Does reduction of dietary sodium improve patient outcomes in chronic kidney disease?

2019 ◽  
Vol Publish Ahead of Print ◽  
Author(s):  
Ravneet Jaura ◽  
Steven Elrod
2015 ◽  
Vol 41 (3) ◽  
pp. 200-209 ◽  
Author(s):  
Sang-Woong Han ◽  
Anca Tilea ◽  
Brenda W. Gillespie ◽  
Fredric O. Finkelstein ◽  
Margaret A. Kiser ◽  
...  

Background: Chronic kidney disease (CKD) patients are prone to both hypo- and hypernatremia. Little has been published on the epidemiology of hypo- and hypernatremia in ambulatory patients with non-dialysis CKD. Methods: Data collected in two contemporaneous CKD cohort studies, the Renal Research Institute (RRI)-CKD study (n = 834) and the Study of Treatment of Renal Insufficiency: Data and Evaluation (STRIDE) (n = 1,348) were combined and analyzed to study the association between serum sodium (Na+) and clinical outcomes. Results: Baseline estimated glomerular filtration rate (eGFR) and Na+ were 26 ± 11 ml/min/1.73 m2 and 140.2 ± 3.4 mEq/l, respectively. The prevalence of Na+ ≤135 mEq/l and ≥144 mEq/l was 6 and 16%, respectively. Higher baseline Na+ was significantly associated with male sex, older age, systolic blood pressure, BMI, serum albumin, presence of heart failure, and lower eGFR. The risk of end-stage renal disease (ESRD) was marginally significantly higher among patients with Na+ ≤135 mEq/l, compared with 140< Na+ <144 mEq/l (referent), in time-dependent models (adjusted hazard ratio, HR = 1.52, p = 0.06). Mortality risk was significantly greater at 135< Na+ ≤140 mEq/l (adjusted HR = 1.68, p = 0.02) and Na+ ≥144 mEq/l (adjusted HR = 2.01, p = 0.01). Conclusion: CKD patients with Na+ ≤135 mEq/l were at a higher risk for progression to ESRD, whereas both lower and higher Na+ levels were associated with a higher risk of mortality. While caring for CKD patients, greater attention to serum sodium levels by clinicians is warranted and could potentially help improve patient outcomes.


2010 ◽  
Vol 45 (4) ◽  
pp. 304-313
Author(s):  
Indu Lew ◽  
Tamira Mullarkey ◽  
Robert T. Adamson ◽  
Maria E. Ashton ◽  
Shilpa Amara

Iron deficiency anemia (IDA), as a result of chronic kidney disease (CKD), has become a worldwide public health issue with increasing prevalence in the United States. An awareness of clinical practice guidelines and safety profiles of intravenous (IV) iron products enables health care professionals to improve patient outcomes in the treatment of CKD-associated IDA. Selection of appropriate IV iron therapy in all patient care settings may encompass considerations such as product premedication and test-dose requirements, preparation and administration, monitoring parameters, safety concerns, cost of care, patient education, and patient self-administration when appropriate. More specifically, a medication use process (prescribing, preparing, dispensing, administering, monitoring, and specific outcomes) should be applied by health systems during the evaluation process to achieve optimal patient outcomes. This performance improvement process serves to promote appropriate medication therapy, improve patient safety, control costs of therapy, stimulate improvements in processes, and provide educational opportunities. This article, the second of a two-part series, describes elements of the medication use process for care of CKD patients with IDA, whereas the preceding article in this series discusses the optimization of IV iron therapy in CKD patients and compares the four parenteral iron agents available on the market.


2013 ◽  
Vol 29 (3) ◽  
pp. 644-649 ◽  
Author(s):  
H. C. Rayner ◽  
J. Baharani ◽  
I. Dasgupta ◽  
V. Suresh ◽  
R. M. Temple ◽  
...  

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.


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.


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.


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