Benefits of dietary sodium restriction in the management of chronic kidney disease

Krikken, Jan A.; Laverman, Gozewijn D.; Navis, Gerjan

doi:10.1097/mnh.0b013e3283312fc8

Cited by 106 publications

(76 citation statements)

References 84 publications

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“…To note, sodium overload increases ACE activity in renal and vascular tissues, which enhances vascular conversion of AngI to AngII and blunts the effects of ACE inhibition in rats and humans with high sodium intake. 29 Independent of BP control, enhanced intrarenal ACE activity has been associated with accelerated renal damage in several experimental models of chronic renal disease 30 and might explain at least part of the excess proteinuria and renal risk associated with high sodium intake observed in this study.…”

Section: Discussionmentioning

confidence: 97%

Sodium Intake, ACE Inhibition, and Progression to ESRD

Vegter

Perna

Postma

et al. 2012

Journal of the American Society of Nephrology

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High sodium intake limits the antihypertensive and antiproteinuric effects of angiotensin-converting enzyme (ACE) inhibitors in patients with CKD; however, whether dietary sodium also associates with progression to ESRD is unknown. We conducted a post hoc analysis of the first and second Ramipril Efficacy in Nephropathy trials to evaluate the association of sodium intake with proteinuria and progression to ESRD among 500 CKD patients without diabetes who were treated with ramipril (5 mg/d) and monitored with serial 24-hour urinary sodium and creatinine measurements. Urinary sodium/creatinine excretion defined low (,100 mEq/g), medium (100 to ,200 mEq/g), and high ($200 mEq/g) sodium intake. During a follow-up of .4.25 years, 92 individuals (18.4%) developed ESRD. Among those with low, medium, and high sodium intakes, the incidence of ESRD was 6.1 (95% confidence interval [95% CI], 3.8-9.7), 7.9 (95% CI, 6.1-10.2), and 18.2 (95% CI, 11.3-29.3) per 100 patient-years, respectively (P,0.001). Patients with high dietary sodium exhibited a blunted antiproteinuric effect of ACE inhibition despite similar BP among groups. Each 100-mEq/g increase in urinary sodium/creatinine excretion associated with a 1.61-fold (95% CI, 1.15-2.24) higher risk for ESRD; adjusting for baseline proteinuria attenuated this association to 1.38-fold (95% CI, 0.95-2.00). This association was independent from BP but was lost after adjusting for changes in proteinuria. In summary, among patients with CKD but without diabetes, high dietary salt (.14 g daily) seems to blunt the antiproteinuric effect of ACE inhibitor therapy and increase the risk for ESRD, independent of BP control.

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Section: Discussionmentioning

confidence: 97%

Sodium Intake, ACE Inhibition, and Progression to ESRD

Vegter

Perna

Postma

et al. 2012

Journal of the American Society of Nephrology

Self Cite

271

179

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“…Excess sodium intake in persons with chronic kidney disease (CKD) 8 is associated with hypertension and proteinuria, and existing studies suggest that sodium reduction produces clinically significant improvements in these endpoints (1)(2)(3)(4)(5). Although higher blood pressure and proteinuria are markers of CKD progression and cardiovascular disease events, data from epidemiologic studies with the use of 24-h urine sodium excretion as a marker of dietary sodium intake have reported conflicting results on CKD progression and cardiovascular disease events in CKD, with some studies suggesting that there are benefits from lower sodium intake, and others suggesting harm (3,(6)(7)(8)(9)(10)(11).…”

Section: Introductionmentioning

confidence: 99%

Spot urine sodium measurements do not accurately estimate dietary sodium intake in chronic kidney disease 1,2

