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Estimated 24-Hour Urinary Sodium Excretion and Incident Cardiovascular Disease and Mortality Among 398 628 Individuals in UK Biobank
Hypertension ( IF 8.3 ) Pub Date : 2020-09-01 , DOI: 10.1161/hypertensionaha.119.14302
Paul Elliott 1, 2, 3, 4, 5 , David C Muller 1 , Deborah Schneider-Luftman 1, 2 , Raha Pazoki 1, 2 , Evangelos Evangelou 1, 2, 6 , Abbas Dehghan 1, 2 , Bruce Neal 1, 7 , Ioanna Tzoulaki 1, 2, 6
Affiliation  

Supplemental Digital Content is available in the text. We report on an analysis to explore the association between estimated 24-hour urinary sodium excretion (surrogate for sodium intake) and incident cardiovascular disease (CVD) and mortality. Data were obtained from 398 628 UK Biobank prospective cohort study participants (40–69 years) recruited between 2006 and 2010, with no history of CVD, renal disease, diabetes mellitus or cancer, and cardiovascular events and mortality recorded during follow-up. Hazard ratios between 24-hour sodium excretion were estimated from spot urinary sodium concentrations across incident CVD and its components and all-cause and cause-specific mortality. In restricted cubic splines analyses, there was little evidence for an association between estimated 24-hour sodium excretion and CVD, coronary heart disease, or stroke; hazard ratios for CVD (95% CIs) for the 15th and 85th percentiles (2.5 and 4.2 g/day, respectively) compared with the 50th percentile of estimated sodium excretion (3.2 g/day) were 1.05 (1.01–1.10) and 0.96 (0.92–1.00), respectively. An inverse association was observed with heart failure, but that was no longer apparent in sensitivity analysis. A J-shaped association was observed between estimated sodium excretion and mortality. Our findings do not support a J-shaped association of estimated sodium excretion with CVD, although such an association was apparent for all-cause and cause-specific mortality across a wide range of diseases. Reasons for these differences are unclear; methodological limitations, including the use of estimating equations based on spot urinary data, need to be considered in interpreting our findings.

中文翻译:

英国生物库中 398 628 人的 24 小时尿钠排泄量和心血管疾病事件及死亡率的估计值

文本中提供了补充数字内容。我们报告了一项分析,以探讨估计的 24 小时尿钠排泄量(钠摄入量的替代指标)与心血管疾病 (CVD) 事件和死亡率之间的关联。数据来自 2006 年至 2010 年间招募的 398 628 名英国生物银行前瞻性队列研究参与者(40-69 岁),他们没有 CVD、肾病、糖尿病或癌症病史,也没有随访期间记录的心血管事件和死亡率。24 小时钠排泄之间的风险比是根据 CVD 事件及其成分的现场尿钠浓度以及全因和原因特异性死亡率估算的。在受限三次样条分析中,几乎没有证据表明估计的 24 小时钠排泄量与 CVD、冠心病、或中风;第 15 个和第 85 个百分位数(分别为 2.5 和 4.2 g/天)的 CVD 风险比(95% CI)与第 50 个百分位数的估计钠排泄量(3.2 g/天)相比分别为 1.05 (1.01–1.10) 和 0.96 ( 0.92-1.00),分别。观察到与心力衰竭呈负相关,但在敏感性分析中不再明显。在估计的钠排泄和死亡率之间观察到 J 形关联。我们的研究结果不支持估计的钠排泄与 CVD 之间存在 J 型关联,尽管这种关联对于多种疾病的全因死亡率和特定原因死亡率而言是显而易见的。这些差异的原因尚不清楚;在解释我们的发现时需要考虑方法学的局限性,包括使用基于现场尿液数据的估计方程。第 15 个和第 85 个百分位数(分别为 2.5 和 4.2 g/天)的 CVD 风险比(95% CI)与第 50 个百分位数的估计钠排泄量(3.2 g/天)相比分别为 1.05 (1.01–1.10) 和 0.96 ( 0.92-1.00),分别。观察到与心力衰竭呈负相关,但在敏感性分析中不再明显。在估计的钠排泄和死亡率之间观察到 J 形关联。我们的研究结果不支持估计的钠排泄与 CVD 之间存在 J 型关联,尽管这种关联对于多种疾病的全因死亡率和特定原因死亡率而言是显而易见的。这些差异的原因尚不清楚;在解释我们的发现时需要考虑方法学的局限性,包括使用基于现场尿液数据的估计方程。第 15 个和第 85 个百分位数(分别为 2.5 和 4.2 g/天)的 CVD 风险比(95% CI)与第 50 个百分位数的估计钠排泄量(3.2 g/天)相比分别为 1.05 (1.01–1.10) 和 0.96 ( 0.92-1.00),分别。观察到与心力衰竭呈负相关,但在敏感性分析中不再明显。在估计的钠排泄和死亡率之间观察到 J 形关联。我们的研究结果不支持估计的钠排泄与 CVD 之间存在 J 型关联,尽管这种关联对于多种疾病的全因死亡率和特定原因死亡率而言是显而易见的。这些差异的原因尚不清楚;在解释我们的发现时需要考虑方法学的局限性,包括使用基于现场尿液数据的估计方程。
更新日期:2020-09-01
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