Genome-Wide Association Study of Blood Pressure Extremes Identifies Variant near UMOD Associated with Hypertension
Hypertension is a heritable and major contributor to the global burden of disease. The sum of rare and common genetic variants robustly identified so far explain only 1%-2% of the population variation in BP and hypertension. This suggests the existence of more undiscovered common variants. We conduc...
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| Vydáno v: | PLoS genetics Ročník 6; číslo 10; s. e1001177 |
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| Médium: | Journal Article |
| Jazyk: | angličtina |
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United States
Public Library of Science
28.10.2010
Public Library of Science (PLoS) |
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| ISSN: | 1553-7404, 1553-7390, 1553-7404 |
| On-line přístup: | Získat plný text |
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| Abstract | Hypertension is a heritable and major contributor to the global burden of disease. The sum of rare and common genetic variants robustly identified so far explain only 1%-2% of the population variation in BP and hypertension. This suggests the existence of more undiscovered common variants. We conducted a genome-wide association study in 1,621 hypertensive cases and 1,699 controls and follow-up validation analyses in 19,845 cases and 16,541 controls using an extreme case-control design. We identified a locus on chromosome 16 in the 5' region of Uromodulin (UMOD; rs13333226, combined P value of 3.6 × 10⁻¹¹). The minor G allele is associated with a lower risk of hypertension (OR [95%CI]: 0.87 [0.84-0.91]), reduced urinary uromodulin excretion, better renal function; and each copy of the G allele is associated with a 7.7% reduction in risk of CVD events after adjusting for age, sex, BMI, and smoking status (H.R. = 0.923, 95% CI 0.860-0.991; p = 0.027). In a subset of 13,446 individuals with estimated glomerular filtration rate (eGFR) measurements, we show that rs13333226 is independently associated with hypertension (unadjusted for eGFR: 0.89 [0.83-0.96], p = 0.004; after eGFR adjustment: 0.89 [0.83-0.96], p = 0.003). In clinical functional studies, we also consistently show the minor G allele is associated with lower urinary uromodulin excretion. The exclusive expression of uromodulin in the thick portion of the ascending limb of Henle suggests a putative role of this variant in hypertension through an effect on sodium homeostasis. The newly discovered UMOD locus for hypertension has the potential to give new insights into the role of uromodulin in BP regulation and to identify novel drugable targets for reducing cardiovascular risk. |
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| AbstractList | Hypertension is a heritable and major contributor to the global burden of disease. The sum of rare and common genetic variants robustly identified so far explain only 1%-2% of the population variation in BP and hypertension. This suggests the existence of more undiscovered common variants. We conducted a genome-wide association study in 1,621 hypertensive cases and 1,699 controls and follow-up validation analyses in 19,845 cases and 16,541 controls using an extreme case-control design. We identified a locus on chromosome 16 in the 5' region of Uromodulin (UMOD; rs13333226, combined P value of 3.610-11). The minor G allele is associated with a lower risk of hypertension (OR [95%CI]: 0.87 [0.84-0.91]), reduced urinary uromodulin excretion, better renal function; and each copy of the G allele is associated with a 7.7% reduction in risk of CVD events after adjusting for age, sex, BMI, and smoking status (H.R.