It is suggested that routinely measured clinical characteristics may help identify populations with greater expected blood pressure response to sodium reduction, and salt sensitivity varied across age, SBP, and body mass index strata.
Abstract
Background
Hypertension guidelines generally recommend uniform sodium restriction although determinants of salt sensitivity, or sodium-blood pressure responsiveness, remain incompletely quantified. We estimated the population sodium-blood pressure dose-response, identified clinical modifiers, quantified high salt sensitivity prevalence, and derived the number needed to restrict sodium intake to prevent 1 cardiovascular event across clinical strata.
Methods
PubMed, Embase, and Cochrane were searched from inception to April 2025 for sodium intervention trials and observational studies. Blood pressure response was standardized per 50-mmol/d sodium difference. Random-effects metaregression evaluated clinical modifiers. A highly salt-sensitive phenotype was defined a priori as a systolic blood pressure (SBP) decrease ≥3 mm Hg per 50-mmol/d reduction.
Results
We included 160 studies (255 estimates; n=16 443). Each 50-mmol/d higher urinary sodium excretion was associated with 1.76-mm Hg higher SBP (95% CI, 1.54-1.98). Age and baseline SBP were the strongest modifiers (0.41 mm Hg per 5 years; 0.23 mm Hg per 5 mm Hg). Salt-sensitive phenotype prevalence rose from 12.5% (age <40 years) to 56.5% (>60 years) and from 16.3% (SBP <120 mm Hg) to 54.1% (≥130 mm Hg). Under a policy-relevant 100-mmol/d sodium reduction, number needed to restrict ranged from ≈1334 in younger, normotensive, lean individuals (age <60 years, SBP <130 mm Hg, and body mass index <25 kg/m2) to ≈87 in older adults with hypertension and elevated body mass index (age ≥60 years, SBP ≥130 mm Hg, and body mass index ≥25 kg/m2), a 15-fold gradient.
Conclusions
Salt sensitivity varied across age, SBP, and body mass index strata. These findings suggest that routinely measured clinical characteristics may help identify populations with greater expected blood pressure response to sodium reduction.
The dietary Na/K ratio emerged as an independent risk marker for hypertension, with significant pathogenic effects observed exclusively in older adults, and the Na/K ratio exhibited synergistic effects with central adiposity in elevating hypertension risk.
Jianuo Yao· Theoretical and Natural Scie...· 0 citations
BACKGROUND AND AIMS
Hypertension carries the highest attributable risk for atrial fibrillation (AF) and strongly influences clinical outcomes such as stroke and death; however, the optimal blood pressure targets in individuals with AF remain poorly defined. We aimed to characterise the dose-response relationship between systolic blood pressure (SBP) and diastolic blood pressure (DBP) and ischaemic stroke, all-cause mortality, and intracranial haemorrhage.
METHODS
We systematically searched MEDLINE, Embase, and Scopus for studies reporting outcomes in AF stratified by SBP and DBP. A two-stage dose-response meta-analysis used restricted cubic splines to model non-linearity, with within-study correlation handled by the Greenland-Longnecker method.
RESULTS
Twenty-three studies (17 cohorts; n = 476,750) were included. SBP demonstrated a U-shaped association with all-cause mortality, with the lowest risk at 134 mmHg (RR 0.92, 0.86-0.98 versus 120 mmHg). DBP exhibited a J-shaped association, with the lowest risk at 83 mmHg (RR 0.99, 0.97-1.02). In contrast to mortality, the risks of ischaemic stroke, intracranial haemorrhage, and stroke or systemic embolism rose progressively with SBP, with a steepening gradient. At 140 versus 120 mmHg, the RR was 1.51 for intracranial haemorrhage against 1.08 for ischaemic stroke, reaching 1.99 versus 1.14 at 150 mmHg.
CONCLUSION
Systolic blood pressure exhibits a U-shaped relationship with all-cause mortality in patients with AF, balancing against a monotonic increase in ischemic stroke and intracranial haemorrhage at higher pressures. A pragmatic target SBP of 120-130 mmHg with DBP kept above approximately 75-80 mmHg, appears to optimize the balance between stroke prevention, bleeding risk, and survival.
