Genetic loci influencing kidney function and chronic kidney disease

John C Chambers, Weihua Zhang, Graham M Lord, Pim van der Harst, Debbie A Lawlor, Joban S Sehmi, Daniel P Gale, Mark N Wass, Kourosh R Ahmadi, Stephan J L Bakker, Jacqui Beckmann, Henk J G Bilo, Murielle Bochud, Morris J Brown, Mark J Caulfield, John M C Connell, H Terence Cook, Ioana Cotlarciuc, George Davey Smith, Ranil de SilvaGuohong Deng, Olivier Devuyst, Lambert D Dikkeschei, Nada Dimkovic, Mark Dockrell, Anna Dominiczak, Shah Ebrahim, Thomas Eggermann, Martin Farrall, Luigi Ferrucci, Jurgen Floege, Nita G Forouhi, Ron T Gansevoort, Xijin Han, Bo Hedblad, Jaap J Homan van der Heide, Bouke G Hepkema, Maria Hernandez-Fuentes, Elina Hypponen, Toby Johnson, Paul E de Jong, Nanne Kleefstra, Vasiliki Lagou, Marta Lapsley, Yun Li, Ruth J F Loos, Jian'an Luan, Karin Luttropp, Céline Maréchal, Olle Melander, Patricia B Munroe, Louise Nordfors, Afshin Parsa, Leena Peltonen, Brenda W Penninx, Esperanza Perucha, Anneli Pouta, Inga Prokopenko, Paul J Roderick, Aimo Ruokonen, Nilesh J Samani, Serena Sanna, Martin Schalling, David Schlessinger, Georg Schlieper, Marc A J Seelen, Alan R Shuldiner, Marketa Sjögren, Johannes H Smit, Harold Snieder, Nicole Soranzo, Timothy D Spector, Peter Stenvinkel, Michael J E Sternberg, Ramasamyiyer Swaminathan, Toshiko Tanaka, Lielith J Ubink-Veltmaat, Manuela Uda, Peter Vollenweider, Chris Wallace, Dawn Waterworth, Klaus Zerres, Gerard Waeber, Nicholas J Wareham, Patrick H Maxwell, Mark I McCarthy, Marjo-Riitta Jarvelin, Vincent Mooser, Goncalo R Abecasis, Liz Lightstone, James Scott, Gerjan Navis, Paul Elliott, Jaspal S Kooner

Research output: Contribution to journalArticleAcademicpeer-review

Abstract

Using genome-wide association, we identify common variants at 2p12-p13, 6q26, 17q23 and 19q13 associated with serum creatinine, a marker of kidney function (P = 10(-10) to 10(-15)). Of these, rs10206899 (near NAT8, 2p12-p13) and rs4805834 (near SLC7A9, 19q13) were also associated with chronic kidney disease (P = 5.0 x 10(-5) and P = 3.6 x 10(-4), respectively). Our findings provide insight into metabolic, solute and drug-transport pathways underlying susceptibility to chronic kidney disease.

Original languageEnglish
Pages (from-to)373-5
Number of pages3
JournalNature Genetics
Volume42
Issue number5
DOIs
Publication statusPublished - May 2010
Externally publishedYes

Keywords

  • Biological Transport
  • Creatinine/blood
  • Cystatin C/metabolism
  • Europe
  • Gene Expression Regulation
  • Genetic Markers/genetics
  • Genetic Predisposition to Disease
  • Genetic Variation
  • Genome-Wide Association Study
  • Genotype
  • Glomerular Filtration Rate
  • Humans
  • Kidney/physiology
  • Kidney Failure, Chronic/genetics
  • Models, Genetic

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