Hyperuricemia In Hypertension Research Articles

9 HYPERURICEMIA AND RISK OF HYPERTENSION RESISTANT TO THERAPY: A SYSTEMATIC REVIEW AND META-ANALYSIS

Background: Hypertension is a common public health problem throughout the world. One of the most common risk factors of hypertension is hyperuricemia. However, there are limited data for the effect of hyperuricemia in hypertension undergoing therapy. The objective of this study is to discover the relationship between hyperuricemia and the risk for resistant hypertension. Methods: Systematic literature search was conducted based on the PRISMA flow diagram, from PubMed, PubMed Central, Cochrane, and Google Scholar with keywords. “hyperuricemia”, “uncontrolled hypertension”, “resistant hypertension”, and “hypertension”. Data extraction was done and Newcastle-Ottawa Scale was used to assess the study quality. The data was then analyzed using Revman 5.4.1 (Cochrane). Results: Four selected cohort studies with a total of 8247 patients. All of the included studies have good quality. From the data analysis, we found that hyperuricemia increased the odds of hypertension becoming resistant to therapy (OR: 2.29 [95% CI 1.26, 4.14]; p: 0.006). Forest plot showed the data was evenly distributed. Conclusion: Hyperuricemia increases the risk of hypertension being resistant to therapy. Therefore, uric acid levels should be controlled in hypertensive patients to optimize the effect of hypertension therapy.

Hyperuricemia in Hypertension and Chronic Kidney Disease: Risk Factors, Prevalence and Clinical Correlates: A Descriptive Comparative Study

Introduction: Uric acid is a product of purine metabolism and elevated serum concentration are very common in, and linked with hypertension and chronic kidney disease, conditions associated with heavy health burden and cardiovascular complications particularly in sub Sahara Africa. An assessment of factors relating hyperuricemia to hypertension and chronic kidney disease would therefore be necessary as way of mitigating the poor quality of life, morbidity and mortality associated with these diseases in low income nations. Methods: A single centre, descriptive comparative study in which the demographic, clinical and laboratory data of hypertensive and non-dialyzed chronic kidney disease (CKD) patients were analyzed. Serum biochemical parameters with uric acid, hematocrit and urine dip strip protein were assessed. Predictors of hyperuricemia were determined using multivariate analysis. Results: One hundred and thirty nine hypertensives and 69 CKD were studied. The mean age of the participants was 54.3 ± 11.7 years, hypertensives (52.9 ± 15.7 years) and CKD (57.3 ± 16.1 years). Both groups had more males, P = 0.8. Majority (78.3%) of the CKD cohorts had stage 4 or 5 (non-dialyzed) disease. The systolic and diastolic blood pressure, creatinine and uric acid were lower in hypertension than in CKD, P = 0.07, P = 0.05, P < 0.001 and P = 0.004 respectively. The hematocrit, albumin and GFR were higher in HTN than CKD, P < 0.001, P < 0.001 and P < 0.001 respectively. The prevalence of hyperuricemia was 56.2%. The mean uric acid was 505.9 ± 23.6 mmol/L, 382 7 ± 10.5 mmol/L for hypertensive and 755.9 ± 14.8 mmol/L for CKD, P < 0.001. The prevalence of systolic HTN, proteinuria, hypoalbuminemia and anemia were 51%, 75%, 46% and 59%, and were higher in males. Hyperuricemia was related to advancing age, proteinuria, elevated creatinine, hypoalbuminemia, anemia and hypertriglyceridemia. Proteinuria (OR—4.66, 95% CI—2.42 - 9.65), elevated creatinine (OR—3.12, 95% CI—2.40 - 6.92), hypoalbuminemia (OR—2.92, 95% CI—1.83 - 5.78) and anemia (OR—4.01, 95% CI—3.78 - 7.99) independently predicted hyperuricemia. Conclusion: Hyperuricemia is commoner in CKD than hypertension and was higher in males and positively correlated with the blood pressure, proteinuria and creatinine, but negatively related to hematocrit, albumin and glomerular filtration rate. Independent predictors of hyperuricemia were proteinuria, elevated creatinine, hypoalbuminemia and anemia. Measures are needed to prevent and treat hyperuricemia to reduce the health burden associated with hypertension and CKD.

Hyperuricemia in hypertension. Domestic experience based on the data of the Hungarian Hypertonia Register 2011., 2013., 2015. Part II.

Hyperuricemia in hypertension. Domestic experience based on the data of the Hungarian Hypertonia Register 2011., 2013., 2015. Part II.

A correlative study of serum uric acid and serum malondialdehyde level in early essential hypertension

Background: Hypertension (HT) posing a major public health challenge to the universe in socioeconomic and epidemiological transition. Hyperuricemia in HT is coupled with augmented cardiovascular morbidity and mortality. It also predates the development of HT and suggests that it is not simply a consequence of HT per se. Increased urate level along with greater production of oxygen-free radical and augmented oxidative stress may contribute to progression of HT. Aims and Objectives: This study aims to assess the correlation between serum uric acid (SUA), serum malondialdehyde S. MDA) level, and blood pressure in early essential HT. Materials and Methods: In this cross-sectional study, after applying inclusion and exclusion criteria, 200 subjects were divided into three groups: 50 subjects as control group, 75 in prehypertensive group, and 75 in hypertensive group. SUA and S. MDA level were estimated in all subjects. Data were analyzed by appropriate statistical methods. Results: A significant and positive correlation was observed between SUA and S. MDA level in HT group. Both parameters were correlated positively and significantly with systolic blood pressure (SBP), but not with diastolic blood pressure (DBP) in hypertensive individuals. Conclusion: An elevated SUA level is predictive for the evolution of both HT and coronary artery disease. Hyperuricemia plays a role in the formation of free radicals and oxidative stress through increased lipid oxidation. Furthermore, positive correlation with SBP further established its potential role in the etiopathogenesis of essential HT.

