What is the issue?
People with chronic kidney disease (CKD) have a reduced kidney function that persists over time. People with CKD are at increased risk of heart disease and worsening kidney function which can lead to the need for dialysis or kidney transplantation to survive. High salt intake is linked to risk factors for both heart disease and worsening kidney function, including high blood pressure, excess protein in the urine and fluid overload. Therefore reducing salt intake may help reduce risk of heart disease and preserve kidney function. We aimed to assess the benefits and harms of reducing salt intake for people with CKD.
What did we do?
We searched the evidence up to October 2020 to find randomised controlled trials comparing two or more levels of salt intake in adults with CKD, including those in the earlier stages of CKD, those treated with dialysis, and those who had received a kidney transplant.
What did we find?
We found 21 studies that included 1197 adults with CKD (725 in low salt and 725 people in high salt group). Study participants included adults who were in the early stages of CKD (779 people in 12 studies), adults who were on dialysis (363 people in seven studies), and adult kidney transplant recipients (55 people in two studies). The average study duration was seven weeks, ranging from one to 36 weeks. We did not find any studies that measured the effect on the incidence of death, heart disease, or need for dialysis or kidney transplantation. Instead, we found studies that measured risk factors for these outcomes.
We found that lowering salt intake reduced blood pressure and protein in the urine in people with CKD. Lowering salt intake may reduce extracellular fluid volume in the earlier stages of CKD. The evidence is very uncertain about the effects on body weight and reductions in blood pressure medications. The effect on kidney function measures was mixed. Lower salt intake may increase dizziness due to low blood pressure.
We found that reducing salt intake reduced risk factors for heart disease and worsening kidney function in people with CKD in the short term. We could not find evidence of the longer term effects of reducing salt intake, which meant we were unable to determine the direct effects of salt intake on death, heart disease, or need for dialysis or kidney transplantation. We need more high quality research in these areas.
We found high certainty evidence that salt reduction reduced blood pressure in people with CKD, and albuminuria in people with earlier stage CKD in the short-term. If such reductions could be maintained long-term, this effect may translate to clinically significant reductions in CKD progression and cardiovascular events. Research into the long-term effects of sodium-restricted diet for people with CKD is warranted.
Evidence indicates that reducing dietary salt may reduce the incidence of heart disease and delay decline in kidney function in people with chronic kidney disease (CKD). This is an update of a review first published in 2015.
To evaluate the benefits and harms of altering dietary salt for adults with CKD.
We searched the Cochrane Kidney and Transplant Register of Studies up to 6 October 2020 through contact with the Information Specialist using search terms relevant to this review. Studies in the Register are identified through searches of CENTRAL, MEDLINE, and EMBASE, conference proceedings, the International Clinical Trials Register (ICTRP) Search Portal and ClinicalTrials.gov.
Randomised controlled trials comparing two or more levels of salt intake in adults with any stage of CKD.
Two authors independently assessed studies for eligibility, conducted risk of bias evaluation and evaluated confidence in the evidence using GRADE. Results were summarised using random effects models as risk ratios (RR) for dichotomous outcomes or mean differences (MD) for continuous outcomes, with 95% confidence intervals (CI).
We included 21 studies (1197 randomised participants), 12 in the earlier stages of CKD (779 randomised participants), seven in dialysis (363 randomised participants) and two in post-transplant (55 randomised participants). Selection bias was low in seven studies, high in one and unclear in 13. Performance and detection biases were low in four studies, high in two, and unclear in 15. Attrition and reporting biases were low in 10 studies, high in three and unclear in eight.
Because duration of the included studies was too short (1 to 36 weeks) to test the effect of salt restriction on endpoints such as death, cardiovascular events or CKD progression, changes in salt intake on blood pressure and other secondary risk factors were examined.
Reducing salt by mean -73.51 mmol/day (95% CI -92.76 to -54.27), equivalent to 4.2 g or 1690 mg sodium/day, reduced systolic/diastolic blood pressure by -6.91/-3.91 mm Hg (95% CI -8.82 to -4.99/-4.80 to -3.02; 19 studies, 1405 participants; high certainty evidence). Albuminuria was reduced by 36% (95% CI 26 to 44) in six studies, five of which were carried out in people in the earlier stages of CKD (MD -0.44, 95% CI -0.58 to -0.30; 501 participants; high certainty evidence). The evidence is very uncertain about the effect of lower salt intake on weight, as the weight change observed (-1.32 kg, 95% CI -1.94 to -0.70; 12 studies, 759 participants) may have been due to fluid volume, lean tissue, or body fat. Lower salt intake may reduce extracellular fluid volume in the earlier stages of CKD (-0.87 L, 95% CI -1.17 to -0.58; 3 studies; 187 participants; low certainty evidence). The evidence is very uncertain about the effect of lower salt intake on reduction in antihypertensive dose (RR 2.45, 95% CI 0.98 to 6.08; 8 studies; 754 participants). Lower salt intake may lead to symptomatic hypotension (RR 6.70, 95% CI 2.40 to 18.69; 6 studies; 678 participants; moderate certainty evidence). Data were sparse for other types of adverse events.