A polymorphism in the major gene regulating serum uric acid associates with clinic SBP and the white-coat effect in a family-based study

Mallamaci, Francesca; Testa, Alessandra; Leonardis, Daniela; Tripepi, Rocco; Pisano, Anna; Spoto, Belinda; Sanguedolce, Maria Cristina; Parlongo, Rosa Maria; Tripepi, Giovanni; Zoccali, Carmine

doi:10.1097/hjh.0000000000000224

Cited by 40 publications

(27 citation statements)

References 30 publications

Supporting

Mentioning

Contrasting

Unclassified

Order By: Relevance

“…Meanwhile, Mendelian randomization studies of genes known to influence uric acid levels have shown that while a genetic predisposition toward hyperuricemia is associated with high risk of gout, it is not associated with higher risk of hypertension (42). However, even these findings are inconsistent with some gene studies showing an association (43,44) and others showing no association (45–47). …”

Section: Discussionmentioning

confidence: 66%

Opposing effects of sodium intake on uric acid and blood pressure and their causal implication

Juraschek

Choi

Tang

et al. 2016

Journal of the American Society of Hypertension

View full text Add to dashboard Cite

Reducing uric acid is hypothesized to lower blood pressure, although evidence is inconsistent. In this ancillary of the DASH-Sodium trial, we examined whether sodium-induced changes in serum uric acid (SUA) were associated with changes in blood pressure. One hundred and three adults with pre- or stage 1 hypertension, were randomly assigned to receive either the DASH diet or a control diet (typical of the average American diet) and were fed each of 3 sodium levels (low, medium, and high) for 30 days in random order. Body weight was kept constant. SUA was measured at baseline and following each feeding period. Participants were 55% women and 75% black. Mean age was 52 (SD, 10) years, and mean SUA at baseline was 5.0 (SD, 1.3) mg/dL. Increasing sodium intake from low to high reduced SUA (−0.4 mg/dL; P < 0.001), but increased systolic (4.3 mm Hg; P < 0.001) and diastolic blood pressure (2.3 mm Hg; P < 0.001). Furthermore, changes in SUA were independent of changes in systolic (P = 0.15) and diastolic (P = 0.63) blood pressure, regardless of baseline blood pressure, baseline SUA, and randomized diet, as well as sodium sensitivity. While both SUA and blood pressure were influenced by sodium, a common environmental factor, their effects were in opposite directions and were unrelated to each other. These findings do not support a consistent causal relationship between SUA and BP.

show abstract

Section: Discussionmentioning

confidence: 66%

Opposing effects of sodium intake on uric acid and blood pressure and their causal implication

Juraschek

Choi

Tang

et al. 2016

Journal of the American Society of Hypertension

View full text Add to dashboard Cite

show abstract

“…These findings are in contrast to a study by Kleber et al [14] wherein a genetic risk score for high uric acid including eight gene variants was related with cardiovascular death. Moreover, in a study by Mallamaci et al [15], a different SNP in the SLC2A9 gene was associated with higher serum uric acid and higher SBP. This was in agreement with a careful analysis of an Amish cohort that revealed an association between a variant of the SLC2A9 gene and hypertension [16].…”

Section: Genetic and Environmental Factors Associated With Serum Uricmentioning

confidence: 96%

Serum uric acid and the risk of cardiovascular and renal disease

Borghi

Rosei

Bardin³

et al. 2015

Journal of Hypertension

420

277

View full text Add to dashboard Cite

Substantial evidence suggests that chronic hyperuricemia is an independent risk factor for hypertension, metabolic syndrome, chronic kidney disease (CKD) and cardiovascular diseases. This highlights the need for greater attention to serum uric acid levels when profiling patients, and suggests that the threshold above which uricemia is considered abnormal is 6 mg/dl, in light of the available evidence. Another important question is whether lowering serum uric acid can improve cardiovascular and renal outcomes, and what therapeutic mechanism of action could provide more clinical benefits to patients; the available literature shows a trend toward improvement associated with administration of urate-lowering drugs, in particular for the xanthine oxidase inhibitors. The demonstrated efficacy of urate-lowering therapy on outcomes other than gout flares leads to the consideration that treatment may be beneficial even in the absence of overt gout when hyperuricemia accompanies other clinical conditions, such as urate deposition, advanced CKD or cardiovascular risk factors.

