Association of three genetic loci with uric acid concentration and risk of gout: a genome-wide association study

Hyperuricaemia, a highly heritable trait, is a key risk factor for gout. We aimed to identify novel genes associated with serum uric acid concentration and gout. Genome-wide association studies were done for serum uric acid in 7699 participants in the Framingham cohort and in 4148 participants in th...

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Veröffentlicht in:	The Lancet (British edition) Jg. 372; H. 9654; S. 1953 - 1961
Hauptverfasser:	Dehghan, Abbas, Köttgen, Anna, Yang, Qiong, Hwang, Shih-Jen, Kao, WH Linda, Rivadeneira, Fernando, Boerwinkle, Eric, Levy, Daniel, Hofman, Albert, Astor, Brad C, Benjamin, Emelia J, van Duijn, Cornelia M, Witteman, Jacqueline C, Coresh, Josef, Fox, Caroline S
Format:	Journal Article
Sprache:	Englisch
Veröffentlicht:	England Elsevier Ltd 06.12.2008 Elsevier Limited
Schlagworte:	Alleles Chromosomes, Human, 4-5 - genetics Chromosomes, Human, 6-12 and X - genetics Chronic illnesses Cohort Studies Eye diseases Family physicians Female Genetic research Genetics, Population Genome, Human - genetics Genome-Wide Association Study Genotype Gout - epidemiology Gout - etiology Gout - genetics Humans Hyperuricemia - complications Hyperuricemia - genetics Hyperuricemia - metabolism Internal Medicine Male Medical ethics Middle Aged Netherlands Polymorphism, Single Nucleotide - genetics Prevalence Risk Factors Sample size Studies Systematic review Uric Acid - blood Netherlands Netherlands, Rotterdam
ISSN:	0140-6736, 1474-547X, 1474-547X
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Abstract	Hyperuricaemia, a highly heritable trait, is a key risk factor for gout. We aimed to identify novel genes associated with serum uric acid concentration and gout. Genome-wide association studies were done for serum uric acid in 7699 participants in the Framingham cohort and in 4148 participants in the Rotterdam cohort. Genome-wide significant single nucleotide polymorphisms (SNPs) were replicated in white (n=11 024) and black (n=3843) individuals who took part in the study of Atherosclerosis Risk in Communities (ARIC). The SNPs that reached genome-wide significant association with uric acid in either the Framingham cohort (p<5·0×10 −8) or the Rotterdam cohort (p<1·0×10 −7) were evaluated with gout. The results obtained in white participants were combined using meta-analysis. Three loci in the Framingham cohort and two in the Rotterdam cohort showed genome-wide association with uric acid. Top SNPs in each locus were: missense rs16890979 in SLC2A9 (p=7·0×10 −168 and 2·9×10 −18 for white and black participants, respectively); missense rs2231142 in ABCG2 (p=2·5×10 −60 and 9·8×10 −4), and rs1165205 in SLC17A3 (p=3·3×10 −26 and 0·33). All SNPs were direction-consistent with gout in white participants: rs16890979 (OR 0·59 per T allele, 95% CI 0·52–0·68, p=7·0×10 −14), rs2231142 (1·74, 1·51–1·99, p=3·3×10 −15), and rs1165205 (0·85, 0·77–0·94, p=0·002). In black participants of the ARIC study, rs2231142 was direction-consistent with gout (1·71, 1·06–2·77, p=0·028). An additive genetic risk score of high-risk alleles at the three loci showed graded associations with uric acid (272–351 μmol/L in the Framingham cohort, 269–386 μmol/L in the Rotterdam cohort, and 303–426 μmol/L in white participants of the ARIC study) and gout (frequency 2–13% in the Framingham cohort, 2–8% in the Rotterdam cohort, and 1–18% in white participants in the ARIC study). We identified three genetic loci associated with uric acid concentration and gout. A score based on genes with a putative role in renal urate handling showed a substantial risk for gout. Netherlands Organisation for Scientific Research (NWO); the National Heart, Lung, and Blood Institute.
