***TASK*** the task is to summarize an input biomedical literature in six sentences 
    ***INPUT*** the input is a biomedical literature 
    ***OUTPUT*** the output is the summary of an input biomedical literature in six sentences 
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    ***EXAMPLES*** 
    Input: Experimental evidence supports a causative role for uric acid in the pathogenesis of  hypertension . Prospect i ve studies have variably adjusted for relevant confounders and have been of relatively limited duration . We prospect ively examined the relationship between uric acid level and the development of hypertension in the Normative Aging Study , a longitudinal cohort of healthy adult men . Of the 2280 initial men in the Normative Aging Study , 2062 had available information for inclusion in the analysis . Cox proportional hazards model was used to examine the relationship between baseline serum uric acid level and the development of hypertension adjusting for age , body mass index , abdominal circumference , smoking , alcohol , plasma triglycerides , total cholesterol , and plasma glucose . A total of 892 men developed hypertension over a mean of 21.5 years of follow-up . Serum uric acid level independently predicted the development of hypertension in age-adjusted ( relative risk [ RR ] : 1.10 ; 95 % CI : 1.06 to 1.15 : P<0.001 ) and multivariable ( RR : 1.05 ; 95 % CI : 1.01 to 1.10 ; P=0.02 ) models . Among 1277 men at risk for the development of hypertension at the time of their first serum creatinine measurement , 508 ( 39.8 % ) developed hypertension over a mean of 10.3±5.5 years of follow-up . Additionally adjusting for calculated glomerular filtration rate in this subset ,  serum  uric acid remained associated with the development of hypertension ( RR : 1.06 ; 95 % CI : 1.01 to 1.12 ; P=0.03 ) . The baseline serum uric acid level is a durable marker of risk for the development of hypertension . The association is independent of elements of the metabolic syndrome , alcohol intake , and renal function We tested the hypothesis that xanthine oxidase inhibition among African Americans receiving the thiazide-type diuretic chlorthalidone  may improve blood pressure control with fewer hyperuricemia-related side effects . We performed a r and omized , double-blind , placebo-controlled study of African Americans with Stage 1 hypertension without clinical ly significant renal disease . One hundred fifty African American men or women between the ages of 18 and 65 years who met the exclusion/ inclusion criteria with untreated or treated hypertension were started on chlorthalidone ( 25 mg/d ) and potassium chloride . After a 5-week run-in on chlorthalidone , baseline testing was performed and they were r and omized to allopurinol ( 300 mg/dL ) or placebo with doses adjusted based on uric acid levels and followed for 8 weeks . One hundred ten subjects completed the study . Baseline systolic blood pressures after the 5-week chlorthalidone run-in were 119.9 ± 13.6 in the allopurinol group and 117 ± 11.2 in the placebo group indicating excellent blood pressure control with the single agent . After at least 4 week postr and omization , the difference in mean change in systolic blood pressure  in allopurinol less placebo from visits 5 to 3 was 4.3 mm Hg ( 95 % confidence interval , -0.2 to 8.7 ; P = .059 ) . The difference in mean change in uric acid levels over the same period was 2.1 mg/dL ( 95 % confidence interval , 1.7 - 2.6 ; P < .001 ) . The use of chlorthalidone with or without allopurinol result ed in excellent blood pressure control . The addition of allopurinol tended to improve clinic blood pressure , but the difference from the group receiving chlorthalidone alone was not statistically significant Abstract Background Topiroxostat , a selective xanthine oxidase inhibitor , shows effective reduction in the serum urate level in hyperuricemic patients with or without gout . The objective of this study was to evaluate the efficacy and safety of topiroxostat in hyperuricemic stage 3 chronic kidney disease patients with or without gout . Methods The study design was a 22-week , r and omized , multicenter , double-blind