Hyperuricemia and cardiovascular disease risk

  title={Hyperuricemia and cardiovascular disease risk},
  author={Claudio Borghi and Federico Maria Verardi and Ilenia Pareo and Crescenzio Bentivenga and Arrigo Francesco Giuseppe Cicero},
  journal={Expert Review of Cardiovascular Therapy},
  pages={1219 - 1225}
Uric acid (UA) is the final end product of purine catabolism and is formed from xanthines and hypoxanthines. Hyperuricemia can be secondary to either an exaggerated production of UA that follows high cellular turnover conditions or, most frequently, to a low renal excretion in patients with impaired renal function. Recent data suggest that serum UA (SUA) at high–normal level is associated with cardiovascular disease risk factors and cardiovascular disease, often being a predictor of incident… 
In response: Hyperuricemia as a risk factor for cardiovascular disease
The explication of the result could be that high SUA level promotes oxidative stress trough the generation of free oxygen radicals, thus inducing an increase in circulating oxLDL, or is more simply an indirect marker of systemic oxidation or exposition to oxidative stress, but probably does not directly affect the LDL resistance to oxidation.
Hyperuricemia: contemporary treatment in patients with cardiovascular disease
The need to reduce the level of uric acid in patients with cardiovascular disease is currently beyond doubt, and lifestyle modification in combination with urate-lowering therapy improves both the quality of life and prognosis.
Hyperuricemia as a risk factor for cardiovascular disease
The authors discuss possible causes and treatments of hyperuricemia as well as the links between elevated serum uric acid (SUA) levels and cardiovascular (CV) risk factors, and the association between elevated SUA levels and stroke.
Hyperuricemia induces hypertension through activation of renal epithelial sodium channel (ENaC).
Sodium-glucose co-transporter 2 inhibitors and serum uric acid
  • T. Kawada
  • Medicine, Biology
    Current medical research and opinion
  • 2019
The effects of SGLT2 inhibitors on SUA should be considered in combination with diabetes, kidney disease and cardiovascular disease, and there are benefits of SUA lowering therapy for improving endothelial dysfunction and systemic inflammation, which would also lead to the prevention of cardiovascular diseases.
Uric Acid and Cognitive Function in Older Individuals
It is concluded that serum uric acid may modulate cognitive function in a different way according to the etiology of dementia, with hypouricemia representing a risk factor for a quicker disease progression and a possible marker of malnutrition.
Sodium-glucose Cotransporter 2 Inhibitors (SGLT2i): Their Role in Cardiometabolic Risk Management.
Multiple metabolic benefits may account for the positive clinical outcomes in the EMPA-REG OUTCOME study, and ongoing CV outcome trials involving other SGLT2i will help establish whether the reported CV and microvascular risk benefits are compound-specific or drug class effects.
Predictors of Microalbuminuria among Hyperuricemia with Hypertension Patients
It seems to be reasonable to consider that treatment for CKD should start at an earlier stage, leading to a better outcome, however early stage of CKD is unlikely to be diagnosed timely, and easily overlooked.


Uric acid, hominoid evolution, and the pathogenesis of salt-sensitivity.
It is hypothesized that the mutation provided a survival advantage to early hominoids because of the ability of hyperuricemia to maintain blood pressure under low-salt dietary conditions, such as prevailed during the Miocene.
Is there anything good in uric acid?
The known negative effects of UA are reviewed, as well as the much less-known possible positive actions, and their therapeutic implications.
Hyperuricemia in primary and renal hypertension.
The present investigation of the population of the Hypertension-Nephritis Clinic of the Presbyterian Hospital in New York City confirms the observation that there is an increased incidence of hyperuricemia among patients with either primary or renal hypertension, treated and untreated.
Uric acid and inflammatory markers.
A positive and significant association between UA and several inflammatory markers was found in a large population-based sample of older persons and in a sub-sample of participants with normal UA, and the prevalence of abnormally high levels of C-reactive protein and IL-6 increased significantly across UA quintiles.
Uric acid predicts clinical outcomes in heart failure: insights regarding the role of xanthine oxidase and uric acid in disease pathophysiology.
Serum concentrations of UA added important prognostic information alone and when combined with measures of cardiac function and patient functional status and were independent of renal function, serum sodium, serum urea, diuretic usage, and patient age.
Editorial comment--Elevated uric acid and ischemic stroke: accumulating evidence that it is injurious and not neuroprotective.
A new study reported in this issue of Stroke 8 examining 2498 subjects admitted with acute stroke found that the admission serum uric acid also independently predicted worse outcome and a higher rate of repeated stroke or other cardiovascular event.
Hyperuricemia induces endothelial dysfunction.
Uric acid was found to inhibit both basal and vascular endothelial growth factor (VEGF)-induced nitric oxide production in bovine aortic endothelial cells and may provide insight into a pathogenic mechanism by which uric acid may induce hypertension and vascular disease.
Towards the physiological function of uric acid.
Uric acid as a danger signal in gout and its comorbidities
Surprisingly, the same mechanisms underlie the inflammatory response to a number of irritant particles, many of which also cause disease, as well as pointing to potential new therapeutic targets for this and other sterile inflammatory diseases.
Elevated Uric Acid Increases Blood Pressure in the Rat by a Novel Crystal-Independent Mechanism
Mild hyperuricemia causes hypertension and renal injury in the rat via a crystal-independent mechanism, with stimulation of the renin-angiotensin system and inhibition of neuronal NO synthase.