ![]() GWAS summary statistics are available from the Kiryluk Lab website. Our IRB determined that the use of the primary genotype data is restricted to genetic studies of kidney disease. Primary genotype data for previously published cohorts are available through dbGAP under accession number phs000431.v2.p1, and the new genotype data are available under dbGAP accession number phs000431.v3.p1. In a comprehensive functional annotation analysis of candidate causal genes, we observed convergence of biological candidates on a common set of inflammatory signaling pathways and cytokine ligand–receptor pairs, prioritizing potential new drug targets. High polygenic score for IgAN was associated with earlier onset of kidney failure. We also observed a positive genetic correlation between IgAN and serum IgA levels. The risk loci were enriched in gene orthologs causing abnormal IgA levels when genetically manipulated in mice. A total of 16 loci were new, including TNFSF4/TNFSF18, REL, CD28, PF4V1, LY86, LYN, ANXA3, TNFSF8/TNFSF15, REEP3, ZMIZ1, OVOL1/RELA, ETS1, IGH, IRF8, TNFRSF13B and FCAR. We defined 30 genome-wide significant risk loci explaining 11% of disease risk. Here we performed a genome-wide association study of 10,146 kidney-biopsy-diagnosed IgAN cases and 28,751 controls across 17 international cohorts. IgA nephropathy (IgAN) is a progressive form of kidney disease defined by glomerular deposition of IgA. Genome-wide association analyses define pathogenic signaling pathways and prioritize drug targets for IgA nephropathy
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