scholarly journals Achieving Salt Restriction in Chronic Kidney Disease

2012 ◽  
Vol 2012 ◽  
pp. 1-10 ◽  
Author(s):  
Emma J. McMahon ◽  
Katrina L. Campbell ◽  
David W. Mudge ◽  
Judith D. Bauer

There is consistent evidence linking excessive dietary sodium intake to risk factors for cardiovascular disease and chronic kidney disease (CKD) progression in CKD patients; however, additional research is needed. In research trials and clinical practice, implementing and monitoring sodium intake present significant challenges. Epidemiological studies have shown that sodium intake remains high, and intervention studies have reported varied success with participant adherence to a sodium-restricted diet. Examining barriers to sodium restriction, as well as factors that predict adherence to a low sodium diet, can aid researchers and clinicians in implementing a sodium-restricted diet. In this paper, we critically review methods for measuring sodium intake with a specific focus on CKD patients, appraise dietary adherence, and factors that have optimized sodium restriction in key research trials and discuss barriers to sodium restriction and factors that must be considered when recommending a sodium-restricted diet.

1989 ◽  
Vol 256 (6) ◽  
pp. E863-E871 ◽  
Author(s):  
H. Hisa ◽  
Y. H. Chen ◽  
K. J. Radke ◽  
J. L. Izzo ◽  
C. D. Sladek ◽  
...  

These experiments evaluated the contribution of alpha- and beta-adrenergic stimulation to plasma renin activity (PRA) during early and long-term dietary sodium restriction, compared with normal sodium intake. Uninephrectomized conscious dogs with catheters in the aorta, vena cava, and remaining renal artery were studied during normal sodium diet (approximately 70 meq/day), after 2-3 days of low-sodium diet (5-7 meq/day), and after greater than or equal to 2 wk of low-sodium diet. Direct renal arterial (ira) infusion of phenoxybenzamine plus propranolol decreased PRA by similar proportions (39-48%) during all three states of dietary sodium intake. The PRA achieved after adrenergic blockade remained higher (P less than 0.05) during early and long-term sodium restriction than during normal sodium intake. The effect on PRA of ira infusion of propranolol alone was not different from that of phenoxybenzamine plus propranolol during normal or low-sodium diet, and the magnitude of decrease in PRA during low-sodium diet was the same whether propranolol (1 microgram.kg-1.min-1) was infused ira or intravenously. In summary, beta-adrenergic stimulation accounts for similar proportions of PRA during early and long-term dietary sodium restriction and during normal sodium intake. Renal alpha-adrenoceptors appear to play little or no role in control of PRA under these conditions.


2020 ◽  
Vol 73 (4) ◽  
Author(s):  
Mailson Marques de Sousa ◽  
Bernadete de Lourdes André Gouveia ◽  
Taciana da Costa Farias Almeida ◽  
Maria Eliane Moreira Freire ◽  
Francisco de Assis Brito Pereira de Melo ◽  
...  

ABSTRACT Objectives: to analyze the scientific production about sodium restriction in patients with heart failure. Methods: integrative literature review from articles published from 2007 to 2017, located in the CINAHL and Scopus databases. Results: thirteen studies were analyzed. Sodium intake restriction was associated with lower unfavorable clinical outcomes in patients with marked symptomatology. The 24-hour urine sodium dosage was the main tool to assess adherence to the low sodium diet. Conclusions: based on the studies included in this review, in symptomatic patients, dietary sodium restriction should be encouraged in clinical practice as a protective measure for health. However, in asymptomatic patients, it should be well studied.