=0.923, 95% CI 0.860-0.991; p=0.027). In a subset of 13,446 individuals with estimated glomerular filtration rate (eGFR) measurements, we show that rs13333226 is independently associated with hypertension (unadjusted for eGFR: 0.89 [0.83-0.96], p=0.004; after eGFR adjustment: 0.89 [0.83-0.96], p=0.003). In clinical functional studies, we also consistently show the minor G allele is associated with lower urinary uromodulin excretion. The exclusive expression of uromodulin in the thick portion of the ascending limb of Henle suggests a putative role of this variant in hypertension through an effect on sodium homeostasis. The newly discovered UMOD locus for hypertension has the potential to give new insights into the role of uromodulin in BP regulation and to identify novel drugable targets for reducing cardiovascular risk. Hypertension is the leading contributor to global mortality with a global prevalence of 26.4% in 2000, projected to increase to 29.2% by 2025. While 50%-60% of population variation in blood pressure can be attributable to additive genetic factors, all the genetic variants robustly identified so far explain only 1%-2% of the population variance indicating the presence of additional undiscovered risk variants. Using an extreme case-control strategy, we have discovered a SNP in the promoter region of the uromodulin gene (UMOD) to be associated with hypertension (minor allele protective against hypertension). We then validated this association using large-scale population and case-control studies, where similar extreme criteria for selection of cases and controls have been used (21,466 cases and 18,240 controls). As the locus was related to uromodulin, a protein exclusively expressed in the kidneys, we show that the association is independent of renal dysfunction. We also show preliminary evidence that the SNP allele which is protective against hypertension is also protective against cardiovascular events in 26,654 Swedish subjects followed-up for 12 years. The newly discovered UMOD locus for hypertension has the potential to give unique insights into the role of uromodulin in BP regulation and to identify novel drugable targets. Hypertension is a heritable and major contributor to the global burden of disease. The sum of rare and common genetic variants robustly identified so far explain only 1%-2% of the population variation in BP and hypertension. This suggests the existence of more undiscovered common variants. We conducted a genome-wide association study in 1,621 hypertensive cases and 1,699 controls and follow-up validation analyses in 19,845 cases and 16,541 controls using an extreme case-control design. We identified a locus on chromosome 16 in the 59 region of Uromodulin (UMOD; rs13333226, combined P value of 3.6x10(-11)). The minor G allele is associated with a lower risk of hypertension (OR [95% CI]: 0.87 [0.84-0.91]), reduced urinary uromodulin excretion, better renal function; and each copy of the G allele is associated with a 7.7% reduction in risk of CVD events after adjusting for age, sex, BMI, and smoking status (H.R. = 0.923, 95% CI 0.860-0.991; p = 0.027). In a subset of 13,446 individuals with estimated glomerular filtration rate (eGFR) measurements, we show that rs13333226 is independently associated with hypertension (unadjusted for eGFR: 0.89 [0.83-0.96], p = 0.004; after eGFR adjustment: 0.89 [0.83-0.96], p = 0.003). In clinical functional studies, we also consistently show the minor G allele is associated with lower urinary uromodulin excretion. The exclusive expression of uromodulin in the thick portion of the ascending limb of Henle suggests a putative role of this variant in hypertension through an effect on sodium homeostasis. The newly discovered UMOD locus for hypertension has the potential to give new insights into the role of uromodulin in BP regulation and to identify novel drugable targets for reducing cardiovascular risk. Hypertension is a heritable and major contributor to the global burden of disease. The sum of rare and common genetic variants robustly identified so far explain only 1%-2% of the population variation in BP and hypertension. This suggests the existence of more undiscovered common variants. We conducted a genome-wide association study in 1,621 hypertensive cases and 1,699 controls and follow-up validation analyses in 19,845 cases and 16,541 controls using an extreme case-control design. We identified a locus on chromosome 16 in the 5' region of Uromodulin (UMOD; rs13333226, combined P value of 3.6 × 10⁻¹¹). The minor G allele is associated with a lower risk of hypertension (OR [95%CI]: 0.87 [0.84-0.91]), reduced urinary uromodulin excretion, better renal function; and each copy of the G allele is associated with