000			03377nam a22005177a 4500
008			150313s20142014 xxu||||| |||| 00| 0 eng d
022			_a1018-4813
040			_aOvid MEDLINE(R)
099			_a24301058
245			_aReplication of the effect of SLC2A9 genetic variation on serum uric acid levels in American Indians.
251			_aEuropean Journal of Human Genetics. 22(7):938-43, 2014 Jul.
252			_aEur J Hum Genet. 22(7):938-43, 2014 Jul.
253			_aEuropean journal of human genetics : EJHG
260			_c2014
260			_fFY2015
266			_d2015-03-17
520			_aIncreased serum uric acid (SUA) or hyperuricemia, a risk factor for gout, renal and cardiovascular diseases, is caused by either increased production or decreased excretion of uric acid or a mix of both. The solute carrier protein 2 family, member 9 (SLC2A9) gene encodes a transporter that mediates urate flux across the renal proximal tubule. Genome-wide association studies have consistently shown the association of single-nucleotide polymorphisms in this gene with SUA in majority populations. American Indian participants of the Strong Heart Family Study, belonging to multigenerational families, have high prevalence of hyperuricemia. We conducted measured genotype analyses, based on variance components decomposition method and accounting for family relationships, to assess whether the association between SUA and SLC2A9 gene polymorphisms generalized to American Indians (n=3604) of this study. Seven polymorphisms were selected for genotyping based on their association with SUA levels in other populations. A strong association was found between SLC2A9 gene polymorphisms and SUA in all centers combined (P-values: 1.3 x 10(-31)-5.1 x 10(-23)) and also when stratified by recruitment center; P-values: 1.2 x 10(-14)-1.0 x 10(-5). These polymorphisms were also associated with the estimated glomerular filtration rate and serum creatinine but not albumin-creatinine ratio. In summary, the association of polymorphisms in the uric acid transporter gene with SUA levels extends to a new population of American Indians.
546			_aEnglish
650			_a*Genetic Predisposition to Disease
650			_a*Genome-Wide Association Study
650			_a*Glucose Transport Proteins, Facilitative/ge [Genetics]
650			_a*Hyperuricemia
650			_a*Indians, North American/ge [Genetics]
650			_a*Polymorphism, Genetic
650			_a*Uric Acid/bl [Blood]
650			_aAdult
650			_aFemale
650			_aGenotype
650			_aGlomerular Filtration Rate/ge [Genetics]
650			_aGlucose Transport Proteins, Facilitative/me [Metabolism]
650			_aHumans
650			_aHyperuricemia/bl [Blood]
650			_aHyperuricemia/ge [Genetics]
650			_aMale
650			_aMiddle Aged
651			_aMedStar Health Research Institute
657			_aClinical Trial
657			_aJournal Article
657			_aMulticenter Study
657			_aResearch Support, American Recovery and Reinvestment Act
657			_aResearch Support, N.I.H., Extramural
700			_aUmans, Jason G
790			_aCole SA, Comuzzie AG, Franceschini N, Haack K, Laston S, MacCluer JW, North KE, Umans JG, Voruganti VS
856			_uhttp://dx.doi.org/10.1038/ejhg.2013.264 _zhttp://dx.doi.org/10.1038/ejhg.2013.264
942			_cART _dArticle
999			_c1551 _d1551