Abstract
We compared the sodium intake and systolic blood pressure (SBP) relationship from complete 24-h urine samples determined by several methods: self-reported no-missed urine, creatinine index ≥0.7, measured 24-h urine creatinine (mCER) within 25% and 15% of Kawasaki predicted urine creatinine, and sex-specific mCER ranges (mCER 15–25 mg/kg/24-h for men; 10–20 mg/kg/24-h for women). We pooled 10,031 BP and 24-h urine sodium data from 2143 participants. We implemented multilevel linear models to illustrate the shape of the sodium–BP relationship using the restricted cubic spline (RCS) plots, and to assess the difference in mean SBP for a 100 mmol increase in 24-h urine sodium. The RCS plot illustrated an initial steep positive sodium–SBP relationship for all methods, followed by a less steep positive relationship for self-reported no-missed urine, creatinine index ≥0.7, and sex-specific mCER ranges; and a plateaued relationship for the two Kawasaki methods. Each 100 mmol/24-h increase in urinary sodium was associated with 0.64 (95% CI: 0.34, 0.94) mmHg higher SBP for self-reported no-missed urine, 0.68 (95% CI: 0.27, 1.08) mmHg higher SBP for creatinine index ≥0.7, 0.87 (95% CI: 0.07, 1.67) mmHg higher SBP for mCER within 25% Kawasaki predicted urine creatinine, 0.98 (95% CI: −0.07, 2.02) mmHg change in SBP for mCER within 15% Kawasaki predicted urine creatinine, and 1.96 (95% CI: 0.93, 2.99) mmHg higher SBP for sex-specific mCER ranges. Studies examining 24-h urine sodium in relation to health outcomes will have different results based on how urine collections are deemed as complete.
Highlights
High systolic blood pressure (SBP) is the largest single risk for death globally [1]
96% of the samples selected by mCER within 15% of Kawasaki predicted urine creatinine, and 94% of samples selected by mCER within 25% of Kawasaki predicted urine creatinine were included by creatinine index ≥0.7
73% of the samples included by the sex-specific range were included by creatinine index ≥0.7, and 67% included by mCER within 15% of Kawasaki predicted urine creatinine were included by the sex-specific mCER range
Summary
High systolic blood pressure (SBP) is the largest single risk for death globally [1]. High intake of sodium is an important dietary risk factor for high blood pressure (BP) [2]. High-quality epidemiological studies and systematic reviews show strong evidence that high sodium intake causes high BP and there is moderately strong evidence from clinical trials for causing cardiovascular diseases [3,4,5,6]. Long-term reduction in sodium intake is one of the most cost-effective strategies to reduce blood pressure and cardiovascular disease [9]. Accurate measurement of daily sodium intake is critical to evaluate the effectiveness of population-based sodium reduction interventions [3]. Sodium measurement in 24-h urine samples is the recommended method to assess daily sodium intake since 93% of ingested sodium is excreted within 24-h [10].
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