AbstractList	Hyperuricaemia, a highly heritable trait, is a key risk factor for gout. We aimed to identify novel genes associated with serum uric acid concentration and gout. Genome-wide association studies were done for serum uric acid in 7699 participants in the Framingham cohort and in 4148 participants in the Rotterdam cohort. Genome-wide significant single nucleotide polymorphisms (SNPs) were replicated in white (n=11 024) and black (n=3843) individuals who took part in the study of Atherosclerosis Risk in Communities (ARIC). The SNPs that reached genome-wide significant association with uric acid in either the Framingham cohort (p<5·0×10 −8) or the Rotterdam cohort (p<1·0×10 −7) were evaluated with gout. The results obtained in white participants were combined using meta-analysis. Three loci in the Framingham cohort and two in the Rotterdam cohort showed genome-wide association with uric acid. Top SNPs in each locus were: missense rs16890979 in SLC2A9 (p=7·0×10 −168 and 2·9×10 −18 for white and black participants, respectively); missense rs2231142 in ABCG2 (p=2·5×10 −60 and 9·8×10 −4), and rs1165205 in SLC17A3 (p=3·3×10 −26 and 0·33). All SNPs were direction-consistent with gout in white participants: rs16890979 (OR 0·59 per T allele, 95% CI 0·52–0·68, p=7·0×10 −14), rs2231142 (1·74, 1·51–1·99, p=3·3×10 −15), and rs1165205 (0·85, 0·77–0·94, p=0·002). In black participants of the ARIC study, rs2231142 was direction-consistent with gout (1·71, 1·06–2·77, p=0·028). An additive genetic risk score of high-risk alleles at the three loci showed graded associations with uric acid (272–351 μmol/L in the Framingham cohort, 269–386 μmol/L in the Rotterdam cohort, and 303–426 μmol/L in white participants of the ARIC study) and gout (frequency 2–13% in the Framingham cohort, 2–8% in the Rotterdam cohort, and 1–18% in white participants in the ARIC study). We identified three genetic loci associated with uric acid concentration and gout. A score based on genes with a putative role in renal urate handling showed a substantial risk for gout. Netherlands Organisation for Scientific Research (NWO); the National Heart, Lung, and Blood Institute. Summary Background Hyperuricaemia, a highly heritable trait, is a key risk factor for gout. We aimed to identify novel genes associated with serum uric acid concentration and gout. Methods Genome-wide association studies were done for serum uric acid in 7699 participants in the Framingham cohort and in 4148 participants in the Rotterdam cohort. Genome-wide significant single nucleotide polymorphisms (SNPs) were replicated in white (n=11 024) and black (n=3843) individuals who took part in the study of Atherosclerosis Risk in Communities (ARIC). The SNPs that reached genome-wide significant association with uric acid in either the Framingham cohort (p<5·0×10−8 ) or the Rotterdam cohort (p<1·0×10−7 ) were evaluated with gout. The results obtained in white participants were combined using meta-analysis. Findings Three loci in the Framingham cohort and two in the Rotterdam cohort showed genome-wide association with uric acid. Top SNPs in each locus were: missense rs16890979 in SLC2A9 (p=7·0×10−168 and 2·9×10−18 for white and black participants, respectively); missense rs2231142 in ABCG2 (p=2·5×10−60 and 9·8×10−4 ), and rs1165205 in SLC17A3 (p=3·3×10−26 and 0·33). All SNPs were direction-consistent with gout in white participants: rs16890979 (OR 0·59 per T allele, 95% CI 0·52–0·68, p=7·0×10−14 ), rs2231142 (1·74, 1·51–1·99, p=3·3×10−15 ), and rs1165205 (0·85, 0·77–0·94, p=0·002). In black participants of the ARIC study, rs2231142 was direction-consistent with gout (1·71, 1·06–2·77, p=0·028). An additive genetic risk score of high-risk alleles at the three loci showed graded associations with uric acid (272–351 μmol/L in the Framingham cohort, 269–386 μmol/L in the Rotterdam cohort, and 303–426 μmol/L in white participants of the ARIC study) and gout (frequency 2–13% in the Framingham cohort, 2–8% in the Rotterdam cohort, and 1–18% in white participants in the ARIC study). Interpretation We identified three genetic loci associated with uric acid concentration and gout. A score based on genes with a putative role in renal urate handling showed a substantial risk for gout. Funding Netherlands Organisation for Scientific Research (NWO); the