{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,9,29]],"date-time":"2026-09-29T23:49:35Z","timestamp":1790725775996,"version":"4.1.0"},"reference-count":79,"publisher":"Frontiers Media SA","license":[{"start":{"date-parts":[[2023,5,25]],"date-time":"2023-05-25T00:00:00Z","timestamp":1684972800000},"content-version":"vor","delay-in-days":0,"URL":"https:\/\/creativecommons.org\/licenses\/by\/4.0\/"}],"content-domain":{"domain":["frontiersin.org"],"crossmark-restriction":true},"short-container-title":["Front. Cardiovasc. Med."],"abstract":"<jats:p>Gout and hyperuricaemia are two clinical situations associated with an elevated risk of developing cardiovascular (heart failure, myocardial infarction, stroke) and metabolic and renal complications. One reason is probably related to the fact that the prevalence of hyperuricaemia and gout is high in clinical situations, which themselves involve a high cardiovascular risk, such as hypertension, diabetes, chronic kidney disease or obesity. However, recent studies suggest that hyperuricaemia may promote cardiovascular complications independently of other cardiovascular risk factors, by inducing chronic inflammation, oxidative stress, and endothelial dysfunction. The questions that arise today concern primarily the treatment of asymptomatic hyperuricaemia. Should it be treated to decrease the patients' cardiovascular risk and if so, starting from which level and towards which target? There are now several pieces of evidence indicating that this might be useful, but data from large studies are not unanimous. This review will discuss this issue as well as new well-tolerated treatments, such as febuxostat or SGLT2 inhibitors, which lower uric acid levels, prevent gout and lower the risk of cardio-renal events.<\/jats:p>","DOI":"10.3389\/fcvm.2023.1190069","type":"journal-article","created":{"date-parts":[[2023,5,25]],"date-time":"2023-05-25T04:25:51Z","timestamp":1684988751000},"update-policy":"https:\/\/doi.org\/10.3389\/crossmark-policy","source":"Crossref","is-referenced-by-count":31,"title":["Gout and hyperuricaemia: modifiable cardiovascular risk factors?"],"prefix":"10.3389","volume":"10","author":[{"given":"Michel","family":"Burnier","sequence":"first","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"1965","published-online":{"date-parts":[[2023,5,25]]},"reference":[{"key":"B1","doi-asserted-by":"publisher","first-page":"130","DOI":"10.1253\/circj.CJ-20-0406","article-title":"Uric acid as a risk factor for chronic kidney disease and cardiovascular disease- Japanese guideline on the management of asymptomatic hyperuricemia","volume":"85","author":"Hisatome","year":"2021","journal-title":"Circ J"},{"key":"B2","doi-asserted-by":"publisher","first-page":"744","DOI":"10.1002\/acr.24180","article-title":"2020 American college of rheumatology guideline for the management of gout","volume":"72","author":"FitzGerald","year":"2020","journal-title":"Arthritis Care Res (Hoboken)"},{"key":"B3","doi-asserted-by":"publisher","first-page":"w20209","DOI":"10.4414\/smw.2020.20209","article-title":"Gout management in Swiss primary care\u2014a retrospective observational study","volume":"150","author":"Meier","year":"2020","journal-title":"Swiss Med Wkly"},{"key":"B4","doi-asserted-by":"publisher","first-page":"100416","DOI":"10.1016\/j.lanepe.2022.100416","article-title":"Management of gout following 2016\/2017 European (EULAR) and British (BSR) guidelines: an interrupted time-series analysis in the United Kingdom","volume":"18","author":"Russell","year":"2022","journal-title":"The Lancet Regional Health\u2014Europe"},{"key":"B5","doi-asserted-by":"publisher","first-page":"29","DOI":"10.1136\/annrheumdis-2016-209707","article-title":"2016 Updated EULAR evidence-based recommendations for the management of gout","volume":"76","author":"Richette","year":"2017","journal-title":"Ann Rheum Dis"},{"key":"B6","doi-asserted-by":"publisher","first-page":"837","DOI":"10.1159\/000519491","article-title":"Mini review: reappraisal of uric acid in chronic kidney disease","volume":"52","author":"Goldberg","year":"2021","journal-title":"Am J Nephrol"},{"key":"B7","doi-asserted-by":"publisher","first-page":"229","DOI":"10.1016\/j.ekir.2022.11.016","article-title":"Uric acid and chronic kidney disease: still more to do","volume":"8","author":"Johnson","year":"2023","journal-title":"Kidney Int Rep"},{"key":"B8","doi-asserted-by":"publisher","first-page":"948","DOI":"10.1161\/HYPERTENSIONAHA.111.00650","article-title":"What are the key arguments against uric acid as a true risk factor for hypertension?","volume":"61","author":"Johnson","year":"2013","journal-title":"Hypertension"},{"key":"B9","doi-asserted-by":"publisher","first-page":"1953","DOI":"10.1097\/HJH.0000000000001940","article-title":"2018 ESC\/ESH guidelines for the management of arterial hypertension: the task force for the management of arterial hypertension of the European society of cardiology and the European society of hypertension: the task force for the management of arterial hypertension of the European society of cardiology and the European society of hypertension","volume":"36","author":"Williams","year":"2018","journal-title":"J Hypertens"},{"key":"B10","doi-asserted-by":"publisher","first-page":"1421","DOI":"10.7326\/0003-4819-34-6-1421","article-title":"Serum uric acid in relation to age and physique in health and in coronary heart disease","volume":"34","author":"Gertler","year":"1951","journal-title":"Ann Intern Med"},{"key":"B11","doi-asserted-by":"publisher","first-page":"7","DOI":"10.7326\/0003-4819-131-1-199907060-00003","article-title":"Serum uric acid and risk for cardiovascular disease and death: the framingham heart study","volume":"131","author":"Culleton","year":"1999","journal-title":"Ann Intern Med"},{"key":"B12","doi-asserted-by":"publisher","first-page":"2404","DOI":"10.1001\/jama.283.18.2404","article-title":"Serum uric acid and cardiovascular mortality the NHANES I epidemiologic follow-up study, 1971-1992. 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