scholarly journals Total Body Sodium Balance in Chronic Kidney Disease

2021 ◽  
Vol 2021 ◽  
pp. 1-10
Author(s):  
Kylie Martin ◽  
Sven-Jean Tan ◽  
Nigel D. Toussaint

Excess sodium intake is a leading but modifiable risk factor for mortality, with implications on hypertension, inflammation, cardiovascular disease, and chronic kidney disease (CKD). This review will focus mainly on the limitations of current measurement methods of sodium balance particularly in patients with CKD who have complex sodium physiology. The suboptimal accuracy of sodium intake and excretion measurement is seemingly more marked with the evolving understanding of tissue (skin and muscle) sodium. Tissue sodium represents an extrarenal influence on sodium homeostasis with demonstrated clinical associations of hypertension and inflammation. Measurement of tissue sodium has been largely unexplored in patients with CKD. Development and adoption of more comprehensive and dynamic assessment of body sodium balance is needed to better understand sodium physiology in the human body and explore therapeutic strategies to improve the clinical outcomes in the CKD population.

2018 ◽  
Vol 315 (5) ◽  
pp. R945-R962 ◽  
Author(s):  
Peter Bie

The classical concepts of human sodium balance include 1) a total pool of Na+ of ≈4,200 mmol (total body sodium, TBS) distributed primarily in the extracellular fluid (ECV) and bone, 2) intake variations of 0.03 to ≈6 mmol·kg body mass−1·day−1, 3) asymptotic transitions between steady states with a halftime (T½) of 21 h, 4) changes in TBS driven by sodium intake measuring ≈1.3 day [ΔTBS/Δ(Na+ intake/day)], 5) adjustment of Na+ excretion to match any diet thus providing metabolic steady state, and 6) regulation of TBS via controlled excretion (90–95% renal) mediated by surrogate variables. The present focus areas include 1) uneven, nonosmotic distribution of increments in TBS primarily in “skin,” 2) long-term instability of TBS during constant Na+ intake, and 3) physiological regulation of renal Na+ excretion primarily by neurohumoral mechanisms dependent on ECV rather than arterial pressure. Under physiological conditions 1) the nonosmotic distribution of Na+ seems conceptually important, but quantitatively ill defined; 2) long-term variations in TBS represent significant deviations from steady state, but the importance is undetermined; and 3) the neurohumoral mechanisms of sodium homeostasis competing with pressure natriuresis are essential for systematic analysis of short-term and long-term regulation of TBS. Sodium homeostasis and blood pressure regulation are intimately related. Real progress is slow and will accelerate only through recognition of the present level of ignorance. Nonosmotic distribution of sodium, pressure natriuresis, and volume-mediated regulation of renal sodium excretion are essential intertwined concepts in need of clear definitions, conscious models, and future attention.


2018 ◽  
Vol 28 (2) ◽  
pp. 125-128
Author(s):  
Chetna M. Pathak ◽  
Joachim H. Ix ◽  
Cheryl A.M. Anderson ◽  
Tyler B. Woodell ◽  
Gerard Smits ◽  
...  

2019 ◽  
Vol 3 (Supplement_1) ◽  
Author(s):  
Matti Marklund ◽  
Gitanjali Singh ◽  
Raquel Greer ◽  
Frederick Cudhea ◽  
Kunihiro Matsushita ◽  
...  

Abstract Objectives Population-level replacement of discretionary (i.e, table/cooking) salt with potassium-enriched salt substitutes is a promising strategy to reduce blood pressure (BP) and prevent cardiovascular disease (CVD). This may be particularly impactful in countries like China where sodium intake is high, mainly from discretionary salt use, and where potassium intake low. However, hyperkalemia resulting from potassium-enriched substitutes and its adverse CVD consequences are of concern for those with chronic kidney disease (CKD). We aimed to estimate the benefits and risks of nationwide replacement of discretionary salt with potassium-enriched salt substitute on CVD mortality in Chinese CKD patients. Methods We used a comparative risk assessment framework and incorporated existing data and corresponding uncertainties from randomized trials, the China National Survey of CKD, the Global Burden of Disease study, and the CKD Prognosis Consortium. We estimated averted CVD mortality from reduced BP subsequent to salt substitution in CKD patients (defined as estimated glomerular filtration rate <60 mL/min per 1.73 m2) stratified by age and sex. Additional CVD deaths from hyperkalemia due to salt substitution were modelled in CKD patients stratified by kidney function. The robustness of the primary model was evaluated in a series of sensitivity analyses where key model assumptions and inputs were altered. Results Nationwide implementation of potassium-enriched salt substitution would prevent an estimated 29,735 (95% uncertainty interval: 13,018–50,403) CVD deaths/year among CKD patients by reducing BP, while the increased potassium intake could potentially produce an estimated 9791 (6078–15,941) additional hyperkalemia-related deaths (Table). The net effect would be 19,558 (3430–37,959) fewer CVD deaths/year, corresponding to 7.4% (1.4–13.4) of annual CVD deaths in Chinese CKD patients. Net benefits were consistent in sensitivity analyses (Table). Conclusions Despite the risks of hyperkalemia, nationwide potassium-enriched salt substitution in China would result in significant net benefit among CKD patients. Funding Sources This analysis was conducted in collaboration with Resolve to Save Lives, an initiative of Vital Strategies. Resolve to Save Lives is funded by Bloomberg Philanthropies, the Bill & Melinda Gates Foundation, and Gates Philanthropy Partners, which is funded with support from the Chan Zuckerberg Foundation. Funding for this work was also provided by the National Health and Medical Research Council and UNSW Sydney. Supporting Tables, Images and/or Graphs


2020 ◽  
Vol 21 (13) ◽  
pp. 4744
Author(s):  
Silvio Borrelli ◽  
Michele Provenzano ◽  
Ida Gagliardi ◽  
Michael Ashour ◽  
Maria Elena Liberti ◽  
...  

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.


2019 ◽  
Vol 33 (1) ◽  
pp. 119-127
Author(s):  
Nicos Mitsides ◽  
Damien McHugh ◽  
Agnieszka Swiecicka ◽  
Roshni Mitra ◽  
Paul Brenchley ◽  
...  

2009 ◽  
Vol 19 (1) ◽  
pp. 61-62 ◽  
Author(s):  
Eberhard Ritz ◽  
Nadezda Koleganova ◽  
Grzegorz Piecha

2014 ◽  
Vol 22 (4) ◽  
pp. 530-539 ◽  
Author(s):  
Yvette Meuleman ◽  
Lucia ten Brinke ◽  
Arjan J. Kwakernaak ◽  
Liffert Vogt ◽  
Joris I. Rotmans ◽  
...  

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