National Heart, Lung, and Blood Institute. Hyperuricaemia, a highly heritable trait, is a key risk factor for gout. We aimed to identify novel genes associated with serum uric acid concentration and gout. Genome-wide association studies were done for serum uric acid in 7699 participants in the Framingham cohort and in 4148 participants in the Rotterdam cohort. Genome-wide significant single nucleotide polymorphisms (SNPs) were replicated in white (n=11 024) and black (n=3843) individuals who took part in the study of Atherosclerosis Risk in Communities (ARIC). The SNPs that reached genome-wide significant association with uric acid in either the Framingham cohort (p<5.0 x 10(-8)) or the Rotterdam cohort (p<1.0 x 10(-7)) were evaluated with gout. The results obtained in white participants were combined using meta-analysis. Three loci in the Framingham cohort and two in the Rotterdam cohort showed genome-wide association with uric acid. Top SNPs in each locus were: missense rs16890979 in SLC2A9 (p=7.0 x 10(-168) and 2.9 x 10(-18) for white and black participants, respectively); missense rs2231142 in ABCG2 (p=2.5 x 10(-60) and 9.8 x 10(-4)), and rs1165205 in SLC17A3 (p=3.3 x 10(-26) and 0.33). All SNPs were direction-consistent with gout in white participants: rs16890979 (OR 0.59 per T allele, 95% CI 0.52-0.68, p=7.0 x 10(-14)), rs2231142 (1.74, 1.51-1.99, p=3.3 x 10(-15)), and rs1165205 (0.85, 0.77-0.94, p=0.002). In black participants of the ARIC study, rs2231142 was direction-consistent with gout (1.71, 1.06-2.77, p=0.028). An additive genetic risk score of high-risk alleles at the three loci showed graded associations with uric acid (272-351 mumol/L in the Framingham cohort, 269-386 mumol/L in the Rotterdam cohort, and 303-426 mumol/L in white participants of the ARIC study) and gout (frequency 2-13% in the Framingham cohort, 2-8% in the Rotterdam cohort, and 1-18% in white participants in the ARIC study). We identified three genetic loci associated with uric acid concentration and gout. A score based on genes with a putative role in renal urate handling showed a substantial risk for gout. Hyperuricaemia, a highly heritable trait, is a key risk factor for gout. We aimed to identify novel genes associated with serum uric acid concentration and gout.BACKGROUNDHyperuricaemia, a highly heritable trait, is a key risk factor for gout. We aimed to identify novel genes associated with serum uric acid concentration and gout.Genome-wide association studies were done for serum uric acid in 7699 participants in the Framingham cohort and in 4148 participants in the Rotterdam cohort. Genome-wide significant single nucleotide polymorphisms (SNPs) were replicated in white (n=11 024) and black (n=3843) individuals who took part in the study of Atherosclerosis Risk in Communities (ARIC). The SNPs that reached genome-wide significant association with uric acid in either the Framingham cohort (p<5.0 x 10(-8)) or the Rotterdam cohort (p<1.0 x 10(-7)) were evaluated with gout. The results obtained in white participants were combined using meta-analysis.METHODSGenome-wide association studies were done for serum uric acid in 7699 participants in the Framingham cohort and in 4148 participants in the Rotterdam cohort. Genome-wide significant single nucleotide polymorphisms (SNPs) were replicated in white (n=11 024) and black (n=3843) individuals who took part in the study of Atherosclerosis Risk in Communities (ARIC). The SNPs that reached genome-wide significant association with uric acid in either the Framingham cohort (p<5.0 x 10(-8)) or the Rotterdam cohort (p<1.0 x 10(-7)) were evaluated with gout. The results obtained in white participants were combined using meta-analysis.Three loci in the Framingham cohort and two in the Rotterdam cohort showed genome-wide association with uric acid. Top SNPs in each locus were: missense rs16890979 in SLC2A9 (p=7.0 x 10(-168) and 2.9 x 10(-18) for white and black participants, respectively); missense rs2231142 in ABCG2 (p=2.5 x 10(-60) and 9.8 x 10(-4)), and rs1165205 in SLC17A3 (p=3.3 x 10(-26) and 0.33). All SNPs were direction-consistent with gout in white participants: rs16890979 (OR 0.59 per T allele, 95% CI 0.52-0.68, p=7.0 x 10(-14)), rs2231142 (1.74, 1.51-1.99, p=3.3 x 10(-15)), and rs1165205 (0.85, 0.77-0.94, p=0.002). In black