Uric Acid is a Key Ingredient in the Treatment Recipe for Cardiorenaal Metabolic Syndrome

Abstract

Elevated serum uric acid levels are frequently observed in individuals with obesity, hypertension, cardiovascular diseases (CVD), kidney diseases, and cardiorenal metabolic syndrome (CRS). The increased consumption of fructose-rich Western diets has contributed to the growing prevalence of CVD, obesity, and diabetes, particularly in industrialized countries. Emerging evidence suggests that high dietary fructose intake plays a causal role in elevating uric acid levels, thereby contributing to CRS. Animal and epidemiological studies support the notion that elevated serum uric acid levels play a key role in the development of insulin resistance and arterial hypertension, suggesting potential pathophysiological mechanisms that drive CVD, associated cardiovascular disorders, and chronic kidney disease (CKD). Elevated serum uric acid levels appear to disrupt nitric oxide production, endothelial function, arterial stiffness, and activate the renin-angiotensin-aldosterone system (RAAS). Additionally, oxidative stress and maladaptive immune and inflammatory responses contribute to vascular, cardiac, and renal fibrosis, leading to associated functional impairments. Small clinical trials have shown that uric acid-lowering therapy may benefit such patients; however, there is no consensus on treating asymptomatic hyperuricemia. Larger randomized controlled trials are necessary to critically evaluate the benefits of serum uric acid reduction in patients with heart failure, diabetes, and/or hypertension.