In humans uric acid (UA) is the end product of degradation of purines. The handling of UA by the renal system is a complex process which is not fully understood. To date, several urate transporters in the renal proximal tubule have been identified. Among them, urate transporter 1 (URAT1) and a glucose transporter 9 (GLUT9) are considered of greater importance, as potential targets for treatment of hyperuricemia and the potential associated cardio-metabolic risk. Therefore, the recognition of the metabolic pathway of UA and elucidation of occurrence of hyperuricemia may provide important insights about the relationship between UA, pre-hypertension (preHT) and the metabolic syndrome (MetS). We also review the available clinical studies in this field, including experimental studies dealing with the mechanisms of UA transport via different transporters, as well as current treatment options for hyperuricemia in patients with MetS, preHT or cardiovascular risk factors.
|Numero di pagine||0|
|Rivista||Current Vascular Pharmacology|
|Stato di pubblicazione||Published - 2013|
All Science Journal Classification (ASJC) codes
- Cardiology and Cardiovascular Medicine
Montalto, G., Rizzo, M., Nikolic, D., Isenovic, E. R., Mikhailidis, D. P., Labudovic-Borovic, M., Nikolic, D., Obradovic, M., Rizzo, M., Rizvi, A. A., & Rizzo, M. (2013). Uric acid metabolism in pre-hypertension and the metabolic syndrome. Current Vascular Pharmacology, 00, 572-585.