Clinical Question

In patients with chronic kidney disease (CKD), does altering dietary salt intake affect risk factors or delay cardiovascular or renal complications?

Evidence-Based Answer

Reducing salt intake lowers blood pressure and reduces proteinuria in patients with CKD, but there is no evidence to determine whether lowering salt consumption leads to clinically significant reductions in end-stage renal disease, cardiovascular events, or all-cause mortality.¹ (Strength of Recommendation: C, based on a review of limited, though consistent, high-quality disease-oriented studies.)

Practice Pointers

CKD is a progressive condition often encountered by family physicians; it is both a complication of commonly encountered disease (e.g., hypertension, diabetes mellitus)² and an independent risk factor for cardiovascular disease.³ Patients with end-stage renal disease incur dramatically higher costs of care⁴ and have markedly increased mortality.⁵ Reliable interventions that may delay or prevent progression of CKD have not been fully elucidated. Restriction of dietary sodium (salt) intake is often recommended in these patients. This review sought to evaluate the benefits and harms of this intervention in patients with CKD.

The authors identified eight randomized controlled trials of parallel or crossover design that compared salt-restricted to higher-salt diets in 258 participants.¹ Some of the studies provided supplemental salt tablets to achieve a high-salt diet, and others used dietary counseling as the intervention for the low-salt diet. Patients on a low-salt diet had a reduction in blood pressure, with an effect size comparable to that of a single antihypertensive medication. Systolic blood pressure was reduced by 9 mm Hg (95% confidence interval, 6 to 11) and diastolic blood pressure was reduced by 4 mm Hg (95% confidence interval, 2 to 5).

The two studies conducted in patients with more advanced kidney disease (one study in patients receiving dialysis and one study in patients following transplant) showed similar results. Other biomarkers were assessed as secondary outcomes; only proteinuria showed consistent improvement with salt restriction, with relative risk reductions ranging from 21% to 49% across studies.

This review does not provide long-term evidence that reduced salt intake affects cardiovascular mortality or progression of kidney disease, because it was limited by the small number of studies of relatively short duration (one to 26 weeks) and heterogeneity among patient populations. Only two of the included studies assessed harms of salt reduction and found a nonsignificant increase in symptomatic hypotension. Other studies have found an increased risk of hospitalization and mortality associated with long-term sustained salt-restricted diets.⁶

This review is consistent with the current state of knowledge that salt restriction has a positive effect on disease-oriented markers such as blood pressure and proteinuria. Long-term effects of sustained dietary salt restriction are unknown. The general lack of data is reflected in the heterogeneity of dietary recommendations. The National Kidney Foundation recommends that dietary sodium intake be limited to less than 2,400 mg per day in patients with CKD and hypertension.⁷ A more recent clinical practice guideline issued by Kidney Disease: Improving Global Outcomes recommends lowering sodium intake to less than 2,000 mg per day in patients with CKD.⁸ Future work should be directed at clarifying the long-term effects of reduced salt intake and its desired effect on delaying progression of CKD to end-stage renal disease.

The practice recommendations in this activity are available at http://www.cochrane.org/CD010070.