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Hyperuricemia and uncontrolled hypertension in treated hypertensive patients: K-MetS Study.

ABSTRACT: Previous epidemiological studies have suggested that uric acid is an independent risk factor for incident hypertension, whereas few studies have evaluated the effect of hyperuricemia on blood pressure control in hypertensive patients. We investigated whether hyperuricemia predicts uncontrolled hypertension through a large-scale prospective cohort study with hypertensive patients treated with fimasartan in the Republic of Korea (the Kanarb-Metabolic Syndrome study).Of the 10,601 hypertensive patients who were recruited from 582 private clinics and 11 university hospitals at baseline, 7725 completed the follow-up after 3 months of fimasartan medication, and 6506 were included in the analysis after excluding those with missing values. We estimated the risk of uncontrolled hypertension after 3 months (?130/80 mm Hg in those with diabetes or chronic renal failure and ?140/90 mm Hg in the remaining patients) related with baseline hyperuricemia (serum uric acid ?7?mg/dL in males ?6?mg/dL in females) using multiple logistic regression models.Hyperuricemia increased the risk of uncontrolled hypertension after 3 months of fimasartan medication (odds ratio, 1.247; 95% confidence interval, 1.063-1.462). Males in the highest quartile of uric acid level were at a 1.322 (95% confidence interval, 1.053-1.660) times higher risk of uncontrolled hypertension in reference to the lowest quartile; the same analyses in females were not significant. Patients without metabolic syndrome had significantly higher odds of uncontrolled hypertension with hyperuricemia (odds ratio, 1.328; 95% confidence interval, 1.007-1.751).Hyperuricemia predicted uncontrolled hypertension even after 3 months of fimasartan treatment in hypertensive patients.

SUBMITTER: Cho J

PROVIDER: S-EPMC4956806 | biostudies-other | 2016 Jul

REPOSITORIES: biostudies-other

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Hyperuricemia and uncontrolled hypertension in treated hypertensive patients: K-MetS Study.

Cho Jaelim J Kim Changsoo C Kang Dae Ryong DR Park Jeong Bae JB

Medicine 20160701 28

Previous epidemiological studies have suggested that uric acid is an independent risk factor for incident hypertension, whereas few studies have evaluated the effect of hyperuricemia on blood pressure control in hypertensive patients. We investigated whether hyperuricemia predicts uncontrolled hypertension through a large-scale prospective cohort study with hypertensive patients treated with fimasartan in the Republic of Korea (the Kanarb-Metabolic Syndrome study).Of the 10,601 hypertensive pati ...[more]

PMID: 27428212

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Project description:BackgroundHigh blood pressure represents a major public health problem. Worldwide, approximately one-fourth of the adult population has hypertension. Epidemiological and experimental studies suggest a link between hyperuricemia and hypertension. Hyperuricemia affects 25% to 40 % of individuals with untreated hypertension; a much lower prevalence has been reported in normotensives or in the general population. However, whether lowering serum uric acid (UA) might lower blood pressure (BP) is an unanswered question.ObjectivesTo determine whether UA-lowering agents reduce BP in patients with primary hypertension or prehypertension compared with placebo.Search methodsThe Cochrane Hypertension Information Specialist searched the following databases for randomized controlled trials up to February 2016: the Cochrane Hypertension Specialised Register, the Cochrane Central Register of Controlled Trials (CENTRAL) (2016, Issue 2), MEDLINE (from 1946), Embase (from 1974), the World Health Organization International Clinical Trials Registry Platform, and ClinicalTrials.gov. We also searched LILACS up to March 2016 and contacted authors of relevant papers regarding further published and unpublished work.Selection criteriaTo be included in this review, the studies had to meet the following criteria: 1) randomized or quasi-randomized, with a group assigned to receive a UA-lowering agent and another group assigned to receive placebo; 2) double-blind, single-blind or open-label; 3) parallel or cross-over trial; 4) cross-over trials had to have a washout period of at least two weeks; 5) minimum treatment duration of four weeks; 6) participants had to have a diagnosis of essential hypertension or prehypertension, and hyperuricemia (serum UA greater than 6 mg/dL in women, 7 mg/dL in men and 5.5 mg/dL in children/adolescents); 7) outcome measures assessed included change in clinic systolic, diastolic or 24-hour ambulatory BP.Data collection and analysisThe two review authors independently collected the data using a data extraction form, and resolved any disagreements via discussion. We assessed risk of bias using the Cochrane Collaboration' Risk of bias' tool.Main resultsIn this review update, we examined the abstracts of 349 identified papers and selected 21 for evaluation. We also identified three ongoing studies, the results of which are not yet available. Three other randomized controlled trials (RCTs) (two new), enrolling individuals with hypertension or prehypertension, and hyperuricemia, met the inclusion criteria for the review and were included in the meta-analysis. Low quality of evidence from three RCTs indicate no reduction in systolic (MD -6.2 mmHg, 95% CI -12.8 to 0.5) or diastolic (-3.9 mmHg, 95% CI -9.2 to 1.4) 24-hour ambulatory BP with UA-lowering drugs compared with placebo. Low quality of evidence from two RCTs reveal a reduction of systolic clinic BP (-8.43 mmHg, 95% CI -15.24 to -1.62) but not diastolic clinic BP (-6.45 mmHg, 95% CI -13.60 to 0.70). High quality of evidence from three RCTs indicates that serum UA levels were reduced by 3.1 mg/dL (95% CI 2.4 to 3.8) in the participants that received UA-lowering drugs. Very low quality of evidence from three RCTs suggests that withdrawals due to adverse effects were not increased with UA-lowering therapy (RR 1.86, 95% CI 0.43 to 8.10).Authors' conclusionsIn this updated systematic review, the RCT data available at present are insufficient to know whether UA-lowering therapy also lowers BP. More studies are needed.

