{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,2,13]],"date-time":"2026-02-13T07:52:59Z","timestamp":1770969179577,"version":"3.50.1"},"reference-count":42,"publisher":"Oxford University Press (OUP)","issue":"9","license":[{"start":{"date-parts":[[2020,4,8]],"date-time":"2020-04-08T00:00:00Z","timestamp":1586304000000},"content-version":"vor","delay-in-days":0,"URL":"https:\/\/academic.oup.com\/pages\/standard-publication-reuse-rights"}],"funder":[{"name":"Nancy CHRU"},{"name":"French Ministry of Health"},{"name":"Contrat de Plan Etat-Lorraine and FEDER Lorraine"},{"DOI":"10.13039\/501100001665","name":"French National Research Agency","doi-asserted-by":"publisher","id":[{"id":"10.13039\/501100001665","id-type":"DOI","asserted-by":"publisher"}]},{"name":"FIGHT-HF","award":["ANR-15-RHU-0004"],"award-info":[{"award-number":["ANR-15-RHU-0004"]}]},{"name":"French PIA","award":["ANR-15-IDEX-04-LUE"],"award-info":[{"award-number":["ANR-15-IDEX-04-LUE"]}]},{"name":"European Fibro-Targets Project","award":["SP7#602904"],"award-info":[{"award-number":["SP7#602904"]}]},{"name":"European HOMAGE project","award":["# 305507"],"award-info":[{"award-number":["# 305507"]}]},{"name":"MEDIA","award":["261409"],"award-info":[{"award-number":["261409"]}]},{"name":"FOCUS-MR","award":["ANR-15-CE14-0032-01"],"award-info":[{"award-number":["ANR-15-CE14-0032-01"]}]},{"name":"ERA-CVD EXPERT","award":["ANR-16-ECVD-0002-02"],"award-info":[{"award-number":["ANR-16-ECVD-0002-02"]}]},{"name":"Fondation de Recherche en Hypertension Art\u00e9rielle"}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":[],"published-print":{"date-parts":[[2020,9,10]]},"abstract":"<jats:title>Abstract<\/jats:title>\n               <jats:sec>\n                  <jats:title>BACKGROUND<\/jats:title>\n                  <jats:p>Recent studies have shown that hyperuricemia may be associated with incident hypertension (HTN). We examined whether serum uric acid (SUA) is a predictor of HTN and target organ damage (TOD) 20 years later in initially healthy middle-aged individuals.<\/jats:p>\n               <\/jats:sec>\n               <jats:sec>\n                  <jats:title>METHODS<\/jats:title>\n                  <jats:p>Participants from the Suivi Temporaire Annuel Non-Invasif de la Sant\u00e9 des Lorrains Assur\u00e9s Sociaux (STANISLAS) a single-center familial longitudinal cohort study (961 initially healthy adults and 570 children) underwent clinical and laboratory measurements at baseline and after approximately 20 years. Blood pressure (BP: using ambulatory BP measurements), urine albumin-to-creatinine ratio, estimated glomerular filtration rate (eGFR), left ventricular hypertrophy (LVH), diastolic dysfunction, and carotid\u2013femoral pulse wave velocity (PWV) were measured at the end of follow-up.<\/jats:p>\n               <\/jats:sec>\n               <jats:sec>\n                  <jats:title>RESULTS<\/jats:title>\n                  <jats:p>In the parent population, higher baseline or last SUA levels and higher change in SUA (\u0394UA) were significantly associated with an increased risk of HTN development, even after adjusting for known HTN risk factors (all P &amp;lt; 0.01). Higher baseline SUA was marginally associated with an increased risk of having high carotid\u2013femoral PWV (P = 0.05). The association of SUA with BP increase was body mass index dependent (the increase in BP being greater in leaner subjects; interactionp &amp;lt; 0.05), and the association of SUA with eGFR decline was age dependent (the decline in eGFR being greater in older subjects; interactionp &amp;lt; 0.05). There was no significant association between SUA and diastolic dysfunction or LVH. In the whole population (i.e. including children), a significant association between SUA at baseline and the risk of HTN and higher carotid\u2013femoral PWV was also found (both P &amp;lt; 0.02).