1980 ◽  
Vol 238 (6) ◽  
pp. H889-H894 ◽  
Author(s):  
H. Munoz-Ramirez ◽  
R. E. Chatelain ◽  
F. M. Bumpus ◽  
P. A. Khairallah

In Sprague-Dawley rats with unilateral renal artery stenosis and an intact contralateral kidney, administration of a low-sodium diet did not prevent the development of hypertension. Despite an elevated blood pressure, hyponatremia, marked activation of the renin-angiotensin system, and increased hematocrit values, only 10% of the rats showed lesions of malignant hypertension. Systolic blood pressures of one- and two-kidney sham-operated rats fed a low-sodium diet were significantly higher than that of normotensive controls fed a normal diet. Uninephrectomy did not reduce plasma renin activity. The low-sodium diet increased plasma renin activity to about the same level in one- and two-kidney normotensive rats. However, the increase in plasma renin activity elicited by dietary sodium restriction was markedly less in one-kidney Goldblatt hypertension. Systolic blood pressure reached similar levels in one- and two-kidney Goldblatt hypertensive rats fed a low-sodium diet. These data indicate that a decrease in sodium intake does not prevent the development of two-kidney Goldblatt hypertension.


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.


1990 ◽  
Vol 124 (3) ◽  
pp. 507-513 ◽  
Author(s):  
E. A. P. Steegers ◽  
Th. J. Benraad ◽  
H. W. Jongsma ◽  
A. C. I. T. L. Tan ◽  
P. R. Hein

ABSTRACT The effects of dietary sodium restriction and posture on plasma concentrations of atrial natriuretic peptide (ANP), aldosterone and free aldosterone were investigated in ten women between weeks 29 and 33 of normal pregnancy. Hormone levels were studied during unrestricted sodium intake and on day 6 of a low sodium diet. On both occasions venous blood was obtained in the sitting as well as in the left lateral tilt position. Plasma concentrations of ANP during the unrestricted sodium intake were not raised compared with control values in healthy non-pregnant females. Recovery experiments showed no differences in the degradation of ANP in blood from pregnant and non-pregnant women. Plasma concentrations of ANP significantly decreased (by 32%) in response to the low sodium regime in both positions. Concentrations of aldosterone and free aldosterone (in women in the sitting position) increased twofold after sodium restriction. Mean values of ANP were higher in women in the left lateral tilt position that in those in the sitting position, but the difference was not significant. Concentrations of aldosterone and free aldosterone were significantly lower (by around 30%) in women in the left lateral tilt position compared with those in the sitting posture. Journal of Endocrinology (1990) 124, 507–513


2020 ◽  
Vol 68 (7) ◽  
pp. 1271-1275
Author(s):  
Wei Wang ◽  
Michel Chonchol ◽  
Douglas R Seals ◽  
Kristen L Nowak

Increased aortic stiffness may contribute to kidney damage by transferring excessive flow pulsatility to susceptible renal microvasculature, leading to constriction or vessel loss. We previously demonstrated that 5 weeks of dietary sodium restriction (DSR) reduces large-elastic artery stiffness as well as blood pressure in healthy middle-aged/older adults with moderately elevated systolic blood pressure (SBP) who are free from chronic kidney disease (CKD). We hypothesized that DSR in this cohort would also reduce urinary concentrations of renal tubular injury biomarkers, which predict incident CKD in the general population. We performed a post hoc analysis using stored 24 hours urine samples collected in 13 participants as part of a randomized, double-blind, crossover clinical trial of DSR (low sodium (LS) target: 50 mmol/day; normal sodium (NS) target: 150 mmol/day). Participants were 61±2 (mean±SEM) years (8 M/5 F) with a baseline blood pressure of 139±2/82±2 mm Hg and an estimated glomerular filtration rate of 79±3 mL/min/1.73 m2. Twenty-four hour urinary sodium excretion was reduced from 149±7 to 66±8 mmol/day during week 5. Despite having preserved kidney function, participants had a 31% reduction in urinary neutrophil gelatinase-associated lipocalin concentrations with just 5 weeks of DSR (LS: 2.8±0.6 vs NS: 4.2±0.8 ng/mL, p<0.05). Results were similar when normalized to urinary creatinine (urinary creatinine did not change between conditions). Concentrations of another kidney tubular injury biomarker, kidney injury molecule-1, were below the detectable limit in all but one sample. In conclusion, DSR reduces an established clinical biomarker of kidney tubular damage in adults with moderately elevated SBP who are free from prevalent kidney disease.


