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review here concludes:
The results of many clinical and experimental studies clearly demonstrate that an increasing serum uric acid level may be a useful biomarker of hypertension and its consequently deranged renal hemodynamics. It is also evident that chronic hyperuricemia may adversely affect cardiovascular and renal structure and function and, therefore, may be a contributory event in the pathogenesis of cardiovascular and renal disorders. Thus, at present, there is no clear or convincing evidence that hyperuricemia is a causative factor in hypertensive disease or that lowering the uric acid concentration may reduce arterial pressure. Therefore, conventional pharmacotherapy, without uricosuric agents, is recommended in the treatment of hypertensive cardiovascular disease unless there is concern about tissue deposition of urate. One exception may be the population of obese hypertensive adolescents in whom reduction of hyperuricemia has been shown to result in a decreased arterial pressure.
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