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Uric acid and hypertension

a focused review and practical recommendations

De Becker, Benjamina; Borghi, Claudiob; Burnier, Michelc; van de Borne, Philippea

doi: 10.1097/HJH.0000000000001980
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Uric acid levels are higher in humans than in other mammals. Best known as an extracellular antioxidant, uric acid also increases salt sensitivity, fat storage, and lipogenesis. Xanthine oxidase-related oxidative stress may also induce endothelial dysfunction and renal vasoconstriction. Renal structure abnormalities contribute to salt-sensitive and uric acid-independent hypertension. Maternal hyperuricemia during pregnancy and hyperuricemia early in life are likewise independent risk factors for hypertension. Genetic polymorphism is potentially involved in the activity of xanthine oxidoreductase, but further studies are needed. Xanthine oxidase inhibition consistently decreases blood pressure in younger hypertensive patients, albeit modestly. Hyperuricemia affects one out of five adults as a result of the Western diet, insulin resistance, and renal dysfunction. This review advocates lifestyle changes to maintain uric acid levels within the normal range in young (pre)hypertensive individuals or normotensives with a family history of hypertension, metabolic disorders, or obesity; moreover, antihypertensive medications that increase uric acid levels should be avoided.

aService de Cardiologie, Université Libre de Bruxelles – Hôpital Erasme, Brussels, Belgium

bUnità Operative di Medicina Interna, Policlinico S.Orsola-Malpighi, Bologna, Italy

cService de Néphrologie et Hypertension, Centre Hospitalier Universitaire Vaudois, Lausanne, Switzerland

Correspondence to Benjamin De Becker, MD, Service de Cardiologie, Université Libre de Bruxelles – Hôpital Erasme, Route de Lennik 808, 1070 Anderlecht, Brussels, Belgium. Tel: +32 2 555 39 07; fax: +32 2 555 66 52; e-mail: Benjamin.De.Becker@erasme.ulb.ac.be

Abbreviations: CRP, C-reactive protein; eNOS, endothelial nitric oxide synthase; GLUT9, glucose transporter type 9; MCP-1, monocyte chemoattractant protein-1; NO, nitric oxide; RAS, renin–angiotensin system; ROS, reactive oxygen species; URAT1, urat transporter 1; XDH, xanthine dehydrogenase; XOR, xanthine oxidoreductase

Received 30 May, 2018

Accepted 30 September, 2018

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