show abstract

“…16 In addition, a recent article by Mallamaci et al 17 showed that rs7345555 variant in SLC2A9 gene is associated with systolic blood pressure in 449 cardiovascular complication-free individuals. In another Mendelian Randomization study, Palmer et al 18 studied the association of a variant in SLC2A9 gene with systolic and diastolic blood pressure.…”

Section: Discussionmentioning

confidence: 99%

Association of Uric Acid Genetic Risk Score With Blood Pressure

et al. 2014

View full text Add to dashboard Cite

Abstract-High levels of serum uric acid are associated with hypertension in observational studies. The aim of this study was to investigate the association of uric acid gene variants with blood pressure. We studied 5791 participants aged ≥55 years from the Rotterdam Study. Thirty gene variants identified for serum uric acid level were used to compile genetic risk score (GRS). We used linear regression models to investigate the association of the uric acid GRS with systolic and diastolic blood pressure in the whole study population and separately in participants with and without comorbidities and medication use. In the age-and sex-adjusted model, each SD increase in uric acid GRS was associated with 0.75 mm Hg lower systolic blood pressure (95% confidence interval, −1.31 to −0.19) and 0.42 mm Hg lower diastolic blood pressure (95% confidence interval, −0.72 to −0.13). The association did not attenuate after further adjustment for antihypertensive medication use and conventional cardiovascular risk factors. In subgroup analysis, the association of uric acid GRS with systolic blood pressure was significantly stronger in participants (n=885) on diuretic treatment (P for interaction, 0.007).In conclusion, we found that higher uric acid GRS is associated with lower systolic and diastolic blood pressure. Diuretics treatment may modify the association of uric acid genetic risk score and systolic blood pressure. Measurement of Serum Uric Acid and Blood PressureValues of serum uric acid were obtained from nonfasting blood samples, which were centrifuged for 10 minutes at 3000 rpm and subsequently stored at −20°C for 1 week. Uric acid activity was ascertained with Kone Diagnostica reagent kit and Kone autoanalyzer. To check the calibration, for every 10 samples, 3 control samples were included. In each run (100 samples), if the average values of the control samples were not within 2.5% of the true value, the run was repeated. Calibration was also done on day-by-day variation, which had to be within 5%. 10After a resting period of 5 minutes, blood pressure was measured twice in a single visit using a random-zero sphygmomanometer (cuff size of 32×17) on the right arm of participants in sitting position. The average of 2 measurements, separated by a count of the pulse rate, was used in the analyses. 11 CovariatesBody mass index was calculated by dividing weight in kilograms by height in meters squared. Information on alcohol consumption was acquired from the questionnaires. Participants were asked for the average daily consumption of alcohol. Medication use information was based on home interview. Diabetes mellitus was defined as the use of blood glucose-lowering medications or a random nonfasting glucose >11.1 mmol/L.12 Coronary heart disease was considered as having experienced myocardial infarction or undergone coronary revascularization procedures.13 Serum creatinine was determined using nonkinetic alkaline picrate (Jaffé) method. Estimated glomerular filtration rate was calculated using the simplified Modification of Di...

show abstract

A polymorphism in the major gene regulating serum uric acid associates with clinic SBP and the white-coat effect in a family-based study

Abstract: Results in this family-based study are compatible with the hypothesis that uric acid is a causal risk factor for hypertension. Trials testing uric acid-lowering interventions are needed to definitively establish the causal implication of hyperuricemia in human hypertension. [Corrected]

Cited by 40 publications

References 30 publications

Opposing effects of sodium intake on uric acid and blood pressure and their causal implication

Opposing effects of sodium intake on uric acid and blood pressure and their causal implication

Serum uric acid and the risk of cardiovascular and renal disease

Association of Uric Acid Genetic Risk Score With Blood Pressure

Contact Info

Product

Resources

About