scholarly journals A Randomized Trial of Distal Diuretics versus Dietary Sodium Restriction for Hypertension in Chronic Kidney Disease

2020 ◽  
Vol 31 (3) ◽  
pp. 650-662 ◽  
Author(s):  
Dominique M. Bovée ◽  
Wesley J. Visser ◽  
Igor Middel ◽  
Anneke De Mik–van Egmond ◽  
Rick Greupink ◽  
...  
Keyword(s):  
Chronic Kidney Disease ◽  
Body Weight ◽  
Kidney Disease ◽  
Extracellular Volume ◽  
Free Water ◽  
Dietary Sodium ◽  
Sodium Restriction ◽  
Ckd Stage ◽  
Lower Egfr ◽  
Dietary Sodium Restriction

BackgroundDistal diuretics are considered less effective than loop diuretics in CKD. However, data to support this perception are limited.MethodsTo investigate whether distal diuretics are noninferior to dietary sodium restriction in reducing BP in patients with CKD stage G3 or G4 and hypertension, we conducted a 6-week, randomized, open-label crossover trial comparing amiloride/hydrochlorothiazide (5 mg/50 mg daily) with dietary sodium restriction (60 mmol per day). Antihypertension medication was discontinued for a 2-week period before randomization. We analyzed effects on BP, kidney function, and fluid balance and related this to renal clearance of diuretics.ResultsA total of 26 patients (with a mean eGFR of 39 ml/min per 1.73 m2) completed both treatments. Dietary sodium restriction reduced sodium excretion from 160 to 64 mmol per day. Diuretics produced a greater reduction in 24-hour systolic BP (SBP; from 138 to 124 mm Hg) compared with sodium restriction (from 134 to 129 mm Hg), as well as a significantly greater effect on extracellular water, eGFR, plasma renin, and aldosterone. Both interventions resulted in a similar decrease in body weight and NT-proBNP. Neither approaches decreased albuminuria significantly, whereas diuretics did significantly reduce urinary angiotensinogen and β2-microglobulin excretion. Although lower eGFR and higher plasma indoxyl sulfate correlated with lower diuretic clearance, the diuretic effects on body weight and BP at lower eGFR were maintained. During diuretic treatment, higher PGE2 excretion correlated with lower free water clearance, and four patients developed mild hyponatremia.ConclusionsDistal diuretics are noninferior to dietary sodium restriction in reducing BP and extracellular volume in CKD. Diuretic sensitivity in CKD is maintained despite lower diuretic clearance.Clinical Trial registry name and registration numberDD-study: Diet or Diuretics for Salt-sensitivity in Chronic Kidney Disease (DD), NCT02875886

Barriers and facilitators of dietary sodium restriction amongst Bangladeshi chronic kidney disease patients

2010 ◽  
Vol 24 (1) ◽  
pp. 86-95 ◽  
Author(s):  
I. de Brito-Ashurst ◽  
L. Perry ◽  
T. A. B. Sanders ◽  
J. E. Thomas ◽  
M. M. Yaqoob ◽  
...  
Keyword(s):  
Chronic Kidney Disease ◽  
Kidney Disease ◽  
Barriers And Facilitators ◽  
Dietary Sodium ◽  
Sodium Restriction ◽  
Dietary Sodium Restriction

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
Keyword(s):  
Chronic Kidney Disease ◽  
Kidney Disease ◽  
Sodium Intake ◽  
Epidemiological Studies ◽  
Dietary Sodium ◽  
Sodium Restriction ◽  
Restricted Diet ◽  
Salt Restriction ◽  
Low Sodium Diet ◽  
Low Sodium

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.

scholarly journals Dietary sodium restriction decreases urinary NGAL in older adults with moderately elevated systolic blood pressure free from chronic kidney disease

2020 ◽  
Vol 68 (7) ◽  
pp. 1271-1275
Author(s):  
Wei Wang ◽  
Michel Chonchol ◽  
Douglas R Seals ◽  
Kristen L Nowak
Keyword(s):  
Blood Pressure ◽  
Older Adults ◽  
Chronic Kidney Disease ◽  
Kidney Disease ◽  
Systolic Blood Pressure ◽  
Dietary Sodium ◽  
Sodium Restriction ◽  
Tubular Injury ◽  
Urinary Creatinine ◽  
Elevated Systolic Blood Pressure

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.

scholarly journals Enteral Ca-Intake May Be Low and Affects Serum-PTH-Levels in Pre-school Children With Chronic Kidney Disease

2021 ◽  
Vol 9 ◽  
Author(s):  
Lilith Schmitz ◽  
Pamela Hoermann ◽  
Birgit Trutnau ◽  
Augustina Jankauskiene ◽  
Ariane Zaloszyc ◽  
...  
Keyword(s):  
Chronic Kidney Disease ◽  
Body Weight ◽  
Kidney Disease ◽  
Data Collection ◽  
Phosphate Binders ◽  
Ca Deficiency ◽  
Ckd Stage ◽  
Pediatric Ckd ◽  
Data Collections ◽  
Dietary Data