2013 ◽  
Vol 304 (3) ◽  
pp. R260-R266 ◽  
Author(s):  
Julie O'Neill ◽  
Alan Corbett ◽  
Edward J. Johns

Angiotensin II at the kidney regulates renal hemodynamic and excretory function, but the actions of an alternative metabolite, angiotensin (1–7), are less clear. This study investigated how manipulation of dietary sodium intake influenced the renal hemodynamic and excretory responses to intrarenal administration of angiotensin (1–7). Renal interstitial infusion of angiotensin (1–7) in anesthetized rats fed a normal salt intake had minimal effects on glomerular filtration rate but caused dose-related increases in urine flow and absolute and fractional sodium excretions ranging from 150 to 200%. In rats maintained for 2 wk on a low-sodium diet angiotensin (1–7) increased glomerular filtration rate by some 45%, but the diuretic and natriuretic responses were enhanced compared with those in rats on a normal sodium intake. By contrast, renal interstitial infusion of angiotensin (1–7) in rats maintained on a high-sodium intake had no effect on glomerular filtration rate, whereas the diuresis and natriuresis was markedly attenuated compared with those in rats fed either a normal or low-sodium diet. Plasma renin and angiotensin (1–7) were highest in the rats on the low-sodium diet and depressed in the rats on a high-sodium diet. These findings demonstrate that the renal hemodynamic and excretory responses to locally administered angiotensin (1–7) is dependent on the level of sodium intake and indirectly on the degree of activation of the renin-angiotensin system. The exact way in which angiotensin (1–7) exerts its effects may be dependent on the prevailing levels of angiotensin II and its receptor expression.


2019 ◽  
Vol 3 (Supplement_1) ◽  
Author(s):  
Katerina Lembrikova ◽  
Jonathan Leong ◽  
Georgiana Yang ◽  
Jessamine Fazli ◽  
Matthew Moy ◽  
...  

Abstract Objectives Adherence to the DASH (Dietary Approaches to Stop Hypertension) diet is associated with slower progression of kidney disease and decreased cardiovascular risk. We evaluated the association between knowledge of the DASH diet, DASH scores and nutrient intake in an inner-City population. Methods A random sample of patients from CKD (37), medicine/diabetes (18) and transplant clinic (31) was studied using 24-hour food recall, with nutrient intake analyzed by ASA24 software used to calculate DASH score. Patients were asked to respond to the question “Do you know what the DASH diet is?” Results Mean age was 63.8 ± 14.1yrs; 50% (43) had diabetes; 85% (73) had hypertension. 45% (39) reported income < $20 K/yr. 78% (67) stated that they were familiar with the DASH diet and defined it as decreased or “low” intake of sodium or salt (LoNa); 33% (28) were not familiar (NoAns). No patient was able to provide a correct explanation of the DASH diet as per the U.S. Department of Health and Human Services. Most common answers were “no salt” (26), “low salt” (38), 3 pts described the limit of sodium as 2gm (2) or <80 mg (1). Several patients commented “nasty” or “tasteless”. Mean DASH scores were poor and did not differ between the two groups (LoNa 3.75 ± 0.88 vs NoAns 3.8 ± 0.8, P = NS), nor did intake of sodium (LoNa 2.51 ±0.96 g vs NoAns 2.59 ± 1.3 g, P = NS). There was no difference in creatinine (LoNa 2.0 ± 1.6 vs 1.79 ± 1.3 mg/dl, P = NS), BMI, blood pressure systolic or diastolic, income, education or marital status between the two groups. 92% (57/62) pts in the LoNa group answered yes to the question “Are you familiar with a low sodium diet” vs 1% (1/16) in the NoAns group, P < 0.0001. Conclusions In our population of inner-City pts: 1. Understanding of the DASH diet was poor and equated with low or absent sodium intake with unclear understanding of actual amount. 2. DASH adherence was poor in all groups. 3. There was no difference in sodium intake between pts who stated that they knew about the DASH diet and those who did not. Neither group met the recommendations for < 2gm/d intake. 4. Pts who answered they knew what a DASH diet was were more likely to report familiarity with low sodium diets. 5. Confusion regarding the DASH diet and sodium restriction is common. As the DASH eating pattern is a more comprehensive change in dietary habits, targeted education may be needed in this population to improve overall adherence. Funding Sources none.


Sign in / Sign up

Export Citation Format

Share Document