A Self-management Approach for Dietary Sodium Restriction in Patients With CKD: A Randomized Controlled Trial

Humalda, Jelmer K.; Klaassen, Gerald; Meuleman, Yvette; Straathof, Elisabeth J.M.; Laverman, Gozewijn D.; Bos, Willem Jan W.; Vermeulen, Karin M.; Navis, Gerjan; Boog, Paul J.M. van der; Dijk, S. van; Verschuur, Lara C.; Henkemans, O.A. Blanson; Borst, Martin H. de; Otten, W.; Vries, Herman de

doi:10.1053/j.ajkd.2019.10.012

Cited by 45 publications

(59 citation statements)

References 24 publications

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“…Other possible trial designs include those that are internet based, though the feasibility of achieving a sufficient separation in sodium intake is unclear. One web based trial in patients with chronic kidney disease achieved a short term but not long term reduction in sodium excretion 55. However, as with all nutritional evidence, long term randomised trials are unlikely to be possible because of practical issues.…”

Section: How To Resolve the Controversymentioning

confidence: 99%

Sodium and health—concordance and controversy

Cook

MacGregor

et al. 2020

BMJ

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Section: How To Resolve the Controversymentioning

confidence: 99%

Sodium and health—concordance and controversy

Cook

MacGregor

et al. 2020

BMJ

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“…Epidemiological studies have verified an association between high salt intake and cardiovascular diseases ( Malta et al, 2018 ; Neupane et al, 2020 ; Xue et al, 2020 ). Clinical trials have demonstrated that reduced sodium intake was associated with a decrease in blood pressure, forming the basis for guideline thresholds ( Dorsch et al, 2018 ; Humalda et al, 2020 ; Xu et al, 2020 ). Salt sensitivity is defined as the association between sodium intake and the increased risk of cardiovascular diseases in certain populations or individuals.…”

Section: Introductionmentioning

confidence: 99%

Nitric Oxide Alleviated High Salt–Induced Cardiomyocyte Apoptosis and Autophagy Independent of Blood Pressure in Rats

Mao

et al. 2021

Front. Cell Dev. Biol.

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The present study aimed to explore whether high-salt diet (HSD) could cause cardiac damage independent of blood pressure, and whether nitric oxide (NO) could alleviate high-salt–induced cardiomyocyte apoptosis and autophagy in rats. The rats received 8% HSD in vivo. H9C2 cells or primary neonatal rat cardiomyocytes (NRCM) were treated with sodium chloride (NaCl) in vitro. The levels of cleaved-caspase 3/caspase 3, cleaved-caspase 8/caspase 8, Bax/Bcl2, LC3 II/LC3 I, Beclin-1 and autophagy related 7 (ATG7) were increased in the heart of HSD rats with hypertension (HTN), and in hypertension-prone (HP) and hypertension-resistant (HR) rats. Middle and high doses (50 and 100 mM) of NaCl increased the level of cleaved-caspase 3/caspase 3, cleaved-caspase 8/caspase 8, Bax/Bcl2, LC3 II/LC3 I, Beclin-1, and ATG7 in H9C2 cells and NRCM. The endothelial NO synthase (eNOS) level was increased, but p-eNOS level was reduced in the heart of HSD rats and H9C2 cells treated with 100 mM NaCl. The level of NO was reduced in the serum and heart of HSD rats. NO donor sodium nitroprusside (SNP) reversed the increases of cleaved-caspase 3/caspase 3, cleaved-caspase 8/caspase 8, Bax/Bcl2 induced by NaCl (100 mM) in H9C2 cells and NRCM. SNP treatment attenuated the increases of cleaved-caspase 3/caspase 3, Bax/Bcl2, LC3 II/LC3 I, Beclin-1, and ATG7 in the heart, but had no effect on the blood pressure of HSD rats with HR. These results demonstrated that HSD enhanced cardiac damage independently of blood pressure. Exogenous NO supplementarity could alleviate the high salt–induced apoptosis and autophagy in cardiomyocytes.

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“…Surprisingly, in the following maintenance phase, no difference in sodium intake was detected between the two groups, due to the inadvertent adoption of the intervention by the control group. Notably, the largest effect was reported in the first 3 months, when participants actively used the web-based self-management program [24].…”

Section: Adherence To Low-salt Diet: Definition and Assessment In Ckdmentioning

confidence: 98%

Sodium Intake and Chronic Kidney Disease

Borrelli

Provenzano

Gagliardi

et al. 2020

IJMS

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In Chronic Kidney Disease (CKD) patients, elevated blood pressure (BP) is a frequent finding and is traditionally considered a direct consequence of their sodium sensitivity. Indeed, sodium and fluid retention, causing hypervolemia, leads to the development of hypertension in CKD. On the other hand, in non-dialysis CKD patients, salt restriction reduces BP levels and enhances anti-proteinuric effect of renin–angiotensin–aldosterone system inhibitors in non-dialysis CKD patients. However, studies on the long-term effect of low salt diet (LSD) on cardio-renal prognosis showed controversial findings. The negative results might be the consequence of measurement bias (spot urine and/or single measurement), reverse epidemiology, as well as poor adherence to diet. In end-stage kidney disease (ESKD), dialysis remains the only effective means to remove dietary sodium intake. The mismatch between intake and removal of sodium leads to fluid overload, hypertension and left ventricular hypertrophy, therefore worsening the prognosis of ESKD patients. This imposes the implementation of a LSD in these patients, irrespective of the lack of trials proving the efficacy of this measure in these patients. LSD is, therefore, a rational and basic tool to correct fluid overload and hypertension in all CKD stages. The implementation of LSD should be personalized, similarly to diuretic treatment, keeping into account the volume status and true burden of hypertension evaluated by ambulatory BP monitoring.

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A Self-management Approach for Dietary Sodium Restriction in Patients With CKD: A Randomized Controlled Trial

Cited by 45 publications

References 24 publications

Sodium and health—concordance and controversy

Sodium and health—concordance and controversy

Nitric Oxide Alleviated High Salt–Induced Cardiomyocyte Apoptosis and Autophagy Independent of Blood Pressure in Rats

Sodium Intake and Chronic Kidney Disease

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