Serum uric acid and the risk of hypertension and chronic kidney disease

Purpose of reviewTo discuss the evolving data regarding uric acid as a potential cause of hypertension and progressive renal dysfunction and its clinical and research implications.Recent findingsThe potential mechanisms by which uric acid could cause vasoconstriction and a progressive ateriolopathy were established in animal models between 1999 and 2004. Since then, there has been a growing interest in the topic and numerous retrospective and prospective observational studies. The preponderance of data support the hypothesis that serum uric acid is a cause or exacerbating factor of hypertension and progressive kidney disease. Over the last couple of years clinical intervention trials, including randomized controlled trials in the young have supported this mechanistic role.SummaryCurrent evidence supports the role of uric acid as marker and mediator of risk for both hypertension and progressive decline in renal function. Data on the impact of xanthine oxidase inhibitors or uricosurics on clinical hypertension and chronic kidney disease are suggestive but inconclusive. Considerably, more data will be required to determine if uric acid lowering therapy will become a mainstay of management in diseases other than gout and tumor lysis syndrome.