Uric acid (UA) is generated as part of the normal turnover of nucleic acid. Purine bases and their nucleotides are captured by the liver and converted into xanthines, metabolized by UA, or recycled by salvage pathways or de novo synthesis. UA formation by xanthine occurs via hypoxanthine by the action of xanthine oxidase (XO), an enzyme present in the peroxisomes of most cells, which is an important source of reactive oxygen species involved in various forms of ischemic and other types of vascular injuries and chronic heart failure. In humans, higher primates, and in a particular species of dog (Dalmatians), UA is the final product of the purine catabolism. In most other mammals, the enzyme uricase further oxidizes UA to allantoin, reducing serum uric acid (SUA).UA circulates in plasma predominantly in the form of a monovalent sodium salt (urate). Hyperuricemia (HU) is commonly observed in hypertensive patients, especially in those with metabolic syndrome (MetS), where it may be a marker of insulin resistance as well as of renal dysfunction and diuretic use. Moreover, a significant association between SUA and the intrarenal resistance index measured by duplex ultrasound has been described, suggesting that HU in patients with essential hypertension (EH)
Journal of Clinical Hypertension – Wiley
Published: Jan 1, 2018
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