study . The enrolled patients were r and omly assigned to treatment with topiroxostat 160 mg/day ( n = 62 ) or to the placebo ( n = 61 ) . The endpoints were the percent change in the serum urate level , change in the estimated glomerular filtration rate , the urinary albumin-to-creatinine ratio , the proportion of patients with serum urate levels of 356.88 μmol/L or less , blood pressure , and serum adiponectin . Results After 22 weeks , although the changes in the estimated glomerular filtration rate and blood pressure were not significant , the percent change in the serum urate level ( −45.38 vs. −0.08 % , P < 0.0001 ) and the percent change in urinary albumin-to-creatinine ratio ( −33.0 vs. −6.0 % , P = 0.0092 ) were found to have decreased in the topiroxostat as compared with the placebo . Although the incidence of ‘ alanine aminotransferase increased ’ was higher in the topiroxostat , serious adverse event rates were similar in the two groups . Conclusion Topiroxostat 160 mg effectively reduced the serum urate level in the hyperuricemic stage 3 chronic kidney disease patients with or without gout Background : Hyperuricemia has been associated with the development of high blood pressure ( BP ) . We studied the effects of allopurinol therapy in hyperuricemic hemodialysis ( HD ) patients with high BP . Material s and Methods : This single-blind , r and omized cross-over clinical study involved 55 HD patients with serum uric acid level > 6.5 ( men ) and > 5.5 mg/dL ( women ) . They were r and omly divided in two groups , each of which went through two phases . Group-1 in phase-1 received 100 mg/day orally of allopurinol for three months ; while Group-2 was given whatever medication they received prior to the study . After two months of washing period , the groups were crossed-over . The BP levels were measured before and after HD during the eight months study period . Results : Fifty-three patients completed the study ( 33 men and 20 women , with mean age of 55.8 years ) .  Uric acid levels decreased significantly during the12 weeks of allopurinol therapy ( 7.71 ± 1.53 to 5.2 ± 1.2 P < 0.005 ) . Overall , after the 12 weeks of allopurinol  therapy , systolic and diastolic BP also significantly decreased in allopurinol group , 15.8 % ( 139 to 117 , P < 0.0005 ) and 8.6 % ( 81 to 74 , P < .0005 ) , respectively . There were not significant changes in body mass index , blood urea nitrogen , creatinine , albumin , cholesterol , triglyceride , hemoglobin , liver enzymes and serum electrolytes level after treatment . Patients treated with allopurinol had a significant increase in the quality of dialysis ( KT/V ) ( P : 0.043 ) . Conclusions : In HD patients  , allopurinol treatment reduced BP . The results indicate a new potential therapeutic approach for controlling BP in HD patients BACKGROUND AND OBJECTIVES Endothelial dysfunction is an early manifestation of vascular injury and contributes to the development of atherosclerotic cardiovascular disease . Recent studies have implicated hyperuricemia as a risk factor for cardiovascular disease . We hypothesized that lowering uric acid in subjects with asymptomatic hyperuricemia with allopurinol  might improve endothelial dysfunction , BP , estimated GFR ( eGFR ) , and inflammatory markers . DESIGN , SETTING , PARTICIPANTS , & MEASUREMENTS Subjects with asymptomatic hyperuricemia and no history of gout and 30 normouricemic control subjects were enrolled in this 4-month r and omized prospect i ve study . Thirty hyperuricemic patients received 300 mg/d allopurinol and were compared with 37 hyperuricemic patients and 30 normouricemic subjects in matched control groups .  