a 7.7% reduction in risk of CVD events after adjusting for age, sex, BMI, and smoking status (H.R. = 0.923, 95% CI 0.860-0.991; p = 0.027). In a subset of 13,446 individuals with estimated glomerular filtration rate (eGFR) measurements, we show that rs13333226 is independently associated with hypertension (unadjusted for eGFR: 0.89 [0.83-0.96], p = 0.004; after eGFR adjustment: 0.89 [0.83-0.96], p = 0.003). In clinical functional studies, we also consistently show the minor G allele is associated with lower urinary uromodulin excretion. The exclusive expression of uromodulin in the thick portion of the ascending limb of Henle suggests a putative role of this variant in hypertension through an effect on sodium homeostasis. The newly discovered UMOD locus for hypertension has the potential to give new insights into the role of uromodulin in BP regulation and to identify novel drugable targets for reducing cardiovascular risk. Hypertension is a heritable and major contributor to the global burden of disease. The sum of rare and common genetic variants robustly identified so far explain only 1%–2% of the population variation in BP and hypertension. This suggests the existence of more undiscovered common variants. We conducted a genome-wide association study in 1,621 hypertensive cases and 1,699 controls and follow-up validation analyses in 19,845 cases and 16,541 controls using an extreme case-control design. We identified a locus on chromosome 16 in the 5′ region of Uromodulin (UMOD; rs13333226, combined P value of 3.6×10−11). The minor G allele is associated with a lower risk of hypertension (OR [95%CI]: 0.87 [0.84–0.91]), reduced urinary uromodulin excretion, better renal function; and each copy of the G allele is associated with a 7.7% reduction in risk of CVD events after adjusting for age, sex, BMI, and smoking status (H.R. = 0.923, 95% CI 0.860–0.991; p = 0.027). In a subset of 13,446 individuals with estimated glomerular filtration rate (eGFR) measurements, we show that rs13333226 is independently associated with hypertension (unadjusted for eGFR: 0.89 [0.83–0.96], p = 0.004; after eGFR adjustment: 0.89 [0.83–0.96], p = 0.003). In clinical functional studies, we also consistently show the minor G allele is associated with lower urinary uromodulin excretion. The exclusive expression of uromodulin in the thick portion of the ascending limb of Henle suggests a putative role of this variant in hypertension through an effect on sodium homeostasis. The newly discovered UMOD locus for hypertension has the potential to give new insights into the role of uromodulin in BP regulation and to identify novel drugable targets for reducing cardiovascular risk. Hypertension is the leading contributor to global mortality with a global prevalence of 26.4% in 2000, projected to increase to 29.2% by 2025. While 50%–60% of population variation in blood pressure can be attributable to additive genetic factors, all the genetic variants robustly identified so far explain only 1%–2% of the population variance indicating the presence of additional undiscovered risk variants. Using an extreme case-control strategy, we have discovered a SNP in the promoter region of the uromodulin gene (UMOD) to be associated with hypertension (minor allele protective against hypertension). We then validated this association using large-scale population and case-control studies, where similar extreme criteria for selection of cases and controls have been used (21,466 cases and 18,240 controls). As the locus was related to uromodulin, a protein exclusively expressed in the kidneys, we show that the association is independent of renal dysfunction. We also show preliminary evidence that the SNP allele which is protective against hypertension is also protective against cardiovascular events in 26,654 Swedish subjects followed-up for 12 years. The newly discovered UMOD locus for hypertension has the potential to give unique insights into the role of uromodulin in BP regulation and to identify novel drugable targets. Hypertension is a heritable and major contributor to the global burden of disease. The sum of rare and common genetic variants robustly identified so far explain only 1%-2% of the population variation in BP