School of Medicine, University of California San Diego, San Diego, California.
School of Medicine, University of California San Diego, San Diego, California; Division of Nephrology-Hypertension, Department of Medicine, University of California San Diego, San Diego, California; Department of Family Medicine and Public Health, University of California San Diego, San Diego, California; Veterans Affairs San Diego Healthcare System, San Diego, California.
J Ren Nutr. 2018 Mar;28(2):125-128. doi: 10.1053/j.jrn.2017.07.002. Epub 2017 Aug 31.
In the kidney disease clinic setting, higher-than-usual blood pressure is often ascribed to recent dietary sodium indiscretion. While clinical trials demonstrate a clear relationship between salt intake and blood pressure on the population level, it is uncertain whether real-world variation in sodium intake within individual chronic kidney disease (CKD) patients is associated with fluctuations in blood pressure.
We analyzed data from the Phosphorus Normalization Trial, in which participants with CKD eating their usual diets completed at least three 24-hour urine collections over 9 months, from which we measured sodium. Blood pressure was measured at the time of 24-hour urine collections. For each individual participant, we assessed the slope of the relationship between sodium intake and mean arterial blood pressure (MAP).
Among 119 participants (mean age 67 years and mean estimated glomerular filtration rate 31 mL/minute/1.73 m), there was substantial variation in sodium intake as measured by 24-hour urine collections (mean intake 3,903 mg/day, standard deviation 1037 mg/day). Individual participants had highly variable associations between their sodium intake and their MAP; 47% (n = 56) had inverse associations between sodium and MAP, whereas the remainder had positive (salt-sensitive) associations.
Among CKD patients, there is substantial variation in sodium intake but no predictable relationship between dietary sodium and blood pressure in individuals. The frequent dismissal of elevated blood pressure readings as related to recent sodium intake in clinic may be a misapplication of large-scale population data to explain individual variability and may contribute to clinical inertia regarding high blood pressure treatment.
在肾脏疾病门诊中,通常将高于正常的血压归因于近期饮食中钠的摄入不当。虽然临床试验表明人群水平的盐摄入量与血压之间存在明确关系,但尚不确定个体慢性肾脏病(CKD)患者中实际钠摄入量的变化是否与血压波动有关。
我们分析了磷正常化试验的数据,该试验中,食用常规饮食的 CKD 患者在 9 个月内至少完成了 3 次 24 小时尿液收集,从中我们测量了钠。在进行 24 小时尿液收集时测量血压。对于每个个体参与者,我们评估了钠摄入量与平均动脉血压(MAP)之间关系的斜率。
在 119 名参与者(平均年龄 67 岁,平均估计肾小球滤过率 31ml/min/1.73m)中,通过 24 小时尿液收集测量的钠摄入量存在很大差异(平均摄入量为 3903mg/天,标准偏差为 1037mg/天)。个体参与者的钠摄入量与其 MAP 之间存在高度可变的关联;47%(n=56)的人存在钠与 MAP 之间的负相关,而其余人则存在正相关(盐敏感)。
在 CKD 患者中,钠摄入量存在很大差异,但个体之间饮食钠与血压之间没有可预测的关系。在临床上,经常将血压升高归因于近期钠摄入的情况可能是将大规模人群数据错误地应用于解释个体变异性,并可能导致高血压治疗的临床惰性。