Role of uric acid in hypertension, renal disease, and metabolic syndrome (original) (raw)
Related papers
Journal of Comparative Physiology B, 2009
Uric acid has historically been viewed as a purine metabolic waste product excreted by the kidney and gut that is relatively unimportant other than its penchant to crystallize in joints to cause the disease gout. In recent years, however, there has been the realization that uric acid is not biologically inert but may have a wide range of actions, including being both a pro-and anti-oxidant, a neurostimulant, and an inducer of inflammation and activator of the innate immune response. In this paper, we present the hypothesis that uric acid has a key role in the foraging response associated with starvation and fasting. We further suggest that there is a complex interplay between fructose, uric acid and vitamin C, with fructose and uric acid stimulating the foraging response and vitamin C countering this response. Finally, we suggest that the mutations in ascorbate synthesis and uricase that characterized early primate evolution were likely in response to the need to stimulate the foraging "survival" response and might have inadvertently had a role in accelerating the development of bipedal locomotion and intellectual development. Unfortunately, due to marked changes in the diet, resulting in dramatic increases in fructose-and purine-rich foods, these identical genotypic changes may be largely responsible for the epidemic of obesity, diabetes and cardiovascular disease in today's society.
Uric acid: from a biological advantage to a potential danger. A focus on cardiovascular effects
Vascular Pharmacology, 2019
Non-communicable diseases represent nowadays the most common cause of death worldwide, having largely overcome infectious diseases. Among them, cardiovascular diseases constitute the majority. Given these premise, great efforts have been made by scientific societies to emphasize the fundamental role of cardiovascular prevention and risk factors control. In addition to classical cardiovascular risk factors such as smoking, arterial hypertension, hypercholesterolemia and male gender, new risk factors are emerging from international literature. Among them, uric acid is the protagonist. Several evidences show a direct role of hyperuricemia in the determinism of metabolic and vascular disorders. From the other hand, some researchers have demonstrated that uric ac id is only a marker of cardiovascular damage and not a risk factor for its development. Aim of this review is to evaluate the scientific evidences on the role of uric acid in cardiovascular diseases in order to shed light on this confusing topic.
Uric Acid, the Metabolic Syndrome, and Renal Disease
Journal of The American Society of Nephrology, 2006
Metabolic syndrome, characterized by truncal obesity, hypertriglyceridemia, elevated BP, and insulin resistance, is recognized increasingly as a major risk factor for kidney disease and also is a common feature of patients who are on dialysis. One feature that is common to patients with metabolic syndrome is an elevated uric acid. Although often considered to be secondary to hyperinsulinemia, recent evidence supports a primary role for uric acid in mediating this syndrome. Specifically, fructose, which rapidly can cause metabolic syndrome in rats, also raises uric acid, and lowering uric acid in fructose-fed rats prevents features of the metabolic syndrome. Uric acid also can accelerate renal disease in experimental animals and epidemiologically is associated with progressive renal disease in humans. It is proposed that fructose-and purine-rich foods that have in common the raising of uric acid may have a role in the epidemic of metabolic syndrome and renal disease that is occurring throughout the world.
Is There a Pathogenetic Role for Uric Acid in Hypertension and Cardiovascular and Renal Disease?
Hypertension, 2003
Hyperuricemia is associated with hypertension, vascular disease, renal disease, and cardiovascular events. In this report, we review the epidemiologic evidence and potential mechanisms for this association. We also summarize experimental studies that demonstrate that uric acid is not inert but may have both beneficial functions (acting as an antioxidant) as well as detrimental actions (to stimulate vascular smooth muscle cell proliferation and induce endothelial dysfunction). A recently developed experimental model of mild hyperuricemia also provides the first provocative evidence that uric acid may have a pathogenic role in the development of hypertension, vascular disease, and renal disease. Thus, it is time to reevaluate the role of uric acid as a risk factor for cardiovascular disease and hypertension and to design human studies to address this controversy.
Review Article: URIC ACID HOMEOSTASIS AND DISTURBANCES
Folia Medica Indonesiana
This review examined the homeostasis of uric acid in human body and analyzed recent studies of the affecting major variables. Normal uric acid concentration in male is 3.5-7.2 mg/dL and in female is 2.6-6 mg/dL. Daily turnover of normal uric acid ranges from 498-1392 mg/day, miscible pool is 767-1650 mg, reabsorption is 8064 mg/day, renal excretion is 262-620 mg/day and intestine 186-313 mg/day. The dynamics of uric acid is influenced by factors of food, drink, age, history of disease, and genetic. High purine dietary consumption increases blood uric acid by 1-2 mg/dL, 213-290 g/day fructose drinks increases 0.52-1.7 mg/dL, 1.5 g/kgBW sucrose increases 0.61 mg/dL, and 10-20 ml/kgBW beer increases 0.50-0.92 mg/dL. The ABCG2 gene plays a role in bringing uric acid out of the body by 114.31-162.73 mg/dL, SLC2A9 of 5.43-20.17 mg/dL, and SLC22A12 of 5.77-6.71 mg/dL. The data described the homeostasis of uric acid and the magnitude of the impact of environmental (consumption of food, beve...
Uric Acid - Key Ingredient in the Recipe for Cardiorenal Metabolic Syndrome
Cardiorenal Medicine, 2013
Elevated serum uric acid levels are a frequent finding in persons with obesity, hypertension, cardiovascular and kidney disease as well as in those with the cardiorenal metabolic syndrome (CRS). The increased consumption of a fructose-rich Western diet has contributed to the increasing incidence of the CRS, obesity and diabetes especially in industrialized populations. There is also increasing evidence that supports a causal role of high dietary fructose driving elevations in uric acid in association with the CRS. Animal and epidemiological studies support the notion that elevated serum uric acid levels play an important role in promoting insulin resistance and hypertension and suggest potential pathophysiological mechanisms that contribute to the development of the CRS and associated cardiovascular disease and chronic kidney disease. To this point, elevated serum levels of uric acid appear to contribute to impaired nitric oxide production/endothelial dysfunction, increased vascular stiffness, inappropriate activation of the renin-angiotensin-aldosterone system, enhanced oxidative stress, and maladaptive immune and inflammatory responses. These abnormalities, in turn, promote vascular, cardiac and renal fibrosis as well as associated functional abnormalities. Small clinical trials have suggested that uric acid-lowering therapies may be beneficial in such patients; however, a consensus on the treatment of asymptomatic hyperuricemia is lacking. Larger randomized controlled trials need to be performed in order to critically evaluate the beneficial effect of lowering serum uric acid in patients with the CRS and those with diabetes and/or hypertension.