and hypertension. This suggests the existence of more undiscovered common variants. We conducted a genome-wide association study in 1,621 hypertensive cases and 1,699 controls and follow-up validation analyses in 19,845 cases and 16,541 controls using an extreme case-control design. We identified a locus on chromosome 16 in the 5' region of Uromodulin (UMOD; rs13333226, combined P value of 3.6×10-11). The minor G allele is associated with a lower risk of hypertension (OR [95%CI]: 0.87 [0.84-0.91]), reduced urinary uromodulin excretion, better renal function; and each copy of the G allele is associated with a 7.7% reduction in risk of CVD events after adjusting for age, sex, BMI, and smoking status (H.R. = 0.923, 95% CI 0.860-0.991; p = 0.027). In a subset of 13,446 individuals with estimated glomerular filtration rate (eGFR) measurements, we show that rs13333226 is independently associated with hypertension (unadjusted for eGFR: 0.89 [0.83-0.96], p = 0.004; after eGFR adjustment: 0.89 [0.83-0.96], p = 0.003). In clinical functional studies, we also consistently show the minor G allele is associated with lower urinary uromodulin excretion. The exclusive expression of uromodulin in the thick portion of the ascending limb of Henle suggests a putative role of this variant in hypertension through an effect on sodium homeostasis. The newly discovered UMOD locus for hypertension has the potential to give new insights into the role of uromodulin in BP regulation and to identify novel drugable targets for reducing cardiovascular risk. Hypertension is a heritable and major contributor to the global burden of disease. The sum of rare and common genetic variants robustly identified so far explain only 1%-2% of the population variation in BP and hypertension. This suggests the existence of more undiscovered common variants. We conducted a genome-wide association study in 1,621 hypertensive cases and 1,699 controls and follow-up validation analyses in 19,845 cases and 16,541 controls using an extreme case-control design. We identified a locus on chromosome 16 in the 5' region of Uromodulin (UMOD; rs13333226, combined P value of 3.6 × 10⁻¹¹). The minor G allele is associated with a lower risk of hypertension (OR [95%CI]: 0.87 [0.84-0.91]), reduced urinary uromodulin excretion, better renal function; and each copy of the G allele is associated with a 7.7% reduction in risk of CVD events after adjusting for age, sex, BMI, and smoking status (H.R. = 0.923, 95% CI 0.860-0.991; p = 0.027). In a subset of 13,446 individuals with estimated glomerular filtration rate (eGFR) measurements, we show that rs13333226 is independently associated with hypertension (unadjusted for eGFR: 0.89 [0.83-0.96], p = 0.004; after eGFR adjustment: 0.89 [0.83-0.96], p = 0.003). In clinical functional studies, we also consistently show the minor G allele is associated with lower urinary uromodulin excretion. The exclusive expression of uromodulin in the thick portion of the ascending limb of Henle suggests a putative role of this variant in hypertension through an effect on sodium homeostasis. The newly discovered UMOD locus for hypertension has the potential to give new insights into the role of uromodulin in BP regulation and to identify novel drugable targets for reducing cardiovascular risk.Hypertension is a heritable and major contributor to the global burden of disease. The sum of rare and common genetic variants robustly identified so far explain only 1%-2% of the population variation in BP and hypertension. This suggests the existence of more undiscovered common variants. We conducted a genome-wide association study in 1,621 hypertensive cases and 1,699 controls and follow-up validation analyses in 19,845 cases and 16,541 controls using an extreme case-control design. We identified a locus on chromosome 16 in the 5' region of Uromodulin (UMOD; rs13333226, combined P value of 3.6 × 10⁻¹¹). The minor G allele is associated with a lower risk of hypertension (OR [95%CI]: 0.87 [0.84-0.91]), reduced urinary uromodulin excretion, better renal function; and each copy of the G allele is associated with a 7.7% reduction in risk of CVD events after adjusting for age, sex, BMI, and smoking status (H.R. = 0.923, 95% CI 