Project description:Increased plasma uric acid (hyperuricemia) has been associated with worse outcomes for chronic kidney disease (CKD). But some attempts to control uric acid (UA) in large-cohort clinical trials did not produce clinically meaningful benefits for CKD. Some studies suggest that only hyperuricemia with crystals, but not asymptomatic hyperuricemia promotes the progression of CKD. Salt-sensitivity (SS) in blood pressure is a prevalent trait that is sexually dimorphic and results in kidney damage. But the connection between hyperuricemia and SS hypertension (HTN) is still unclear. Here we tested the connection between the two using both male and female Dahl SS rats, a well-establish model of SS HTN. We hypothesized that mild asymptomatic hyperuricemia is beneficial in controlling the progression of SS HTN. A uricase inhibitor, oxonic acid (2%) (Oxo) was used to induce hyperuricemia and high-salt (HS) (4% NaCl) diet was used to induce SS HTN. After 3 weeks, in response to oxonic acid supplementation, both sexes showed a significant increase of UA in plasma compared to their respective HS-only controls (Males: 0.63 ±0.07 vs. 2.17 ±0.34; Females: 0.78 ±0.15 vs. 2.04 ±0.35 mg/dl, HS vs. HS/oxo). Interestingly, only male HS/oxo rats showed a significant increase in uricosuria (Males: 0.23 ±0.03 vs. 0.45 ±0.06; Femaels: 0.26 ±0.06 vs. 0.26 ±0.001 UA/Cre, HS vs. HS/oxo). Moreover, the mild hyperuricemia was associated with a significant attenuation of the progression and magnitude of the mean arterial pressure in male but not female rats (Males: 157 ±3 vs. 136 ±3; Females: 155 ±6 vs. 154 ±5 mmHg, HS vs. HS/oxo). Xanthine oxidase (XO) is one of the enzymes that produce UA, and its activity has been shown to affect HTN as well. Therefore, we examined the level of XO activity in the plasma after the treatment. While there was no difference in the activity based on the diet within each sex, females had significantly lower levels of XO activity compared to males in each of the diets. To further investigate the beneficial phenotype seen in male rats, we evaluate changes in the progression of renal pathology. The HS/oxo group compared to the HS group had a lower kidney weight/body weight ratio and lower protein cast accumulation, indicating lower kidney damage. Furthermore, the HS/Oxo treated males had less oxidative damage in their tubules than the HS-only males. Bulk-RNA seq done on the male kidneys revealed that attenuated HTN phenotype was associated with an increased expression in Mas1 (MAS receptor), Klk-1 (Kallikrein-1), and Pcsk6 (PCSK6 enzyme) which can all lead to the activation of different vasodilatory pathways. Our study showed that in male but not female Dahl SS rats, asymptomatic mild hyperuricemia accompanied by hyperuricosuria ameliorates the progression of SS HTN and protects kidneys from further damage. Thus, our findings challenge the notion of hyperuricemia being inherently detrimental to health and highlight that this is an oversimplified view of UA’s role in disease.

Project description:IntroductionIn most treated patients with hypertension, a two or more drug combination is required to achieve adequate blood pressure (BP) control. In our study we assessed whether the combination of zofenopril + hydrochlorothiazide (HCTZ) was at least as effective as irbesartan + HCTZ in essential hypertensives with at least one additional cardiovascular risk factor, uncontrolled by a previous monotherapy.MethodsAfter a 2-week placebo washout, 361 treated hypertensive patients [office sitting diastolic BP (DBP), ≥90 mmHg], aged 18-75 years, were randomized double blind to 18-week treatment with zofenopril 30 mg plus HCTZ 12.5 mg or irbesartan 150 mg plus HCTZ 12.5 mg once daily, in an international, multicenter study. After the first 6 and 12 weeks, zofenopril and irbesartan doses could be doubled in non-normalized subjects. The primary study end point was the office sitting DBP reduction after 18 weeks of treatment. Secondary end points included office systolic BP (SBP), ambulatory BP and high sensitivity C-reactive protein (hs-CRP).ResultsThe between-treatment difference for office DBP averaged to +1.0 (95% CI -0.4, +0.8) mmHg (P = 0.150), the upper limit of the 95% confidence interval being inferior to the protocol-defined non-inferiority limit (3 mmHg). In the subset of patients with valid ambulatory BP, no difference in 24-h average DBP [n = 181; 6.7 (8.7, 4.6) zofenopril + HCTZ vs. 6.3 (8.8, 3.7) mmHg irbesartan + HCTZ, P = 0.810] and SBP reductions [11.7 (15.4, 8.0) vs. 12.6 (17.2, 8.0) mmHg, P = 0.758] were observed between the two treatment groups. hs-CRP was reduced by zofenopril + HCTZ [-0.52 (-1.05, 0.01) mg/L], while it was increased by irbesartan plus HCTZ [0.97 (0.29, 1.65) mg/L, P = 0.001 between treatments].ConclusionIn previously monotherapy-treated, uncontrolled patients with hypertension, zofenopril 30-60 mg + HCTZ 12.5 mg is as effective as irbesartan 150-300 mg plus HCTZ 12.5 mg, with the added value of a potential protective effect against vascular inflammation.

