Increased Serum Uric Acid Association with Hypertension (original) (raw)
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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.
THE ROLE OF URIC ACID IN CARDIOVASCULAR DISEASE AND ITS CLINICAL IMPLICATIONS
2004
A substantial body of epidemiological and experimental evidence suggests the significance of serum uric acid as an important and independent risk factor of cardiovascular and renal diseases especially in patients with diabetes mellitus, hypertension or heart failure. Elevated serum uric acid is highly predictive of mortality in patients with heart failure or coronary artery disease and of cardiovascular events in patients with diabetes. Moreover patients with hypertension and hyperuricemia have a 3-to 5-fold increased risk of experiencing coronary artery disease or cerebrovascular disease compared with patients with normal uric acid levels.Although the mechanisms by which uric acid may playa pathogenetic role in cardiovascular disease is unclear, hyperuricemia is associated with deleterious effects on endothelial dysfunction, oxidative metabolism, platelet adhesiveness, hemorheology, and aggregation. Xanthine oxidase inhibitors (e.g., allopurinol) or a variety of uricosuric agents (e.g., probenecid, sulfinpyrazone,benzbromarone,and benziodarone) can lower elevated uric acid levels but it is unknown whether these agents reversibly impact cardiovascular outcomes. Overall, serum uric acid may be a powerful tool to help stratify risk for cardiovascular disease. At the very least, it should be carefully considered when evaluating overall cardiovascular risk.
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.
The role of uric acid in the pathogenesis of human cardiovascular disease
Heart, 2013
Hyperuricaemia is common in subjects with cardiovascular disease, but is not commonly considered a true risk factor. Recent studies suggest that uric acid is biologically active and can stimulate oxidative stress, endothelial dysfunction, inflammation and vasoconstriction. Epidemiological studies have found that uric acid can independently predict the development of hypertension, as well as stroke and heart failure. Experimentally raising uric acid in animals increases blood pressure, and pilot studies suggest that lowering uric acid in humans can reduce blood pressure in hypertensive individuals. Uric acid may also have emerging roles in the pathogenesis of kidney disease, metabolic syndrome and diabetes. More studies need to be performed on the pathophysiology and clinical consequences of hyperuricaemia in cardiovascular disease.
ORIGINAL RESEARCH PAPER AN EFFECT OF SERUM URIC ACID LEVELS IN HYPERTENSION
INTERNATIONAL JOURNAL OF SCIENTIFIC RESEARCH, 2022
BACKGROUND: Hypertension (HTN or HT), also known as high blood pressure (HBP), is a long-term medical condition in which the blood pressure in the arteries is persistently elevated. Worldwide, raised blood pressure is estimated to cause 7.5 million deaths, about 12.8% of the total of all deaths. Elevated levels of serum uric acid are strongly associated with development and progression of hypertension and renal diseases, but whether uric acid plays a causal role or whether it simply acts as an indicator in patients at risk for these conditions remains controversial. Many authorities do not consider an increased uric acid to be a true risk factor for cardiovascular diseases, because patients with hyperuricemia mostly have other well established risk factors for cardiovascular conditions like hypertension, renal disease, obesity, dyslipidaemias, and insulin resistance. This study was aimed to evaluate the levels of uric acid in hypertensive cases and normotensive controls. MATERIAL AND METHOD: This study was conducted on 60 individuals in which 30 considered as case and they having hypertension apart from any other noncommunicable diseases. 30 healthy individuals also taken as controls. This study was conducted in a tertiary care centre. As we RESULTS: compared both of groups, we found a signicant corelation between the uric acid and hypertension. Statistical analysis was done on SPSS by using Karl's Pearson's correlation. Analysed levels are shows that as systolic and diastolic blood pressure so that suggestion for future CONCLUSION: references is to maintain the blood pressure according to the guidelines as well as maintain the food restrictions and give preferences to physical exercise.
Background: uric acid, a final metabolic product of purine breakdown, appears as an etiology in gout. Higher levels have also been associated with hypertension, cardiovascular morbidity and mortality. Few studies have been conducted, especially in India, to elucidate the relationship between uric acid and prehypertension. Objective: In this study, the relationship between serum uric acid levels and blood pressure in the normotensive, prehypertensive and hypertensive population was evaluated. Also, it should be checked whether there is an incremental increase in serum uric acid with an increase in blood pressure. Place and Duration: In the Medicine department of Holy Family Hospital Rawalpindi for one year duration from March 2019 to February 2020. Material and methods: Two hundred OPD patients meeting the inclusion and exclusion criteria and were included in the study population. A venipuncture was measured to collect venous blood to measure the blood pressure of each participant and then serum uric acid. According to the classification of the National Joint Committee 7, the participants were divided into 4 groups such as Normal, Prehypertension, Hypertension -Stage 1, Hypertension Stage -2. The data were analyzed to determine and confirm serum uric acid levels from four categories. The relationship of uric acid with blood pressure. Results and conclusion: A gradual increase in serum uric acid levels was observed with an increase in blood pressure. A strong positive linear correlation was observed between serum uric acid levels and mean arterial pressure (Pearson correlation coefficient r = 0.74; p <0.0001). Uric acid was associated with blood pressure in the prehypertensive population (r = 0.442). Serum uric acid levels are associated with prehypertension and hypertension and are strong independent predictors of cardiovascular mortality.
Serum Uric Acid And Cardiovascular Disease.
A substantial body of epidemiological and experimental evidence suggests the significance of serum uric acid as an important and independent risk factor of cardiovascular and renal diseases especially in patients with diabetes mellitus, hypertension or heart failure. Elevated serum uric acid is highly predictive of mortality in patients with heart failure or coronary artery disease and of cardiovascular events in patients with diabetes. Moreover patients with hypertension and hyperuricemia have a 3- to 5-fold increased risk of experiencing coronary artery disease or cerebrovascular disease compared with patients with normal uric acid levels. Although the mechanisms by which uric acid may play pathogenetic role in cardiovascular disease is unclear. Hyperuricemia is associated with deleterious effects on endothelial dysfunction, oxidative metabolism, platelet adhesiveness, hemorheology, and aggregation. Xanthine oxidase inhibitors (e.g., allopurinol) or a variety of uricosuric agents (e.g., probenecid, sulfinpyrazone, benzbromarone, and benziodarone) can lower elevated uric acid levels but it is unknown whether these agents reversibly impact cardiovascular outcomes. Hyperuricemia will become then a meaningful target for the prevention and treatment of cardiovascular disease. Overall, serum uric acid may be a powerful tool to help stratify risk for cardiovascular disease. At the very least, it should be carefully considered when evaluating overall cardiovascular risk. KEYWORDS: Hypertension; uric acid; gout; allopurinol; coronary heart disease.
Uric Acid and Hypertension: An Update With Recommendations
American Journal of Hypertension, 2020
The association between increased serum urate and hypertension has been a subject of intense controversy. Extracellular uric acid drives uric acid deposition in gout, kidney stones, and possibly vascular calcification. Mendelian randomization studies, however, indicate that serum urate is likely not the causal factor in hypertension although it does increase the risk for sudden cardiac death and diabetic vascular disease. Nevertheless, experimental evidence strongly suggests that an increase in intracellular urate is a key factor in the pathogenesis of primary hypertension. Pilot clinical trials show beneficial effect of lowering serum urate in hyperuricemic individuals who are young, hypertensive, and have preserved kidney function. Some evidence suggest that activation of the renin–angiotensin system (RAS) occurs in hyperuricemia and blocking the RAS may mimic the effects of xanthine oxidase inhibitors. A reduction in intracellular urate may be achieved by lowering serum urate con...