Dougher

Rifkin

Anderson

et al. 2016

The American Journal of Clinical Nutrition

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Background: Sodium intake influences blood pressure and proteinuria, yet the impact on long-term outcomes is uncertain in chronic kidney disease (CKD). Accurate assessment is essential for clinical and public policy recommendations, but few large-scale studies use 24-h urine collections. Recent studies that used spot urine sodium and associated estimating equations suggest that they may provide a suitable alternative, but their accuracy in patients with CKD is unknown. Objective: We compared the accuracy of 4 equations [the Nerbass, INTERSALT (International Cooperative Study on Salt, Other Factors, and Blood Pressure), Tanaka, and Kawasaki equations] that use spot urine sodium to estimate 24-h sodium excretion in patients with moderate to advanced CKD. Design: We evaluated the accuracy of spot urine sodium to predict mean 24-h urine sodium excretion over 9 mo in 129 participants with stage 3-4 CKD. Spot morning urine sodium was used in 4 estimating equations. Bias, precision, and accuracy were assessed and compared across each equation. Results: The mean age of the participants was 67 y, 52% were female, and the mean estimated glomerular filtration rate was 31 6 9 mL $ min . The mean 6 SD number of 24-h urine collections was 3.5 6 0.8/participant, and the mean 24-h sodium excretion was 168.2 6 67.5 mmol/d. Although the Tanaka equation demonstrated the least bias (mean: 28.2 mmol/d), all 4 equations had poor precision and accuracy. The INTERSALT equation demonstrated the highest accuracy but derived an estimate only within 30% of mean measured sodium excretion in only 57% of observations. Bland-Altman plots revealed systematic bias with the Nerbass, INTERSALT, and Tanaka equations, underestimating sodium excretion when intake was high. Conclusion: These findings do not support the use of spot urine specimens to estimate dietary sodium intake in patients with CKD and research studies enriched with patients with CKD. The parent data for this study come from a clinical trial that was registered at clinicaltrials. gov as NCT00785629.Am J Clin Nutr 2016;104:298-305.

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“…[4][5][6][7][8][9][10][11][12] The association of hypertensive renal disease with dietary salt is well recognized. [13][14][15][16] Many patients with CKD have salt-sensitive hypertension. 17,18 Although restriction of dietary salt reduces albuminuria, [19][20][21][22] it is not clear how salt per se accelerates the progression of renal glomerular and tubulointerstitial fibrosis.…”

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confidence: 99%

A Salt-Induced Reno-Cerebral Reflex Activates Renin-Angiotensin Systems and Promotes CKD Progression

Cao

Wang

et al. 2015

Journal of the American Society of Nephrology

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Salt intake promotes progression of CKD by uncertain mechanisms. We hypothesized that a salt-induced reno-cerebral reflex activates a renin-angiotensin axis to promote CKD. Sham-operated and 5/6-nephrectomized rats received a normal-salt (0.4%), low-salt (0.02%), or high-salt (4%) diet for 2 weeks. High salt in 5/6-nephrectomized rats increased renal NADPH oxidase, inflammation, BP, and albuminuria. Furthermore, high salt activated the intrarenal and cerebral, but not the systemic, renin-angiotensin axes and increased the activity of renal sympathetic nerves and neurons in the forebrain of these rats. Renal fibrosis was increased 2.2-fold by high versus low salt, but intracerebroventricular tempol, losartan, or clonidine reduced this fibrosis by 65%, 69%, or 59%, respectively, and renal denervation or deafferentation reduced this fibrosis by 43% or 38%, respectively (all P,0.05). Salt-induced fibrosis persisted after normalization of BP with hydralazine. These data suggest that the renal and cerebral renin-angiotensin axes are interlinked by a reno-cerebral reflex that is activated by salt and promotes oxidative stress, fibrosis, and progression of CKD independent of BP.

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Benefits of dietary sodium restriction in the management of chronic kidney disease

Cited by 106 publications

References 84 publications

Sodium Intake, ACE Inhibition, and Progression to ESRD

Sodium Intake, ACE Inhibition, and Progression to ESRD

Spot urine sodium measurements do not accurately estimate dietary sodium intake in chronic kidney disease 1,2

A Salt-Induced Reno-Cerebral Reflex Activates Renin-Angiotensin Systems and Promotes CKD Progression

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