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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Published in:The Lancet (British edition) Vol. 372; no. 9654; pp. 1953 - 1961
Main Authors: 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
Language:English
Published: England Elsevier Ltd 06.12.2008
Elsevier Limited
Subjects:
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 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=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.
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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SourceType Open Access Repository
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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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Volume 372
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