E. Shahmohamadi, Alessandra Pina, Adrian D. Elliott et al.· Europace· 0 citations
Aldosterone dysregulation is an important contributor to suboptimal blood pressure control in essential hypertension. A retrospective study was conducted using electronic health record data from Baylor Scott and White Health. Adults ≥ 18 years with essential hypertension who underwent at least one measurement of serum aldosterone and plasma renin between January 1, 2022 -October 31, 2024 were included. Aldosterone dysregulation was defined as aldosterone-to-renin ratio (ARR) >10 using plasma renin activity (PRA) or ARR >1 using plasma renin concentration (PRC). Primary outcomes included uncontrolled hypertension (systolic blood pressure (SBP) ≥130 mmHg) and stage 2 hypertension (SBP ≥140 mmHg) based on office SBP obtained closest to and within one year following aldosterone measurement. Multivariable logistic regression models were adjusted for diabetes, encounter type, serum potassium, and aldosterone assay type. Among the 9129 patients (age 58.7 [15.7] years; women 4720 [51.7%]), aldosterone dysregulation was present in 39.4% patients, and was more prevalent among those with uncontrolled versus controlled hypertension (41.5% vs 31.9%, respectively). Aldosterone dysregulation was associated with uncontrolled hypertension (odds ratio [OR] 1.40, 95% confidence interval [CI] 1.26-1.56) and stage 2 hypertension (OR 1.38; 95% CI 1.26-1.50) in adjusted analysis. Aldosterone dysregulation was more common in those receiving multiple antihypertensives (44.2% on ≥4 agents, 40.8% on 3, 36.4% on 2, and 33.9% on 1). In conclusion, aldosterone dysregulation is common in patients with essential hypertension and is associated with suboptimal blood pressure control. Currently available treatments may not fully address aldosterone dysregulation.
Javed Butler, K. Hammonds, Muhammad Sameer Arshad et al.· American Journal of Cardiolo...· 0 citations
The identification of a high-risk SSI, based on 24-hour ABPM, is validated as a generalizable implementable approach for the clinical diagnosis of the SSBP, with a potential greater clinical diagnostic value in hypertensive versus normotensive individuals.
Xiangyu Zheng, Leonardo Máximo Cardoso, Christopher Dieffenthaller et al.· American Journal of Physiolo...· 0 citations
We evaluated the efficacy and safety of baxdrostat in adults with uncontrolled or resistant hypertension. We searched PubMed, Scopus, Web of Science, and Cochrane CENTRAL from inception to January 2026. We included randomized controlled trials that involved hypertension patients with resistance type and compared baxdrostat versus placebo. The primary outcomes were the changes in mean seated systolic blood pressure and diastolic blood pressure. Secondary outcomes included changes in estimated glomerular filtration rate (eGFR), serum potassium, and serum aldosterone. Three randomized controlled trials were finally included, comprising 1264 patients were followed for 12-24 weeks. Compared with placebo, baxdrostat reduced seated systolic blood pressure by 8.62 mm Hg [mean difference (MD) = -8.62, 95% confidence interval (CI), -10.55 to -6.70, P < 0.001] and seated diastolic blood pressure by 3.55 mm Hg (MD = -3.55, 95% CI, -4.81 to -2.28, P < 0.001). Baxdrostat lowered serum aldosterone by 4.03 ng/dL, reduced eGFR by 5.49 mL/min/1.73 m2, and increased serum potassium by 0.39 mmol/L. However, baxdrostat was associated with higher adverse events compared with the placebo. Baxdrostat lowers blood pressure and aldosterone levels in uncontrolled and resistant hypertension but increases potassium and modestly reduces eGFR, supporting careful laboratory monitoring and longer trials to evaluate long-term clinical outcomes.
A. Gadelmawla, A. W. Hageen, R. Rateb et al.· Cardiology in Review· 0 citations
