Altered dietary salt intake in chronic kidney disease
The quality of evidence is downgraded by study limitations (unclear allocation concealment, blinding and incomplete outcome data in half of the trials).
A Cochrane review 1 included 21 studies with a total of 1197 subjects. Duration of the included studies was too short (1 to 36 weeks) to test the effect of salt restriction on endpoints such as mortality, cardiovascular events or chronic kidney disease (CKD) progression. There was a significant reduction in 24 hour sodium excretion associated with low salt interventions (range 52 to 141 mmol) ( MD -105.86 mmol/d, 95% CI -119.20 to -92.51; 8 studies, n=258, I²=51%). Reducing salt intake significantly reduced systolic/diastolic blood pressure (-6.91/-3.91 mm Hg. 95% CI -8.82 to -4.99/-4.80 to -3.02; 19 studies, n=1405). Albuminuria was reduced by 36% (95% CI 26 to 44) in 6 studies, 5 of which were carried out in people in the earlier stages of CKD (MD -0.44, 95% CI -0.58 to -0.30; n=501; high certainty evidence).
A prospective cohort study 2 investigated whether an intensive low-salt diet education program effectively attenuated the rate of renal function decline in hypertensive patients with CKD (n=171). During the whole study period, the rate of renal function decline was significantly faster in the conventional group (0.11 ± 4.63 vs. -1.53 ± 3.04 mL/min/1.73 m²/year, p = 0.01). The percent of incremental change in serum creatinine ≥50% was 1.1% in the intensive group and 8.2% in the conventional group (p = 0.025), and the percent of decremental change in eGFR ≥30% was 3.3% in the intensive group and 11.1% in the conventional group (p= 0.048). With logistic regression analysis adjusted for related factors, conventional group showed a higher risk for deterioration in serum creatinine and eGFR.
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