Editor-in-Chief: Dimitri P. Mikhailidis Academic Head, Department of Clinical Biochemistry Royal Free Hospital Campus University College London Medical School University College London (UCL) Pond Street London, NW3 2QG UK
Affiliation: Institute Vinca, University of Belgrade, Laboratory of Radiobiology and Molecular Genetics, P.O. Box 522, 11000 Belgrade, Serbia.
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.