There is a paucity of quality evidence regarding the effects of sodium restriction in patients with CKD, particularly in patients with pre-end stage CKD, where controlling modifiable risk factors may be especially important for delaying CKD progression and cardiovascular events. We conducted a double-blind placebo-controlled randomized crossover trial assessing the effects of high versus low sodium intake on ambulatory BP, 24-hour protein and albumin excretion, fluid status (body composition monitor), renin and aldosterone levels, and arterial stiffness (pulse wave velocity and augmentation index) in 20 adult patients with hypertensive stage 3–4 CKD as phase 1 of the LowSALT CKD study. Overall, salt restriction resulted in statistically significant and clinically important reductions in BP (mean reduction of systolic/diastolic BP, 10/4 mm Hg; 95% confidence interval, 5 to 15 /1 to 6 mm Hg), extracellular fluid volume, albuminuria, and proteinuria in patients with moderate-to-severe CKD. The magnitude of change was more pronounced than the magnitude reported in patients without CKD, suggesting that patients with CKD are particularly salt sensitive. Although studies with longer intervention times and larger sample sizes are needed to confirm these benefits, this study indicates that sodium restriction should be emphasized in the management of patients with CKD as a means to reduce cardiovascular risk and risk for CKD progression.

Food product reformulation is promoted as an effective strategy to reduce population salt intake and address the associated burden of chronic disease. Salt has a number of functions in food processing, including impacting upon physical and sensory properties. Manufacturers must ensure that reformulation of foods to reduce salt does not compromise consumer acceptability. The aim of this systematic review is to determine to what extent foods can be reduced in salt without detrimental effect on consumer acceptability. Fifty studies reported on salt reduction, replacement or compensation in processed meats, breads, cheeses, soups, and miscellaneous products. For each product category, levels of salt reduction were collapsed into four groups: <40%, 40–59%, 60–79% and ≥80%. Random effects meta-analyses conducted on salt-reduced products showed that salt could be reduced by approximately 40% in breads [mean change in acceptability for reduction <40% (−0.27, 95% confidence interval (CI) −0.62, 0.08; p = 0.13)] and approximately 70% in processed meats [mean change in acceptability for reductions 60–69% (−0.18, 95% CI −0.44, 0.07; p = 0.15)] without significantly impacting consumer acceptability. Results varied for other products. These results will support manufacturers to make greater reductions in salt when reformulating food products, which in turn will contribute to a healthier food supply.

Excess salt intake is a major cause of raised blood pressure—the leading risk factor for death and disability worldwide. Although behaviour change interventions such as awareness campaigns and health education programs are implemented to reduce salt intake, their effectiveness is unclear. This global systematic review investigates the impact of population-level behaviour change interventions that aim to reduce salt intake. A search for published and grey literature was conducted using PubMed, Cochrane Library, Embase, Web of Science, Sage, Scopus, OpenGrey, Google Scholar and other relevant organizations’ websites. Studies were included if 1) published between 2005 and 2015; 2) the education or awareness-raising interventions were aimed at the population or sub-population and 3) salt intake and/or salt-related behaviours were outcome measures. Study and intervention characteristics were extracted for the descriptive synthesis and study quality was assessed. Twenty two studies involving 41,448 participants were included. Most were conducted in high income countries (n = 16), targeting adults (n = 21) in the general population (n = 16). Behaviour change interventions were categorised as health education interventions (n = 14), public awareness campaigns (n = 4) and multi-component interventions (including both health education and awareness campaigns, n = 4). 19 of the 22 studies demonstrated significant reductions in estimated salt intake and/or improvement in salt-related behaviours. All studies showed high risk of bias in one or more domains. Of the 10 higher quality studies, 5 found a significant effect on salt intake or salt behaviours based on the more objective outcome assessment method. Based on moderate quality of evidence, population-level behaviour change interventions can improve salt-related behaviours and/or reduce salt intake. However, closer analysis of higher quality studies show inconsistent evidence of the effectiveness and limited effect sizes suggest the implementation of education and awareness-raising interventions alone are unlikely to be adequate in reducing population salt intake to the recommended levels. A framework which guides rigorous research and evaluation of population-level interventions in real-world settings would help understand and support more effective implementation of interventions to reduce salt intake.

Dietary sodium restriction is a key management strategy in chronic kidney disease (CKD). Recent evidence has demonstrated short-term reduction in blood pressure (BP) and proteinuria with sodium restriction, however the effect on other cardiovascular-related risk factors requires investigation in CKD. The LowSALT CKD study involved 20 hypertensive Stage III-IV CKD patients counselled by a dietitian to consume a low-sodium diet (<100 mmol/day). The study was a randomised crossover trial comparing 2 weeks of high-sodium (additional 120 mmol sodium tablets) and low-sodium intake (placebo). Measurements were taken after each crossover arm including BP (peripheral and central), adipokines (inflammation markers and adiponectin), volume markers (extracellular-to-intracellular [E/I] fluid ratio; N-terminal pro-brain natriuretic peptide [NT-proBNP]), kidney function (estimated Glomerular Filtration Rate [eGFR]) and proteinuria (urine protein-creatinine ratio [PCR] and albumin-creatinine ratio [ACR]). Outcomes were compared using paired t-test for each cross-over arm. BP-lowering benefits of a low-sodium intake (peripheral BP (mean ± SD) 148/82 ± 21/12 mmHg) from high-sodium (159/87 ± 15/10 mmHg) intake were reflected in central BP and a reduction in eGFR, PCR, ACR, NTproBNP and E/I ratio. There was no change in inflammatory markers, total or high molecular weight adiponectin. Short-term benefits of sodium restriction on BP were reflected in significant change in kidney function and fluid volume parameters. Larger, long-term adequately powered trials in CKD are necessary to confirm these results. Universal Trial Number U1111-1125-2149 registered on 13/10/2011; Australian New Zealand Clinical Trials Registry Number ACTRN12611001097932 registered on 21/10/2011.