participants of the ARIC study, rs2231142 was direction-consistent with gout (1.71, 1.06-2.77, p=0.028). An additive genetic risk score of high-risk alleles at the three loci showed graded associations with uric acid (272-351 mumol/L in the Framingham cohort, 269-386 mumol/L in the Rotterdam cohort, and 303-426 mumol/L in white participants of the ARIC study) and gout (frequency 2-13% in the Framingham cohort, 2-8% in the Rotterdam cohort, and 1-18% in white participants in the ARIC study).FINDINGSThree loci in the Framingham cohort and two in the Rotterdam cohort showed genome-wide association with uric acid. Top SNPs in each locus were: missense rs16890979 in SLC2A9 (p=7.0 x 10(-168) and 2.9 x 10(-18) for white and black participants, respectively); missense rs2231142 in ABCG2 (p=2.5 x 10(-60) and 9.8 x 10(-4)), and rs1165205 in SLC17A3 (p=3.3 x 10(-26) and 0.33). All SNPs were direction-consistent with gout in white participants: rs16890979 (OR 0.59 per T allele, 95% CI 0.52-0.68, p=7.0 x 10(-14)), rs2231142 (1.74, 1.51-1.99, p=3.3 x 10(-15)), and rs1165205 (0.85, 0.77-0.94, p=0.002). In black participants of the ARIC study, rs2231142 was direction-consistent with gout (1.71, 1.06-2.77, p=0.028). An additive genetic risk score of high-risk alleles at the three loci showed graded associations with uric acid (272-351 mumol/L in the Framingham cohort, 269-386 mumol/L in the Rotterdam cohort, and 303-426 mumol/L in white participants of the ARIC study) and gout (frequency 2-13% in the Framingham cohort, 2-8% in the Rotterdam cohort, and 1-18% in white participants in the ARIC study).We identified three genetic loci associated with uric acid concentration and gout. A score based on genes with a putative role in renal urate handling showed a substantial risk for gout.INTERPRETATIONWe identified three genetic loci associated with uric acid concentration and gout. A score based on genes with a putative role in renal urate handling showed a substantial risk for gout. Background Hyperuricaemia, a highly heritable trait, is a key risk factor for gout. We aimed to identify novel genes associated with serum uric add concentration and gout. Methods Genome-wide association studies were done for serum uric add in 7699 participants in the Framingham cohort and in 4148 participants in the Rotterdam cohort. Genome-wide significant single nudeotide polymorphisms (SNPs) were replicated in white (n=11 024) and black (n=3843) individuals who took part in the study of Atherosderosis Risk in Communities (ARIC). The SNPs that readied genome-wide significant association with uric add in either the Framingham cohort (p<5 times 0x10 super(-8)) or the Rotterdam cohort (p<1 times 0x10 super(-7)) were evaluated with gout The results obtained in white participants were combined using meta-analysis. Findings Three loci in the Framingham cohort and two in the Rotterdam cohort showed genome-wide association with uric add. Top SNPs in each locus were: missense rs16890979 in SLC2A9 (p=7 times 0x10 super(-168) and 2 times 9x10 super(-18) for white and black participants, respectively); missense rs2231142 in ABCG2 (p=2 times 5x10 super(-60) and 9 times 8x10 super(-4)), and rs1165205 in SLC17A3 (p=3 times 3x10 super(-26) and 0.33). All SNPs were direction-consistent with gout in white participants: rs16890979 (OR 0 times 59 per T allele, 95% CI 0 times 52-0.68, p=7 times 0x10 super(-14)), rs2231142 (1 times 74, 1 times 51-1 times 99, p=3 times 3x10 super(-15)), and rs1165205 (0 times 85, 0 times 77-0 times 94, p=0 times 002). In black partidpants of the ARIC study, rs2231142 was direction-consistent with gout (1 times 71, 1 times 06-2 times 77, p=0 times 028). An additive genetic risk score of high-risk alleles at the three loci showed graded associations with uric add (272-351 mu mol/L in the Framingham cohort, 269-386 mu mol/L in the Rotterdam cohort, and 303-426 mu mol/L in white participants of the ARIC study) and gout (frequency 2-13% in the Framingham cohort, 2-8% in the Rotterdam cohort, and 1-18% in white participants in the ARIC study). Interpretation We identified three genetic loci associated with uric add concentration and gout. A score based on genes with a putative role in renal urate handling showed a substantial risk for gout Funding Netherlands Organisation for Scientific Research (NWO); the National Heart, Lung, and Blood Institute. Hyperuricaemia, a highly heritable trait, is a key risk factor for gout. We aimed to identify novel genes associated with serum uric acid concentration and gout. Genome-wide association studies were done for serum uric acid in 7699 participants in the Framingham cohort and in 4148 participants in the Rotterdam cohort. Genome-wide significant single nucleotide polymorphisms (SNPs) were replicated in white (n=11024) and black (n=3843) individuals who took part in the study of Atherosclerosis Risk in Communities (ARIC). The SNPs that reached genome-wide significant association with uric acid in either the Framingham cohort (p<5.0×10^sup -8^) or the Rotterdam cohort (p<1.0×10×10^sup -7^) were evaluated with gout. The results obtained in white participants were combined using meta-analysis. Three loci in the Framingham cohort and two in the Rotterdam cohort showed genome-wide association with uric acid. Top SNPs in each locus were: missense rs16890979 in SLC2A9 (p=7.0×10^sup -168^ and 2.9×10^sup -18^ for white and black participants, respectively); missense rs2231142 in ABCG2 (p=2.5×10^sup -60^ and 9.8×10^sup -4^), and rs1165205 in SLC17A3 (p=3.3×10^sup -26^ and 0.33). All SNPs were direction-consistent with gout in white participants: rs16890979 (OR 0.59 per T allele, 95% CI 0.52-0.68, p=7.0×10^sup -14^), rs2231142 (1.74, 1.51-1.99, p=3.3×10^sup -15^), and rs1165205 (0.85, 0.77-0.94, p=0.002). In black participants of the ARIC study, rs2231142 was direction-consistent with gout (1.71, 1.06-2.77, p=0.028). An additive genetic risk score of high-risk alleles at the three loci showed graded associations with uric acid (272-351 µmol/L in the Framingham cohort, 269-386 µmol/L in the Rotterdam cohort, and 303-426 µmol/L in white participants of the ARIC study) and gout (frequency 2-13% in the Framingham cohort, 2-8% in the Rotterdam cohort, and 1-18% in white participants in the ARIC study). We identified three genetic loci associated with uric acid concentration and gout. A score based on genes with a putative role in renal urate handling showed a substantial risk for gout.
Author	van Duijn, Cornelia M Hofman, Albert Hwang, Shih-Jen Kao, WH Linda Coresh, Josef Benjamin, Emelia J Witteman, Jacqueline C Yang, Qiong Boerwinkle, Eric Dehghan, Abbas Levy, Daniel Rivadeneira, Fernando Astor, Brad C Köttgen, Anna Fox, Caroline S
AuthorAffiliation	3 Department of Biostatistics, School of Public Health, Boston University, Boston, USA 8 NHLBI’s Framingham Heart Study, and the Center for Population Studies, Framingham, MA, USA 4 Department of School of Medicine, Boston University, Boston, USA 2 Department of Epidemiology and the Welch Center for Prevention, Epidemiology & Clinical Research, Johns Hopkins University, Baltimore, USA 1 Department of Epidemiology & Biostatistics, Erasmus Medical Center, Rotterdam, The Netherlands 5 Human Genetics Center and Institute of Molecular Medicine, University of Texas Health Science Center, Houston, TX, USA 6 Boston University, Boston, MA, USA 7 Brigham and Women’s Hospital Division of Endocrinology, Hypertension, and Diabetes and Harvard Medical School, Framingham, MA, USA 9 the National Heart Lung and Blood Institute, Bethesda, MD, USA
AuthorAffiliation_xml	– name: 3 Department of Biostatistics, School of Public Health, Boston University, Boston, USA – name: 8 NHLBI’s Framingham Heart Study, and the Center for Population Studies, Framingham, MA, USA – name: 9 the National Heart Lung and Blood Institute, Bethesda, MD, USA – name: 1 Department of Epidemiology & Biostatistics, Erasmus Medical Center, Rotterdam, The Netherlands – name: 2 Department of Epidemiology and the Welch Center for Prevention, Epidemiology & Clinical Research, Johns Hopkins University, Baltimore, USA – name: 6 Boston University, Boston, MA, USA – name: 7 Brigham and Women’s Hospital Division of Endocrinology, Hypertension, and Diabetes and Harvard Medical School, Framingham, MA, USA – name: 5 Human Genetics Center and Institute of Molecular Medicine, University of Texas Health Science Center, Houston, TX, USA – name: 4 Department of School of Medicine, Boston University, Boston, USA