Project description:AbstractMedication nonadherence represents a modifiable risk factor for patients with hypertension. Identification of nonadherent patients could have significant clinical and economic implications in the management of uncontrolled hypertension.We analysed the results of 174 urinary adherence screens from patients referred to Addenbrooke's Hospital, Cambridge, for uncontrolled hypertension. Cases were identified for evaluation by results of liquid chromatography-tandem mass spectrometry of urine samples (males: 91; females: 83; age range: 17-87). We performed a binary logistic regression analysis for nonadherence using age, sex, and number of medications prescribed (both antihypertensives and non-antihypertensives separately) as independent predictors. Rates of nonadherence for individual antihypertensive drugs were calculated if prescribed to ≥10 patients.The overall rate of nonadherence to one or more prescribed antihypertensive medications was 40.3%. 14.4% of all patients were nonadherent to all prescribed antihypertensive medications (complete nonadherence), whereas 25.9% of all patients were nonadherent to at least 1, (but not all) prescribed antihypertensive medications (partial nonadherence). 72% of patients were prescribed ≥3 antihypertensives And for every increase in the number of antihypertensive medications prescribed, nonadherence increased with adjusted odds ratios of 2.9 (P < .001). Logistic regression showed that women were 3.3 times more likely to be nonadherent (P = .004). Polypharmacy (≥6 medications prescribed for hypertension and/or concomitant comorbidities) was prevalent in 52%. Bendroflumethiazide and chlortalidone demonstrated the highest and lowest nonadherences respectively (45.5% and 11.8%).Rate of nonadherence in patients with hypertension was significantly impacted by sex and number of antihypertensive medications prescribed. Understanding these factors is crucial in identifying and managing nonadherence.

Project description:BackgroundRacial/ethnic differences in the associations of smoking with uncontrolled blood pressure (BP) and its subtypes (isolated uncontrolled systolic BP (SBP), uncontrolled systolic-diastolic BP, and isolated uncontrolled diastolic BP (DBP)) have not been investigated among diagnosed hypertensive subjects.MethodsA sample of 7,586 hypertensive patients aged ≥18 years were selected from the National Health and Nutrition Examination Survey 1999-2010. Race/ethnicity was classified into Hispanic, non-Hispanic white, and non-Hispanic black. Smoking was categorized as never smoking, ex-smoking, and current smoking. Uncontrolled BP was determined as SBP≥140 or DBP≥90 mm Hg. Isolated uncontrolled SBP was defined as SBP≥140 and DBP<90 mm Hg, uncontrolled SDBP as SBP≥140 and DBP≥90 mm Hg, and isolated uncontrolled DBP as SBP<140 and DBP≥90 mm Hg. Adjusted odds ratios (ORs) with 95% confidence intervals (CIs) of uncontrolled BP and its subtypes were calculated using weighted logistic regression models.ResultsThe interaction effect of race and smoking was significant after adjustment for the full potential confounding covariates (Adjusted p = 0.0412). Compared to never smokers, current smokers were 29% less likely to have uncontrolled BP in non-Hispanic whites (OR = 0.71, 95% CI = 0.56-0.90), although the likelihood for uncontrolled BP is the same for smokers and never smokers in Hispanics and non-Hispanic blacks. Current smokers were 26% less likely than never smokers to have isolated uncontrolled SBP in non-Hispanic whites (OR = 0.74, 95% CI = 0.58-0.95). However, current smoking is associated with an increased likelihood of uncontrolled systolic-diastolic BP in non-Hispanic blacks, and current smokers in this group were 70% more likely to have uncontrolled systolic-diastolic BP than never smokers (OR = 1.70, 95% CI = 1.10-2.65).ConclusionThe associations between current smoking and uncontrolled BP differed over race/ethnicity. Health practitioners may need to be especially vigilant with non-Hispanic black smokers with diagnosed hypertension.

Dataset Information

Hyperuricemia and uncontrolled hypertension in treated hypertensive patients: K-MetS Study.

Publications

Hyperuricemia and uncontrolled hypertension in treated hypertensive patients: K-MetS Study.

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