Please use this identifier to cite or link to this item: https://repository.monashhealth.org/monashhealthjspui/handle/1/32529
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dc.contributor.authorKanellis J.en
dc.contributor.authorFeig D.I.en
dc.contributor.authorJohnson R.J.en
dc.date.accessioned2021-05-14T11:01:15Zen
dc.date.available2021-05-14T11:01:15Zen
dc.date.copyright2004en
dc.date.created20050131en
dc.date.issued2012-10-17en
dc.identifier.citationNephrology. 9 (6) (pp 394-399), 2004. Date of Publication: December 2004.en
dc.identifier.issn1320-5358en
dc.identifier.urihttps://repository.monashhealth.org/monashhealthjspui/handle/1/32529en
dc.description.abstractRecent studies in both humans and experimental animals have led to renewed interest in uric acid and its association with hypertension, cardiovascular events and renal disease progression. This has also refuelled a longstanding debate regarding the precise role of this ubiquitous breakdown product of purine metabolism in these disease processes. Various lines of evidence suggest that uric acid may have a direct role in the pathogenesis of hypertension and vascular disease. Regardless of this possibility, it is apparent that serum uric acid levels serve as a powerful 'biomarker' or independent predictor of prognosis and outcome in certain renal, cardiovascular and cerebrovascular diseases. Whether these outcomes can be improved by specifically treating asymptomatic hyperuricaemia remains inadequately resolved at this stage. Data from various animal studies suggests that lowering uric acid levels may be of benefit, but the crucial human studies are still lacking. This review will examine some of the recent evidence supporting a causal and contributory role for uric acid in cardiovascular and renal disease. How clarification of the role of uric acid may guide future treatment strategies will also be discussed.en
dc.languageEnglishen
dc.languageenen
dc.publisherBlackwell Publishing (550 Swanston Street, Carlton South VIC 3053, Australia)en
dc.titleDoes asymptomatic hyperuricaemia contribute to the development of renal and cardiovascular disease? An old controversy renewed.en
dc.typeReviewen
dc.type.studyortrialReview article (e.g. literature review, narrative review)-
dc.identifier.doihttp://monash.idm.oclc.org/login?url=http://dx.doi.org/10.1111/j.1440-1797.2004.00336.xen
dc.publisher.placeAustraliaen
dc.identifier.pubmedid15663643 [http://www.ncbi.nlm.nih.gov/pubmed/?term=15663643]en
dc.identifier.source40115966en
dc.identifier.institution(Kanellis) Depts. of Nephrology and Medicine, University of Melbourne, Austin Health, Melbourne, Vic., Australia (Feig) Department of Paediatrics, Renal Section, Baylor College of Medicine, Houston, TX, United States (Johnson) Sect. Nephrology, Hypertension T., University of Florida, Gainesville, FL, United States (Kanellis) Department of Nephrology, Monash Medical Centre, Clayton, Vic. 3169, Australiaen
dc.description.addressJ. Kanellis, Department of Nephrology, Monash Medical Centre, Clayton, Vic. 3169, Australia. E-mail: jckanellis@mac.comen
dc.description.publicationstatusEmbaseen
dc.rights.statementCopyright 2012 Elsevier B.V., All rights reserved.en
dc.subect.keywordsAtherosclerosis Cardiovascular disease Hypertension Oxidants Vascular smooth muscle cellsen
dc.identifier.authoremailKanellis J.; jckanellis@mac.comen
item.fulltextNo Fulltext-
item.cerifentitytypePublications-
item.openairecristypehttp://purl.org/coar/resource_type/c_18cf-
item.grantfulltextnone-
item.openairetypeReview-
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