Abstract 1630: Uric Acid Revisited: Interrelationships with Low-Grade Inflammation, Adiponectin and Arterial Stiffness in Essential Hypertension
Introduction: Increased uric acid (UA) levels are associated with high cardiovascular risk, while subclinical inflammation, arterial stiffening and hypoadiponectinemia contribute to atherosclerosis progression.
Hypothesis: Serum UA levels may be related to high-sensitivity C-reactive protein (hs-CRP), adiponectin and arterial stiffness in essential hypertensives.
Methods: In our population of 292 newly diagnosed untreated non-diabetic patients with stage I to II essential hypertension [190 men, aged 50 years, office blood pressure (BP)=148/95 mmHg], the distribution of UA was split by the median (5.3 mg/dl) and accordingly subjects were classified into those with high and low values. In all participants, arterial stiffness was evaluated on the basis of carotid to femoral pulse wave velocity (PWV), by means of a computerized method (Complior SP).
Results: Patients with high UA (n=143) compared to those with low UA (n=149) exhibited higher 24-h systolic BP (139±12 vs 132±11 mmHg, p<0.0001), while did not differ regarding age, body mass index and lipid profile (p=NS). Those with high UA compared to those with low UA had increased levels of hs-CRP (3.1±1.4 vs 2.3±1.2 mg/l, p<0.05) and PWV (8.7±1.2 vs 7.9±1.2 m/sec, p<0.05), whereas exhibited lower adiponectin (8.1±2.4 vs 9.7±2.8 μg/ml, p<0.05). In the entire population, UA was positively associated with 24-h systolic BP (r=0.297, p<0.0001), hs-CRP (r=0.204, p<0.001) and PWV (r=0.165, p=0.009), while it was negatively related to adiponectin (r=−0.218, p<0.0001). In multiple regression analysis, 24-h systolic BP (b=0.246, p<0.001), hs-CRP (b=0.142, p<0.05) and adiponectin (b=−0.154, p≥0.05) were independent predictors of UA. Analysis of covariance revealed that hs-CRP, PWV and adiponectin values were significantly different between groups after adjustment for confounders (p<0.05).
Conclusions: Increased UA levels in essential hypertension are paralleled by a state of pronounced inflammatory activation, hypoadiponectinemia and accelerated arterial stiffening. These findings suggest that UA is interrelated with diverse mediators of vascular dysfunction, underscoring its pluripotent nature in the progression of the hypertensive atherosclerotic disease.