Key result
Serum sodium shows no association with blood pressure progression or incident hypertension.
Why the study?
Cross-sectional studies have suggested higher serum sodium levels may be a marker of elevated blood pressure, but whether serum sodium levels relate to the risk of developing hypertension in the community was unclear.
Does higher baseline serum sodium concentration increase the risk of longitudinal blood pressure progression or incident hypertension in nonhypertensive community-dwelling adults?
Cohort (n=2,172)
No
Does higher baseline serum sodium concentration increase the risk of longitudinal blood pressure progression or incident hypertension in nonhypertensive community-dwelling adults?
Serum sodium concentration is tightly regulated and is not a useful biomarker for predicting future blood pressure progression or incident hypertension in the general nonhypertensive population.
Answers are grounded in this paper and cite their sources.
Serum sodium should not guide hypertension risk prediction in nonhypertensive adults; challenges cross-sectional associations and leaves open causal roles.
BACKGROUND: Recent cross-sectional studies have suggested that higher serum sodium levels may be a marker of elevated blood pressure. It is unclear whether serum sodium levels are related to the risk of developing hypertension in the community. METHODS: We investigated the association of serum sodium with longitudinal blood pressure tracking and incidence of hypertension in 2172 nonhypertensive Framingham Offspring Study participants (mean age 42 years, 54% women). We defined an increase in blood pressure as an increment of at least one category (as defined by the Joint National Committee on Prevention, Detection, Evaluation, and Treatment of High Blood Pressure), and incident hypertension as a systolic blood pressure of at least 140 or a diastolic blood pressure of at least 90 mmHg, or use of antihypertensive medications. Serum sodium was analyzed as a continuous variable, and as categories. RESULTS: Cross-sectionally, serum sodium was not associated with systolic or diastolic blood pressure (P exceeded 0.10). On follow-up (mean 4.4 years), 805 participants (37%, 418 women) progressed by at least one blood pressure category, and 318 (15%, 155 women) developed new-onset hypertension. In multivariable logistic regression analyses (adjusting for age, sex, baseline blood pressure, diabetes, BMI, weight gain and smoking), serum sodium was not associated with blood pressure progression (odds ratio per SD increment 0.93, 95% confidence interval 0.85-1.03), or with hypertension incidence (odds ratio per SD increment 0.94, 95% confidence interval 0.82-1.08). CONCLUSION: In our large community-based sample, serum sodium was not associated with blood pressure cross-sectionally, or with blood pressure tracking or hypertension incidence longitudinally.
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Lago et al. (2008) conducted a cohort in Blood pressure progression and incident hypertension in nonhypertensive individuals (n=2,172). Serum sodium concentration (per SD increment and across 4 categories) vs. Middle two categories of serum sodium (or within 1 SD of the mean) as referent was evaluated on Progression in blood pressure by one or more JNC VI categories at 4-year follow-up (OR 0.93, 95% CI 0.85-1.03). Serum sodium concentration was not associated with longitudinal blood pressure progression (OR 0.93 per SD increment, 95% CI 0.85-1.03) or incident hypertension (OR 0.94, 95% CI 0.82-1.08).
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