Estimation of the influence of photobiomodulation on the endothelial function in patients with arterial hypertension under the conditions of hyperuricemia

Introduction. In 2015, the global prevalence of hypertension in the world was estimated at 1.13 billion. The European Association for the Treatment of Hypertension (ESH) updated its recommendations in 2018 and officially added to the already existing risk factors of hypertension hyperuricemia. In patients with comorbidity of hyperuricemia and hypertension, endothelial dysfunction is observed. The aim of the study is to establish correlation between uric acid level and pulse wave velocity, Tei index, endothelium-dependent vasodilation of the brachial artery and evaluate the effect of photobiomodulation on endothelial dysfunction in patients with hypertension. Materials and methods. The study included 102 patients with hypertension: 48 without hyperuricemia (group 1) and 54 with comorbidity of hypertension and hyperuricemia (group 2). Groups 1A and 2A received antihypertensive therapy. Groups 1B and 2B — antihypertensive therapy with a course of intravenous laser therapy with a wavelength of 635 nm, course 10 procedures. Endothelium-dependent vasodilation of the brachial artery was determined by a breakdown with reactive hyperemia. Tei index was calculated during echocardiography. The pulse wave velocity was measured with a SonoScape S6 Pro. Results. Antihypertensive therapy in group 1A reduced the rate of the pulse wave by 7.8 %. Antihypertensive therapy and intravenous laser therapy in Group 1 reduced uric acid by 5.7 %, pulse rate by 12.2 %, Tei index by 9.5 %, increased endothelium dependent vasodilation of the brachial artery by 19.1 % (p &lt; 0,05). Antihypertensive therapy in Group 2A reduced uric acid by 4.7 %, pulse rate by 8.5 % and increased endothelium-dependent brachial artery vasodilation by 31.7 %. Combined use of antihypertensive therapy and intravenous laser therapy in group 2B reduced uric acid by 19.2 %, pulse wave speed by 21.9 %, Tei index by 29.0 %, increased endothelium- dependent vasodilation of the brachial artery by 97.7 % &lt; 0.05). A correlation was established between uric acid level and endothelium dependent vasodilation of the brachial artery r = - 0.62 (p &lt; 0.001) and between uric acid level and pulse wave velocity r = + 0.68, uric acid level and systolic blood pressure (day ) r = + 0.48 (p &lt; 0.001), uric acid level and Tei index r = + 0.47 (p &lt; 0.05). Conclusion. Given the established negative correlation between the mean strength between uric acid level and endothelium-dependent vasodilation of the brachial artery, it is appropriate to use in clinical practice a combination of antihypertensive therapy with intravenous laser therapy, which significantly reduces the level of uterine fibrillation hypertension and in patients with comorbidity of hypertension and hyperuricemia.

The effects of urate lowering therapy on inflammation, endothelial function, and blood pressure (SURPHER) study design and rationale

BackgroundThe association between hyperuricemia and hypertension is controversial. Animal models, epidemiological data, and small clinical trials have favored a causative role for hyperuricemia in hypertension but more studies are necessary to elucidate putative mechanisms, population susceptibility, and potential for urate-lowering therapies (ULT) to decrease blood pressure (BP). PurposeTo describe the background and design of the Serum Urate Reduction to Prevent Hypertension (SURPHER) study. MethodsSURPHER is a single center, double-blinded, crossover trial in which participants are randomly assigned to allopurinol (300mg) or placebo. Enrollment focused on adults 18–40years old with baseline systolic blood pressure≥120 and <160mmHg or diastolic blood pressure≥80 and <100mmHg, and serum urate ≥5.0mg/dL or ≥4.0mg/dL for men or women, respectively. SURPHER recruitment targets participants without chronic kidney disease (estimated glomerular filtration rate>60mL/min/1.73m2), and without prior diagnosis of gout or use of ULT to treat gout. The primary outcome is change from baseline in blood pressure assessed by 24hour ambulatory blood pressure monitoring and mechanistic outcomes include changes in endothelial function as measured by flow-mediated dilation, as well as C-reactive protein levels. ResultsSince June 16, 2014 until present, SURPHER is recruiting participants in the city of Birmingham, Alabama. LimitationsThe study aims to enroll otherwise healthy young adults for a pharmacological intervention study with multiple study-related procedures. Challenges related to recruitment are anticipated and multiple strategies for increasing recruitment and retention are planned if necessary.

Serum uric acid and the renin-angiotensin system in hypertension.

To study whether the renin-angiotensin system is related to hyperuricemia in hypertension, the serum concentration of uric acid was determined in 96 patients with various types of hypertension and various degrees of plasma renin activity (PRA). In malignant hypertension, both PRA and the serum uric acid level were higher than in essential hypertension; but in primary aldosteronism or desoxycorticosterone-excess hypertension, they were lower than in the essential type. In renovascular hypertension, PRA was higher than in essential hypertension, but the serum uric acid levels were similar. There were no differences in PRA and serum uric acid concentration between Cushing's syndrome and essential hypertension. The serum uric acid level in high-renin essential hypertension was higher than in either the normal-renin or the low-renin type. There was a significant correlation between serum uric acid concentration and PRA in the basal state, and between the change in PRA and the change in serum uric acid induced by administration of furosemide. Apparently the close correlation between the renin-angiotensin system and the concentration of serum uric acid is related to changes in extracellular fluid volume, although an intrarenal effect of angiotensin II cannot be excluded.