0.860-0.991; p = 0.027). In a subset of 13,446 individuals with estimated glomerular filtration rate (eGFR) measurements, we show that rs13333226 is independently associated with hypertension (unadjusted for eGFR: 0.89 [0.83-0.96], p = 0.004; after eGFR adjustment: 0.89 [0.83-0.96], p = 0.003). In clinical functional studies, we also consistently show the minor G allele is associated with lower urinary uromodulin excretion. The exclusive expression of uromodulin in the thick portion of the ascending limb of Henle suggests a putative role of this variant in hypertension through an effect on sodium homeostasis. The newly discovered UMOD locus for hypertension has the potential to give new insights into the role of uromodulin in BP regulation and to identify novel drugable targets for reducing cardiovascular risk. |
| Author | Hedner, Thomas Grassi, Guido Siscovick, David S. Luan, Jian'an Montagnana, Martina Hastie, Claire E. McDonald, Robert A. Shields, Denis Colm Welsh, Paul Pell, Jill P. Caulfield, Mark J. Farrall, Martin Kwakernaak, Arjan J. Signorini, Stefano Nolte, Ilja M. Strachan, David P. Miller, William H. Melander, Olle Zhang, Feng Loos, Ruth J. F. Stanton, Alice Connell, John M. C. Graham, Delyth Danese, Elisa Wareham, Nicholas J. Cesana, Giancarlo Snieder, Harold Arora, Pankaj Zanchetti, Alberto Navis, Gerjan Burnier, Michel Wichmann, H. Erich Laan, Maris Rettig, Rainer Vollenweider, Peter Sjögren, Marketa Kathiresan, Sekar Baker, Andrew H. Padmanabhan, Sandosh Monti, Maria Cristina Eyheramendy, Susana Gentilini, Davide Soranzo, Nicole van der Harst, Pim Torffvit, Ole Hedblad, Bo Samani, Nilesh J. McBride, Martin Völzke, Henry Johnson, Toby Mancia, Giuseppe Nicklin, Stuart A. Menni, Cristina Bochud, Murielle Sever, Peter Fava, Cristiano Maillard, Marc Newton-Cheh, Christopher Delles, Christian Kjeldsen, Sverre Corso, Barbara Spector, Timothy D. Lucas, Gavi |
| AuthorAffiliation | 40 MRC Epidemiology Unit, Institute of Metabolic Science, Cambridge, United Kingdom 4 Istituto Auxologico Italiano, Milan, Italy 10 Service of Nephrology, Centre Hospitalier Universitaire Vaudois and University of Lausanne, Lausanne, Switzerland 15 Department of Nephrology, Institution of Clinical Sciences, University Hospital of Lund, Lund, Sweden 17 College of Medicine, Dentistry and Nursing, Ninewells Hospital, University of Dundee, Dundee, United Kingdom 36 Department of Twin Research and Genetic Epidemiology, King's College London, London, United Kingdom 45 University of Milano, Milano, Italy 28 Conway Institute of Biomolecular and Biomedical Research, University College Dublin, Dublin, Ireland 26 Division of Community Health Sciences, St George's, University of London, London, United Kingdom 24 Institute of Medical Informatics, Biometry and Epidemiology, Chair of Epidemiology, Ludwig-Maximilians-Universität, Munich, Germany 14 Department of Life and Reproduction Sciences, Section of Clinic |
| AuthorAffiliation_xml | – name: 3 Clinical Pharmacology and Barts and the London Genome Centre, William Harvey Research Institute, Barts and the London School of Medicine, Queen Mary University of London, London, United Kingdom – name: 42 Department of Psychiatry, Leiden University Medical Center, Leiden, The Netherlands – name: 14 Department of Life and Reproduction Sciences, Section of Clinical Chemistry, University of Verona, Verona, Italy – name: 1 Institute of Cardiovascular and Medical Sciences, College of Medical Veterinary and Life Sciences, University of Glasgow, Glasgow, United Kingdom – name: 7 Department of Nephrology, University Medical Center Groningen, University of Groningen, Groningen, The Netherlands – name: 18 Clinical Pharmacology Unit, University of Cambridge, Addenbrookes Hospital, Cambridge, United Kingdom – name: 27 International Centre for Circulatory Health National Heart and Lung Institute, Imperial College, London, United Kingdom – name: 16 Unit of Genetic Epidemiology and Bioinformatics, Department of Epidemiology, University Medical Center Groningen, University of Groningen, Groningen, The Netherlands – name: 4 Istituto Auxologico Italiano, Milan, Italy – name: 36 Department of Twin Research and Genetic Epidemiology, King's College London, London, United Kingdom – name: 24 Institute of Medical Informatics, Biometry and Epidemiology, Chair of Epidemiology, Ludwig-Maximilians-Universität, Munich, Germany – name: 25 Institute of Molecular and Cell Biology, University of Tartu, Tartu, Estonia – name: 23 Institute of Epidemiology, Helmholtz Zentrum München, German Research Center for Environmental Health, Neuherberg, Germany – name: 5 Università Milano-Bicocca, Dipartimento di Medicina Clinica e Prevenzione, Ospedale San Gerardo, Monza, Milano, Italy – name: University of California San Diego and The Scripps Research Institute, United States of America – name: 35 Program in Medical and Population Genetics, Broad Institute, Cambridge, Massachusetts, United States of America – name: 20 Department of Cardiovascular Medicine, Wellcome Trust Centre for Human Genetics, Oxford, United Kingdom – name: 22 Department of Statistics, Pontificia Universidad Catolica de Chile, Santiago, Chile – name: 8 Department of Cardiology, University Medical Center Groningen, University of Groningen, Groningen, The Netherlands – name: 26 Division of Community Health Sciences, St George's, University of London, London, United Kingdom – name: 33 Institute of Physiology, University of Greifswald, Greifswald, Germany – name: 12 Department of Cardiology, University of Oslo, Ullevaal Hospital, Oslo, Norway – name: 19 Department of Cardiovascular Sciences, University of Leicester, Glenfield Hospital, Leicester, United Kingdom – name: 38 Cardiovascular Epidemiology and Genetics Group, Institut Municipal d'Investigacio Medica, Barcelona, Spain – name: 39 Cardiovascular Health Research Unit, Departments of Medicine and Epidemiology, University of Washington, Seattle, Washington, United States of America – name: 45 University of Milano, Milano, Italy – name: 6 Department of Health Science, University of Pavia, Pavia, Italy – name: 21 Azienda Ospedaliera di Desio e Vimercate, Milano, Italy – name: 37 Wellcome Trust Sanger Institute, Genome Campus, Hinxton, United Kingdom – name: 10 Service of Nephrology, Centre Hospitalier Universitaire Vaudois and University of Lausanne, Lausanne, Switzerland – name: 41 Department of Psychiatry/EMGO Institute, Neuroscience Campus, VU University Medical Center, Amsterdam, The Netherlands – name: 32 Institute for Community Medicine, University of Greifswald, Greifswald, Germany – name: 44 Public Health and Health Policy Section, University of Glasgow, Glasgo, United Kingdom – name: 30 Department of Internal Medicine, Centre Hospitalier Universitaire Vaudois and University of Lausanne, Lausanne, Switzerland – name: 31 Interfaculty Institute for Genetics and Functional Genomics, University of Greifswald, Greifswald, Germany – name: 40 MRC Epidemiology Unit, Institute of Metabolic Science, Cambridge, United Kingdom – name: 9 University Institute of Social and Preventive Medicine, Centre Hospitalier Universitaire Vaudois and University of Lausanne, Lausanne, Switzerland – name: 43 Department of Psychiatry, University Medical Center Groningen, University of Groningen, Groningen, The Netherlands – name: 28 Conway Institute of Biomolecular and Biomedical Research, University College Dublin, Dublin, Ireland – name: 11 Institute of Medicine, The Sahlgrenska Academy, University of Gothenburg, Gothenburg, Sweden – name: 29 Molecular and Cellular Therapeutics, Royal College of Surgeons in Ireland, Dublin, Ireland – name: 2 Department of Clinical Sciences, Hypertension and Cardiovascular Diseases, University Hospital Malmö, Lund University, Malmö, Sweden – name: 15 Department of Nephrology, Institution of Clinical Sciences, University Hospital of Lund, Lund, Sweden – name: 34 Center for Human Genetic Research and Cardiovascular Research Center, Massachusetts General Hospital, Harvard Medical School, Boston, Massachusetts, United States of America – name: 13 Department of Medicine, Section of Internal Medicine C, University of Verona, Verona, Italy – name: 17 College of Medicine, Dentistry and Nursing, Ninewells Hospital, University of Dundee, Dundee, United Kingdom |
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| BackLink | https://www.ncbi.nlm.nih.gov/pubmed/21082022$$D View this record in MEDLINE/PubMed https://gup.ub.gu.se/publication/139274$$DView record from Swedish Publication Index (Göteborgs universitet) |