Author_xml	– sequence: 1 givenname: Abbas surname: Dehghan fullname: Dehghan, Abbas organization: Department of Epidemiology, Erasmus Medical Centre, Rotterdam, Netherlands – sequence: 2 givenname: Anna surname: Köttgen fullname: Köttgen, Anna organization: Department of Epidemiology and the Welch Center for Prevention, Epidemiology, and Clinical Research, Johns Hopkins University, Baltimore, MD, USA – sequence: 3 givenname: Qiong surname: Yang fullname: Yang, Qiong organization: Departments of Biostatistics, School of Public Health, Boston University, Boston, MA, USA – sequence: 4 givenname: Shih-Jen surname: Hwang fullname: Hwang, Shih-Jen organization: National Heart, Lung, and Blood Institute, Framingham Heart Study, and the Center for Population Studies, Framingham, MA, USA – sequence: 5 givenname: WH Linda surname: Kao fullname: Kao, WH Linda organization: Department of Epidemiology and the Welch Center for Prevention, Epidemiology, and Clinical Research, Johns Hopkins University, Baltimore, MD, USA – sequence: 6 givenname: Fernando surname: Rivadeneira fullname: Rivadeneira, Fernando organization: Department of Internal Medicine, Erasmus Medical Centre, Rotterdam, Netherlands – sequence: 7 givenname: Eric surname: Boerwinkle fullname: Boerwinkle, Eric organization: Human Genetics Center and Institute of Molecular Medicine, University of Texas Health Science Center, Houston, TX, USA – sequence: 8 givenname: Daniel surname: Levy fullname: Levy, Daniel organization: National Heart, Lung, and Blood Institute, Framingham Heart Study, and the Center for Population Studies, Framingham, MA, USA – sequence: 9 givenname: Albert surname: Hofman fullname: Hofman, Albert organization: Department of Epidemiology, Erasmus Medical Centre, Rotterdam, Netherlands – sequence: 10 givenname: Brad C surname: Astor fullname: Astor, Brad C organization: Department of Epidemiology and the Welch Center for Prevention, Epidemiology, and Clinical Research, Johns Hopkins University, Baltimore, MD, USA – sequence: 11 givenname: Emelia J surname: Benjamin fullname: Benjamin, Emelia J organization: Department of Cardiology, Boston University School of Medicine, Boston, MA, USA – sequence: 12 givenname: Cornelia M surname: van Duijn fullname: van Duijn, Cornelia M organization: Department of Epidemiology, Erasmus Medical Centre, Rotterdam, Netherlands – sequence: 13 givenname: Jacqueline C surname: Witteman fullname: Witteman, Jacqueline C organization: Department of Epidemiology, Erasmus Medical Centre, Rotterdam, Netherlands – sequence: 14 givenname: Josef surname: Coresh fullname: Coresh, Josef organization: Department of Epidemiology and the Welch Center for Prevention, Epidemiology, and Clinical Research, Johns Hopkins University, Baltimore, MD, USA – sequence: 15 givenname: Caroline S surname: Fox fullname: Fox, Caroline S email: foxca@nhlbi.nih.gov organization: Brigham and Women's Hospital Division of Endocrinology, Hypertension, and Diabetes and Harvard Medical School, Boston, MA, USA
BackLink	https://www.ncbi.nlm.nih.gov/pubmed/18834626$$D View this record in MEDLINE/PubMed
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Snippet	Hyperuricaemia, a highly heritable trait, is a key risk factor for gout. We aimed to identify novel genes associated with serum uric acid concentration and... Summary Background Hyperuricaemia, a highly heritable trait, is a key risk factor for gout. We aimed to identify novel genes associated with serum uric acid... Background Hyperuricaemia, a highly heritable trait, is a key risk factor for gout. We aimed to identify novel genes associated with serum uric add...
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StartPage	1953
SubjectTerms	Alleles Chromosomes, Human, 4-5 - genetics Chromosomes, Human, 6-12 and X - genetics Chronic illnesses Cohort Studies Eye diseases Family physicians Female Genetic research Genetics, Population Genome, Human - genetics Genome-Wide Association Study Genotype Gout - epidemiology Gout - etiology Gout - genetics Humans Hyperuricemia - complications Hyperuricemia - genetics Hyperuricemia - metabolism Internal Medicine Male Medical ethics Middle Aged Netherlands Polymorphism, Single Nucleotide - genetics Prevalence Risk Factors Sample size Studies Systematic review Uric Acid - blood
Title	Association of three genetic loci with uric acid concentration and risk of gout: a genome-wide association study
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