title: Serum uric acid and the risk of cardiovascular and renal disease.
abstract: Substantial evidence suggests that chronic hyperuricemia is an independent risk factor for hypertension, metabolic syndrome, chronic kidney disease (CKD) and cardiovascular diseases. This highlights the need for greater attention to serum uric acid levels when profiling patients, and suggests that the threshold above which uricemia is considered abnormal is 6  mg/dl, in light of the available evidence. Another important question is whether lowering serum uric acid can improve cardiovascular and renal outcomes, and what therapeutic mechanism of action could provide more clinical benefits to patients; the available literature shows a trend toward improvement associated with administration of urate-lowering drugs, in particular for the xanthine oxidase inhibitors. The demonstrated efficacy of urate-lowering therapy on outcomes other than gout flares leads to the consideration that treatment may be beneficial even in the absence of overt gout when hyperuricemia accompanies other clinical conditions, such as urate deposition, advanced CKD or cardiovascular risk factors.
authors.affiliation: aDepartment of Medical and Surgical Sciences, University of Bologna, Bologna, Italy bDepartment of Clinical and Experimental Sciences, University of Brescia, Department of Medicine, Spedali Civili, Brescia, Italy cAssistance Publique Hôpitaux de Paris, Hôpital Lariboisière dUniversité Paris Diderot, Sorbonne Paris Cité eINSERM, UMR 1132, Paris, France fInstitute of Cardiovascular and Medical Sciences, College of Medical, Veterinary and Life Sciences, University of Glasgow, Glasgow, UK gDepartment of Nephrology and Hypertension, Hannover Medical School, Hannover, Germany hCardiology Department, Asklepeion Hospital, Athens, Greece iRheumatology Division, Hospital Universitario Cruces and Biocruces Health Research Institute, Vizcaya, Spain jUniversità Milano-Bicocca, IRCCS Istituto Auxologico Italiano, Milan, Italy.
authors.forename: Claudio
authors.initials: C
authors.lastname: Borghi
authors.forename: Enrico Agabiti
authors.initials: EA
authors.lastname: Rosei
authors.forename: Thomas
authors.initials: T
authors.lastname: Bardin
authors.forename: Jesse
authors.initials: J
authors.lastname: Dawson
authors.forename: Anna
authors.initials: A
authors.lastname: Dominiczak
authors.forename: Jan T
authors.initials: JT
authors.lastname: Kielstein
authors.forename: Athanasios J
authors.initials: AJ
authors.lastname: Manolis
authors.forename: Fernando
authors.initials: F
authors.lastname: Perez-Ruiz
authors.forename: Giuseppe
authors.initials: G
authors.lastname: Mancia
mesh_terms: D002318:Cardiovascular Diseases / Q000453:epidemiology*; D006074:Gout Suppressants / Q000627:therapeutic use; D006801:Humans; D006973:Hypertension / Q000453:epidemiology; D033461:Hyperuricemia / Q000097:blood* / Q000188:drug therapy / Q000453:epidemiology / Q000235:genetics / Q000503:physiopathology; D024821:Metabolic Syndrome / Q000453:epidemiology; D051436:Renal Insufficiency, Chronic / Q000453:epidemiology* / Q000209:etiology; D012307:Risk Factors; D014527:Uric Acid / Q000097:blood*
chemical_list: D006074:Gout Suppressants; D014527:Uric Acid