<\/jats:p>\n               <\/jats:sec>\n               <jats:sec>\n                  <jats:title>CONCLUSIONS<\/jats:title>\n                  <jats:p>Increased SUA is associated with the development of HTN and vascular\/renal TOD in initially healthy midlife subjects.<\/jats:p>\n               <\/jats:sec>","DOI":"10.1093\/ajh\/hpaa030","type":"journal-article","created":{"date-parts":[[2020,4,7]],"date-time":"2020-04-07T11:08:17Z","timestamp":1586257697000},"page":"869-878","source":"Crossref","is-referenced-by-count":18,"title":["Impact of Uric Acid on Hypertension Occurrence and Target Organ Damage: Insights From the STANISLAS Cohort With a 20-Year Follow-up"],"prefix":"10.1093","volume":"33","author":[{"given":"Mehmet","family":"Kanbay","sequence":"first","affiliation":[{"name":"Department of Medicine, Division of Nephrology, Koc University School of Medicine , Istanbul, Turkey"}]},{"given":"Nicolas","family":"Girerd","sequence":"additional","affiliation":[{"name":"Universit\u00e9 de Lorraine, INSERM CIC-P 1433, CHRU de Nancy, INSERM U1116, FCRIN INI-CRCT (Cardiovascular and Renal Clinical Trialists) , Nancy, France"}]},{"given":"Jean-Loup","family":"Machu","sequence":"additional","affiliation":[{"name":"Universit\u00e9 de Lorraine, INSERM CIC-P 1433, CHRU de Nancy, INSERM U1116, FCRIN INI-CRCT (Cardiovascular and Renal Clinical Trialists) , Nancy, France"}]},{"given":"Erwan","family":"Bozec","sequence":"additional","affiliation":[{"name":"Universit\u00e9 de Lorraine, INSERM CIC-P 1433, CHRU de Nancy, INSERM U1116, FCRIN INI-CRCT (Cardiovascular and Renal Clinical Trialists) , Nancy, France"}]},{"given":"Kevin","family":"Duarte","sequence":"additional","affiliation":[{"name":"Universit\u00e9 de Lorraine, INSERM CIC-P 1433, CHRU de Nancy, INSERM U1116, FCRIN INI-CRCT (Cardiovascular and Renal Clinical Trialists) , Nancy, France"}]},{"given":"Jean-Marc","family":"Boivin","sequence":"additional","affiliation":[{"name":"Universit\u00e9 de Lorraine, INSERM CIC-P 1433, CHRU de Nancy, INSERM U1116, FCRIN INI-CRCT (Cardiovascular and Renal Clinical Trialists) , Nancy, France"}]},{"given":"Sandra","family":"Wagner","sequence":"additional","affiliation":[{"name":"Universit\u00e9 de Lorraine, INSERM CIC-P 1433, CHRU de Nancy, INSERM U1116, FCRIN INI-CRCT (Cardiovascular and Renal Clinical Trialists) , Nancy, France"}]},{"given":"Jo\u00e3o Pedro","family":"Ferreira","sequence":"additional","affiliation":[{"name":"Universit\u00e9 de Lorraine, INSERM CIC-P 1433, CHRU de Nancy, INSERM U1116, FCRIN INI-CRCT (Cardiovascular and Renal Clinical Trialists) , Nancy, France"}]},{"given":"Faiez","family":"Zannad","sequence":"additional","affiliation":[{"name":"Universit\u00e9 de Lorraine, INSERM CIC-P 1433, CHRU de Nancy, INSERM U1116, FCRIN INI-CRCT (Cardiovascular and Renal Clinical Trialists) , Nancy, France"}]},{"given":"Patrick","family":"Rossignol","sequence":"additional","affiliation":[{"name":"Universit\u00e9 de Lorraine, INSERM CIC-P 1433, CHRU de Nancy, INSERM U1116, FCRIN INI-CRCT (Cardiovascular and Renal Clinical Trialists) , Nancy, France"}]}],"member":"286","published-online":{"date-parts":[[2020,4,8]]},"reference":[{"key":"2022100315501365800_CIT0001","doi-asserted-by":"crossref","first-page":"381","DOI":"10.1097\/HJH.0b013e3282f29876","article-title":"Pathogenesis of essential hypertension: historical paradigms and modern insights","volume":"26","author":"Johnson","year":"2008","journal-title":"J Hypertens"},{"key":"2022100315501365800_CIT0002","doi-asserted-by":"crossref","first-page":"3","DOI":"10.1016\/j.ejim.2015.11.026","article-title":"Uric acid in metabolic syndrome: from an innocent bystander to a central player","volume":"29","author":"Kanbay","year":"2016","journal-title":"Eur J Intern 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