<p>Hyperuricemia and Hypertension: Links and Risks</p>

Abstract

Hyperuricemia has long been recognized to be associated with increased cardiovascular risk, including risk of developing hypertension. Epidemiological findings suggest that the link with hypertension is stronger in children and adolescents. Uric acid acts as a strong antioxidant compound in the extracellular environment but has pro-inflammatory effects within the intracellular setting. A chronic phase of microvascular injury is known to occur after prolonged periods of hyperuricemia. This is proposed to contribute to afferent arteriolopathy and elevation of blood pressure that may become unresponsive to uric acid-lowering therapies over time. Studies have struggled to infer direct causality of hyperuricemia due to a vast number of confounders including body mass index. The aim of this review is to present the available data and highlight the need for large scale prospective randomized controlled trials in this area. At present, there is limited evidence to support a role for uric acid-lowering therapies in helping mitigate the risk of hypertension.

Uric Acid and Hypertension: Prognostic Role and Guide for Treatment

“…UA is a weak acid, and in normal blood pH values it exists predominantly as urate anion. XOR catalyzes the generation of urate from hypoxanthine and xanthine, which are the last metabolites of endogenous and exogenous purine mononucleotide catabolism [ 40 , 42 , 60 ]. XOR has two forms: Xanthine dehydrogenase (XDH), the most prevalent, and xanthine oxidase (XO) [ 61 ].…”

“…XOR has two forms: Xanthine dehydrogenase (XDH), the most prevalent, and xanthine oxidase (XO) [ 61 ]. Hyperuricemia is defined as SUA > 6 mg/dL in women, SUA > 7 mg/dL in men, and SUA > 5.5 mg/dL in the pediatric population, and its prevalence is increasing worldwide [ 42 , 62 ]. During the Miocene epoch, humans lost the capacity to metabolize UA into allantoin due to nonsense mutations in the gene codifying the enzyme uricase [ 63 ].…”

“…However, polymorphisms involving major urate transporters genes (e.g., SLC2A9) have not been demonstrated to correlate with hypertension [ 38 , 39 ]. XOR is involved in intracellular UA production, while urate transporters play a major role in regulating extracellular UA concentration and UA excretion [ 40 , 41 , 42 , 43 ]. Thus, the results of genetic studies may underlie a critical role of intracellular UA production in the development and progression of hypertension.…”

Why Hyperuricemia Does Not Necessarily Induce Gout?

“…The oxidant-antioxidant paradox of UA [37] may suggest UA could have different molecular behaviours under various pathological conditions. At the hydrophilic condition, it shows the protective effects of antioxidant [38]. Reducing SUA could decline the protecting effect to radiation damage [39], and total bone mineral density [40,41] or a protective effect on bone loss in rheumatoid arthritis [42].…”

Analyzing the Association between Hyperuricemia and Periodontitis: A Cross-Sectional Study Using KoGES HEXA Data

“…Accelerated purine degradation and higher production or reduced excretion of uric acid could cause elevated uric acid levels [5]. They are also associated with health conditions such as cardiovascular disease, renal disease, metabolic syndrome, and diabetes [6,7]. Additionally, hyperuricemia could be related to osteolytic diseases such as osteoporosis [8].…”