Uric Acid and Hypertension: a Review of Evidence and Future Perspectives for the Management of Cardiovascular Risk

Abstract

Uric acid is the final product of purine metabolism, and its increased serum levels have been directly involved in the pathogenesis and natural history of hypertension. The relationship between elevated uric acid and hypertension has been proven in both animals and humans, and its relevance is already evident in childhood and adolescent population. The mechanism responsible for blood pressure increase in hyperuricemic subjects is implicating both oxidative stress and intracellular urate activity with a primary involvement of XOR (xanthine-oxidoreductase activity). An increase in the relative risk of hypertension has been confirmed by genetic data and by large meta-analyses of epidemiological data. The effects of urate-lowering treatment on blood pressure control in patients with elevated serum uric acid has been investigated in a small number of reliable studies with a large heterogeneity of patient populations and study designs. However, 2 large meta-analyses suggest a significant effect of urate-lowering treatment on blood pressure, thus confirming the significant relationship between high serum urate and blood pressure. The future research should be focused on a more appropriate identification of patients with cardiovascular hyperuricemia by considering the correct cardiovascular threshold of serum urate, the time-course of uricemia fluctuations, and the identification of reliable markers of urate overproduction that could significantly clarify the clinical and therapeutic implications of the interaction between serum uric acid and hypertension.

Ganoderma lucidumpolysaccharide peptide alleviates hyperuricemia by regulating adenosine deaminase and urate transporters

“…1 HUA is a critical risk factor for the development of gout, kidney disease, hypertension, insulin resistance, and cardiovascular diseases. [2][3][4][5] HUA occurs as a result of overproduction and/or renal underexcretion and/or gut underexcretion of uric acid (UA). 6 UA overproduction is caused by purine metabolism abnormalities mainly in the liver, bone marrow and muscle.…”

Impact of Early Life Factors on Metabolic Phenotypes of Obesity in Preschool Children

“…In sensitivity analyses, we chose UA ≥5.5 mg/dL (327 μmol/L) to define the high UA levels, from which the probability of primary hypertension increases significantly ( 22 ); moreover, we used the cutoff points established by the World Obesity Federation to categorize childhood BMI status ( 23 , 24 ).…”

Anti-Inflammatory and Hypouricemic Effect of Bioactive Compounds: Molecular Evidence and Potential Application in the Management of Gout

“…If not treated, gout leads to severe damage of articular tissues and subchondral bones with consequent disability. Furthermore, the persistent increase in serum levels of uric acid leads to comorbidities, in particular those related to cardiovascular diseases [ 6 ].…”