Urinary sodium excretion and the risk of CVD: a community-based cohort study in Taiwan.

Yi-Jie Wang,Ming-Fong Chen,Yuan-Teh Lee,Hung-Ju Lin,Ta-Chen Su,Kuo-Liong Chien,Hsiu-Ching Hsu

doi:10.1017/s0007114521001768

Yi-Jie Wang, Ming-Fong Chen + Show 5 more

Open Access

https://doi.org/10.1017/s0007114521001768

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Abstract

Urinary Na excretion is a potential risk factor for CVD. However, the underlying biological mechanisms and effects of salt sensitivity are unclear. The purpose of this study was to characterise the relative contribution of biological factors to the Na-CVD association. A total of 2112 participants were enrolled in this study. Structured questionnaires and blood and urine samples were obtained. Twenty-four-hour Na excretion was estimated using a single overnight urine sample. Hypertension, the metabolic syndrome and overweight status were considered to indicate salt sensitivity. Cox proportional hazard models were used to investigate the effects of salt sensitivity on urinary Na excretion and CVD risk. The traditional mediation approach was used to calculate the proportion of mediation. The mean age (sd) of the 2112 participants was 54·5 (sd 12·2) years, and they were followed up for a mean of 14·1 (sd 8·1) years. Compared with those in the lowest quartile, the highest baseline urinary Na excretion (>4·2 g/24 h) was associated with a 43 % higher CVD risk (hazard ratio, 1·43; 95 % CI 1·02, 1·99). Participants with high urinary Na excretion, hypertension or the metabolic syndrome had a significantly high risk of CVD. The carotid intima-media thickness had the largest mediating effect (accounting for 35 % of the Na-CVD association), followed by systolic blood pressure (BP) (33 %), left ventricular mass (28 %) and diastolic BP (14 %). Higher urinary Na excretion increased the risk of CVD, which was explained largely by carotid media-thickness and systolic BP.

Highlights

CVD, including CHD and stroke, is a major leading cause of global mortality[1]
We aimed to investigate the association between urinary Na excretion and CVD risk, to explore the effects of salt sensitivity predisposing factors between urinary Na excretion and CVD risk and to quantify the contribution of novel biological factors to the Na–CVD association
The correlations between urinary Na and other risk factors, ranging from −0·018 for LDL-cholesterol to 0·110 for systolic BP (SBP), are shown in Supplementary Table S1

Summary

Introduction

CVD, including CHD and stroke, is a major leading cause of global mortality[1]. Practically, 50 % of the non-communicable disease-related deaths were attributed to CVD[2]. Na consumption was associated with CVD risk in both high-v.-low and dose–response meta-analyses[4]. A study suggested that low Na excretion is associated with high CVD mortality[12]. A few studies have indicated a non-significant relationship between dietary Na intake and CVD risk[14,15]. Mediation analysis linking Na intake and CVD risk is necessary. In nutritional epidemiology, both urinary Na excretion and dietary assessment tools are widely used to evaluate dietary Na intake. Spot, overnight and 24-h urinary Na excretion are the usual methods for assessing Na intake. The use of spot urine and overnight urine collection to estimate dietary Na intake is simpler and has been

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