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| Copyright | Padmanabhan et al. 2010 2010 Padmanabhan et al. This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited: Padmanabhan S, Melander O, Johnson T, Di Blasio AM, Lee WK, et al. (2010) Genome-Wide Association Study of Blood Pressure Extremes Identifies Variant near UMOD Associated with Hypertension. PLoS Genet 6(10): e1001177. doi:10.1371/journal.pgen.1001177 |
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| CorporateAuthor | Global BPgen Consortium Nephrology Njurmedicin Institutionen för kliniska vetenskaper, Lund Sektion II Lunds universitet Section II Profile areas and other strong research environments Department of Clinical Sciences, Malmö Lund University Kardiovaskulär forskning - hypertoni Department of Clinical Sciences, Lund Strategiska forskningsområden (SFO) EpiHealth: Epidemiology for Health Faculty of Medicine Strategic research areas (SRA) Medicinska fakulteten Profilområden och andra starka forskningsmiljöer Cardiovascular Research - Hypertension Institutionen för kliniska vetenskaper, Malmö |
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| Notes | ObjectType-Article-1 SourceType-Scholarly Journals-1 ObjectType-Feature-2 content type line 23 Conceived and designed the experiments: S Padmanabhan, O Melander, C Delles, A Zanchetti, AF Dominiczak. Performed the experiments: S Padmanabhan, AM Di Blasio, WK Lee, D Gentilini, S Laing, M Sjögren, P Welsh. Analyzed the data: S Padmanabhan, T Johnson, CE Hastie, C Menni, MC Monti, B Corso, G Navis, AJ Kwakernaak, P van der Harst, M Bochud, C Fava, M Montagnana, E Danese, M Farrall, S Eyheramendy, DP Strachan, A Teumer, R Rettig, C Newton-Cheh, P Arora, F Zhang, N Soranzo, G Lucas, J Luan, RJF Loos. Contributed reagents/materials/analysis tools: O Melander, G Navis, P van der Harst, M Bochud, M Maillard, M Burnier, T Hedner, S Kjeldsen, B Wahlstrand, O Torffvit, B Hedblad, H Snieder, JMC Connell, M Brown, NJ Samani, M Farrall, G Cesana, G Mancia, S Signorini, G Grassi, S Eyheramendy, HE Wichmann, M Laan, DP Strachan, P Sever, DC Shields, A Stanton, P Vollenweider, A Teumer, H Volzke, R Rettig, C Newton-Cheh, P Arora, F Zhang, N Soranzo, TD Spector, G Lucas, S Kathiresan, DS Siscovick, J Luan, RJF Loos, NJ Wareham, BW Penninx, IM Nolte, P Munroe, MJ Caulfield, A Zanchetti, AF Dominiczak. Wrote the paper: S Padmanabhan, O Melander, T Johnson, C Delles, G Navis, M Bochud, M McBride, WH Miller, SA Nicklin, AH Baker, D Graham, RA McDonald, JP Pell, N Sattar, P Munroe, MJ Caulfield, A Zanchetti, AF Dominiczak. For more information on the Global BPgen Consortium please see Text S1. |
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| PMID | 21082022 |
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| PublicationDate | 20101028 |
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| SubjectTerms | Age Aged Alleles Blood Pressure Body mass index burden Cardiology and Cardiovascular Disease Cardiovascular Disorders/Hypertension Chromosomes, Human, Pair 16 - genetics chronic kidney-disease Clinical Medicine Confidence intervals feasibility Female Gene Frequency Genetic Predisposition to Disease Genetics and Genomics/Complex Traits Genetics and Genomics/Genetics of Disease Genome-Wide Association Study - methods Genome-Wide Association Study - statistics & numerical data Genomes Genotype Glomerular Filtration Rate Health risk assessment Heart attacks Humans Hypertension - genetics Hypertension - physiopathology Kardiologi och kardiovaskulära sjukdomar Klinisk medicin Linear Models loci Male Medical and Health Sciences Medicin och hälsovetenskap Meta-Analysis as Topic Middle Aged Mortality Multivariate Analysis mutations nephropathy Polymorphism, Single Nucleotide Population Proportional Hazards Models Risk assessment Risk Factors Studies Survival Analysis tamm-horsfall protein urinary-excretion Uromodulin - blood Uromodulin - genetics |
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| Title | Genome-Wide Association Study of Blood Pressure Extremes Identifies Variant near UMOD Associated with Hypertension |
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