Vnitr Lek 2025, 71(1):18-23 | DOI: 10.36290/vnl.2025.003

Hyperuricaemia and metabolic syndrome

Lukáš Rozsíval¹, Michael Jenšovský², Jana Urbanová³, Natálie Michalcová¹, Ludmila Brunerová³, Jana Malinovská¹, Juraj Michalec¹, Jan Brož¹

¹ Interní klinika, 2. LF UK a FN Motol, Praha

² Kardiologická klinika, 2. LF UK a FN Motol, Praha

³ Interní klinika, 3. LF UK a FN Královské Vinohrady, Praha

Uric acid (UA) is predominantly formed in the liver, intestine and vascular endothelium as an end product of the metabolism of purines derived from food and endogenously from damaged or dead cells. The kidneys play a major role in the excretion of UA, eliminating about 70 % of the daily production. The remainder (approximately 30 %) is excreted by the intestine. If the production of UA exceeds the capacity of its excretion, hyperuricaemia results. Overexpression of urate transporter 1 (URAT1), glucose transporter 9 (GLUT9) and impaired glycolysis due to insulin resistance may be related to the development of hyperuricaemia in metabolic syndrome. Hyperuricemia is associated with the development and severity of metabolic syndrome. Previously, hyperuricaemia was thought to be the main cause of gout and gouty arthritis only. It was also assumed that hyperuricemia in patients with renal disease was a consequence of inadequate UA excretion due to renal failure and therefore was not a target for intensive treatment. Basic scientific evidence now suggests that hyperuricemia plays a pathogenic role in the development of chronic kidney disease and cardiovascular disease by causing endothelial dysfunction, vascular smooth muscle cell proliferation, and activation of the renin- angiotensin system. Lowering UA levels is an effective method for improving the condition, but not all UA lowering agents work the same. In clinical practice, these agents should be used with caution. Further accumulating data suggest that UA-lowering therapy slows the progression of these diseases.

Keywords: uric acid, hyperuricemia, metabolic syndrome, risk, hyperuricemia therapy.

Accepted: February 6, 2025; Published: February 18, 2025  Show citation