Please use this identifier to cite or link to this item: http://hdl.handle.net/2440/119907
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dc.contributor.authorVan Zuydam, N.en
dc.contributor.authorAhlqvist, E.en
dc.contributor.authorSandholm, N.en
dc.contributor.authorDeshmukh, H.en
dc.contributor.authorWilliam Rayner, N.en
dc.contributor.authorAbdalla, M.en
dc.contributor.authorLadenvall, C.en
dc.contributor.authorZiemek, D.en
dc.contributor.authorFauman, E.en
dc.contributor.authorRobertson, N.en
dc.contributor.authorMcKeigue, P.en
dc.contributor.authorValo, E.en
dc.contributor.authorForsblom, C.en
dc.contributor.authorHarjutsalo, V.en
dc.contributor.authorPerna, A.en
dc.contributor.authorRurali, E.en
dc.contributor.authorLoredana Marcovecchio, M.en
dc.contributor.authorIgo, R.en
dc.contributor.authorSalem, R.en
dc.contributor.authorPerico, N.en
dc.contributor.authoret al.en
dc.date.issued2018en
dc.identifier.citationDiabetes, 2018; 67(7):1414-1427en
dc.identifier.issn0012-1797en
dc.identifier.issn1939-327Xen
dc.identifier.urihttp://hdl.handle.net/2440/119907-
dc.description.abstractIdentification of sequence variants robustly associated with predisposition to diabetic kidney disease (DKD) has the potential to provide insights into the pathophysiological mechanisms responsible. We conducted a genome-wide association study (GWAS) of DKD in type 2 diabetes (T2D) using eight complementary dichotomous and quantitative DKD phenotypes: the principal dichotomous analysis involved 5,717 T2D subjects, 3,345 with DKD. Promising association signals were evaluated in up to 26,827 subjects with T2D (12,710 with DKD). A combined T1D+T2D GWAS was performed using complementary data available for subjects with T1D, which, with replication samples, involved up to 40,340 subjects with diabetes (18,582 with DKD). Analysis of specific DKD phenotypes identified a novel signal near GABRR1 (rs9942471, P = 4.5 × 10−8) associated with microalbuminuria in European T2D case subjects. However, no replication of this signal was observed in Asian subjects with T2D or in the equivalent T1D analysis. There was only limited support, in this substantially enlarged analysis, for association at previously reported DKD signals, except for those at UMOD and PRKAG2, both associated with estimated glomerular filtration rate. We conclude that, despite challenges in addressing phenotypic heterogeneity, access to increased sample sizes will continue to provide more robust inference regarding risk variant discovery for DKD.en
dc.description.statementofresponsibilityNatalie R. van Zuydam, Emma Ahlqvist, Niina Sandholm, Harshal Deshmukh, N. William Rayner ... Ville-Petteri Makinen ... et al.en
dc.language.isoenen
dc.publisherAmerican Diabetes Associationen
dc.rightsCopyright status unknownen
dc.subjectFinnish Diabetic Nephropathy Study (FinnDiane); Hong Kong Diabetes Registry Theme-based Research Scheme Project Group; Warren 3 and Genetics of Kidneys in Diabetes (GoKinD) Study Group; GENIE (GEnetics of Nephropathy an International Effort) Consortium; Diabetes Control and Complications Trial (DCCT)/Epidemiology of Diabetes Interventions and Complications (EDIC) Research Group; SUrrogate markers for Micro- and Macrovascular hard endpoints for Innovative diabetes Tools (SUMMIT) Consortium; Humans; Diabetic Nephropathies; Kidney Failure, Chronic; Diabetes Mellitus, Type 2; Genetic Predisposition to Disease; Case-Control Studies; Polymorphism, Single Nucleotide; Adult; Aged; Aged, 80 and over; Middle Aged; Female; Male; Renal Insufficiency, Chronic; Genome-Wide Association Studyen
dc.titleA genome-wide association study of diabetic kidney disease in subjects with type 2 diabetesen
dc.typeJournal articleen
dc.identifier.rmid0030109990en
dc.identifier.doi10.2337/db17-0914en
dc.identifier.pubid462128-
pubs.library.collectionMedicine publicationsen
pubs.library.teamDS10en
pubs.verification-statusVerifieden
pubs.publication-statusPublisheden
Appears in Collections:Medicine publications

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