Flow-mediated dilation ( FMD ) , eGFR , ambulatory BP monitoring , spot urine protein-creatine ratio , and highly sensitive C-reactive protein were measured at baseline and at 4 months . RESULTS Age , gender , lipid profile , eGFR , hemoglobin , glucose , and level of proteinuria were similar in hyperuricemic subjects and controls at baseline . As expected , hyperuricemic patients had higher levels of highly sensitive C-reactive protein and lower FMD compared with normouricemic patients . Allopurinol treatment result ed in a decrease in serum uric acid , a decrease in systolic BP , an increase in FMD , and an increase in eGFR compared with baseline . No significant difference was observed in the control hyperuricemic and normouricemic groups . In a multiple regression analysis , FMD levels were independently related to uric acid both before ( beta = -0.55 ) and after ( beta = -0.40 ) treatment . CONCLUSIONS Treatment of hyperuricemia with allopurinol improves endothelial dysfunction and eGFR in subjects with asymptomatic hyperuricemia OBJECTIVE To evaluate the effects of diet and medication , either isolated or associated , on serum levels of uric acid in patients with hyperuricemia . METHODS We studied patients from the Hypertension Unit of the University of Goias who had hyperuricemia ( men > or = 8.5 mg/dL and women > or = 7.5 mg/dL ) . We divided the patients into three groups : G1 ( low purine diet ) , G2 ( low purine diet + medication ) , and G3 ( medication only ) . Patients received allopurinol , 150 mg/day titrated up to 300 mg/dL when necessary . Patients were evaluated with regards to their lifestyles ( diet , smoking , physical , activity , alcohol consumption ) , uric acid , blood pressure , use of medication , body mass index , cholesterol , and triglyceride . Follow-up took place in weeks 0 ( M1 ) , 6 ( M2 ) , 12 ( M3 ) during the intervention and in week 36 ( M4 ) after the study was completed . RESULTS Fifty-five patients participated in the study , 31 women , mean age 54.4+/-10.6 years , body mass index 28.6+/-3.9 kg/m2 . A similar reduction ( p<0.001 ) in uric acid levels occurred in the three intervention groups . In week 36 ( M4 ) , after 24 weeks without intervention , a tendency toward elevation of uricemia was noted in G2 and G3 , and a continuous drop in uricemia was noted in G1 . No significant modifications were observed in the other variables analyzed . CONCLUSION Considering the cost x benefit relationship , a diet low in purine should be the 1st therapeutic option for controlling hyperuricemia in patients with similar characteristic to the ones presented in this study Abstract Background . Arterial hypertension is commonly associated with hyperuricemia . Several studies have shown that allopurinol reduces arterial blood pressure in animal models and in adolescent patients with newly diagnosed hypertension . Moreover , allopurinol has shown beneficial effects on endothelial function and arterial wave reflection in contrast to uricosuric agents . Antihypertensive drugs produce different effects on serum uric acid levels . Objective . The aim of the study was to evaluate the influence of allopurinol on blood pressure and aortic compliance in patients with arterial hypertension depending on hypotensive therapy with angiotensin-converting enzyme inhibitor ( ACE-I ) or thiazide diuretic , hypotensive drugs with distinct effects on serum uric acid levels and conversely , a positive influence on pulse wave velocity ( PWV ) in the aorta . Material and Methods . Sixty-six patients aged 25–70 ( mean age 46.17 ± 10.89 ) with mild and moderate arterial hypertension diagnosed on the basis of office blood pressure , were studied . They were r and omized to antihypertensive therapy on either perindopril ( n = 35 ) or hydrochlorothiazide ( n = 31 ) . After 8 weeks of antihypertensive therapy , 150 mg of allopurinol daily was added for the next 8 weeks . Measurement of the serum uric acid level , PWV and 24-h ambulatory blood pressure monitoring ( ABPM ) were performed at baseline , after 8 weeks antihypertensive therapy and again after the final 8 weeks with the additional allopurinol . Results . No significant changes in systolic ( SBP ) and diastolic blood pressure ( DBP ) or ABPM were observed after allopurinol treatment in either of the subgroups receiving ACE-I or thiazide-based antihypertensive therapy . The mean PWV decreased from 10.7 ± 1.4 m/s to 10.0 ± 1.2 m/s ( p = 0.00008 ) in the ACE-I-based therapy subgroup and from 11.5 ±1.7 m/s to 10.4 ± 1.5 m/s ( p = 0.00002 ) in the th 
    Output:
    
In this up date d systematic review , the RCT data available at present are insufficient to know whether UA-lowering therapy also lowers BP .