Treatment of chronic kidney disease (CKD) mineral bone disorder (MBD) is challenging in growing children due to the high amount of calcium needed for normal bone mineralization and the required dietary phosphate restriction, which often includes intake of calcium-rich products such as milk. Therefore, enteral calcium-intake (Ca-I) was calculated.Patients: We looked at pediatric CKD-Patients aged 0–6 years.Design: We used a retrospective analysis of Ca-I from dietary data collections. Ca-I below 60% or above 100% of the D-A-CH and the KDOQI reference values were considered as severe Ca deficiency or Ca overload, respectively.Results: We had 41 children, median age 1.1 (range 0-5.8) years, body weight 7.3 (2.4–19.9) kg, and length 68 (48-105) cm at the time of first dietary data collection. Renal function was classified as CKD stage III in 20, IV in 28, V in 44, and VD in 142 dietary data collections. At the first dietary data collection, 5 children were in the CKD stage III, 10 in IV, 9 in V, and 17 were on dialysis. Only one child progressed to a higher CKD stage. In total, 234 dietary data collections were analyzed, and 65 follow-up collections were available from 33 children after a time interval of 26 (1–372) days. The median caloric intake was 120 (47–217)% of D-A-CH RDI. In 149 (63.6%) of the dietary data collections, enteral Ca-I was below the target (&lt;100% of the D-A-CH and KDOQI RDI). Severe Ca-deficiency was found in 11 (26%) and 4 (12%) of the children at the first and second dietary data collection, respectively. In total, 11 children were on Ca-containing phosphate binders. In dietary data collection 1 and 2, there were seven children. From these, 4/7 and 4/7 patients had an enteral total Ca-I above the 100% D-A-CH-limit or above the KDOQI limit, respectively. Absolute dietary Ca-I and Ca-I normalized to body weight correlated negatively with PTH (r = −0.196, p &lt; 0.005 and r = −0.13, p &lt; 0.05).Conclusion: Enteral Ca-I should repeatedly be monitored in CKD children because many may may otherwise be underexposed to enteral calcium and overexposed when calcium-containing phosphate binders are given. Our findings suggest a major impact of dietary calcium supply on bone health in pediatric CKD.

scholarly journals Acid retention in chronic kidney disease is inversely related to GFR

2018 ◽  
Vol 314 (5) ◽  
pp. F985-F991 ◽  
Author(s):  
Nimrit Goraya ◽  
Jan Simoni ◽  
Lauren N. Sager ◽  
Jessica Pruszynski ◽  
Donald E. Wesson
Keyword(s):  
Chronic Kidney Disease ◽  
Kidney Disease ◽  
Cross Sectional ◽  
Time Points ◽  
Ckd Stage ◽  
Lower Egfr ◽  
Gfr Decline ◽  
The Difference ◽  
Stage 1 ◽  
Egfr Decline

Greater H+ retention in animal models of chronic kidney disease (CKD) mediates faster glomerular filtration rate (GFR) decline and dietary H+ reduction slows eGFR decline in CKD patients with reduced eGFR and H+ retention due to the high acid (H+) diets of developed societies. We examined if H+ retention in CKD is inversely associated with estimated GFR (eGFR) using cross-sectional and longitudinal analysis of individuals with CKD stage 1 (>90 ml·min− 1·1.73 m−2), CKD stage 2 (60–89 ml/min per 1.73 m2), and CKD stage 3 (30–59 ml·min− 1·1.73 m−2) eGFR. H+ retention was assessed using the difference between observed and expected plasma total CO2 2 h after 0.5 meq/kg body wt oral NaHCO3. H+ retention was higher in CKD 2 vs. CKD 1 ( P < 0.01) and in CKD 3 vs. CKD 2 ( P < 0.02) at baseline and 5 yr, and was higher in CKD 2 vs. CKD 1 ( P < 0.01) at 10 yr. All groups had lower eGFR at subsequent time points ( P < 0.01) but H+ retention was not different among the three time points for CKD 1. By contrast, eGFR decrease was associated with higher H+ retention in CKD 2 at 5 yr ( P = 0.04) and 10 yr ( P < 0.01) and with higher H+ retention in CKD 3 at 5 yr ( P < 0.01). Yearly eGFR decline rate was faster in CKD 2 vs. CKD 1 ( P < 0.01) and in CKD 3 vs. CKD 2 ( P < 0.01). The data show that H+ retention is inversely associated with eGFR, with faster eGFR decline, and support the need for greater dietary H+ reduction therapy for CKD individuals with lower eGFR.

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