Key result
Decreasing sodium intake from >100 to ≤100 mmol/d over 1 year was associated with a significantly greater decrease in mean arterial pressure compared to increasing sodium intake (-7.44 vs -0.23 mmHg).
Why the study?
Does decreasing sodium intake improve blood pressure control and arterial stiffness in patients with early-stage CKD in primary care?
Cohort (n=1,607)
Yes
Does decreasing sodium intake improve blood pressure control and arterial stiffness in patients with early-stage CKD in primary care?
Decreasing sodium intake to below 100 mmol/d over 1 year is independently associated with improved blood pressure control and reduced arterial stiffness in patients with early-stage CKD in primary care.
May support sodium reduction to ≤100 mmol/d for BP control in early CKD; hypothesis-generating, needs RCTs before practice change.
Decreasing sodium intake has been associated with improvements in blood pressure (BP) and proteinuria, two important risk factors for CVD and chronic kidney disease (CKD) progression. We aimed to investigate the role of sodium intake by examining the effect of changes in sodium intake over 1 year on BP and proteinuria in people with early stage CKD. From thirty-two general practices, 1607 patients with previous estimated glomerular filtration rate of 59-30 ml/min per 1.73 m² and mean age of 72.9 (sd 9.0) years were recruited. Clinical assessment, urine and serum biochemistry testing were performed at baseline and after 1 year. Sodium intake was estimated from early morning urine specimens using an equation validated for this study population. We found that compared with people who increased their sodium intake from ≤ 100 to >100 mmol/d over 1 year, people who decreased their intake from >100 to ≤ 100 mmol/d evidenced a greater decrease in all BP variables (Δmean arterial pressure (ΔMAP) = -7.44 (SD 10.1) v. -0.23 (SD 10.4) mmHg; P<0.001) as well as in pulse wave velocity (ΔPWV = -0.47 (SD 1.3) v. 0.08 (SD 1.88) m/s; P<0.05). Albuminuria improved only in albuminuric patients who decreased their sodium intake. BP improved in people who maintained low sodium intake at both times and in those with persistent high intake, but the number of anti-hypertensive increased only in the higher sodium intake group, and PWV improved only in participants with lower sodium intake. Decreasing sodium intake was an independent determinant of ΔMAP. Although more evidence is needed, our results support the benefits of reducing and maintaining sodium intake below 100 mmol/d (2.3-2.4 g/d) in people with early stages of CKD.
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Nerbass et al. (2015) conducted a cohort in chronic kidney disease (n=1,607). Decreased sodium intake (from >100 to ≤100 mmol/d) vs. Increased sodium intake (from ≤100 to >100 mmol/d) was evaluated on Change in mean arterial pressure (ΔMAP) (p=<0.001). Decreasing sodium intake from >100 to ≤100 mmol/d over 1 year was associated with a significantly greater decrease in mean arterial pressure compared to increasing sodium intake (-7.44 vs -0.23 mmHg).
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