Key result
Estimated 24-h urinary sodium excretion was not associated with the incidence of a composite of end-stage kidney disease and kidney-related death (HR 1.03 per 1-g increment).
Why the study?
Sodium reduction lowers blood pressure and albuminuria, but the hypothesized association between sodium intake and kidney-related endpoints remained unproven.
Does lower 24-h urinary sodium excretion reduce the incidence of end-stage kidney disease and kidney-related death in community-dwelling adults?
Cohort (n=444,086)
Yes
Does lower 24-h urinary sodium excretion reduce the incidence of end-stage kidney disease and kidney-related death in community-dwelling adults?
Hazard Ratio: 1.03 (95% CI 0.91–1.16)
Estimated 24-h urinary sodium excretion was not associated with the incidence of ESKD or kidney-related death, challenging the hypothesis that population-level sodium reduction prevents hard kidney endpoints.
No association of estimated urinary sodium excretion with ESKD or kidney death; leaves open effects of sodium restriction on renal outcomes.
Background Sodium reduction lowers blood pressure and albuminuria, indicating a hypothesized but yet-to-be proven association between sodium intake and kidney-related endpoints. Objectives We aimed to investigate the associations of 24-h urinary sodium excretion, reflecting daily sodium intake, with kidney-related outcomes. Methods Prospective cohort of 444,086 middle- to early late-aged participants from the UK Biobank. The primary outcome was a composite of incident end-stage kidney disease (ESKD) and death due to a kidney-related cause, each of which was separately examined as a secondary outcome. Death due to a non-kidney related cause prior to ESKD was considered a competing event. Results The mean 24-h urinary sodium excretion estimated from spot urinary biomarkers was 3.3 g. During a median follow-up of 11.8 years, 1,256 composite events occurred. Multivariable-adjusted cause-specific hazards models showed that, with every 1-g increment in 24-h urinary sodium excretion, hazard ratios (95% confidence intervals) were 1.03 (0.91-1.16), 1.08 (0.88-1.32), and 1.01 (0.88-1.16) for the composite outcome, incident ESKD, and kidney-related death, respectively. Similar null results were observed when the exposure was treated as binary (<2 g/d vs. ≥2 g/d) or multicategorical (quartiles). Nonlinear associations were not detected with restricted cubic splines. The findings also held constant in prespecified sensitivity and subgroup analyses. Conclusions Estimated 24-h urinary sodium excretion was not linearly or nonlinearly associated with the incidence of ESKD or death due to kidney-related causes. Our findings did not support the hypothesized notion that sodium intake should be reduced to prevent kidney-related endpoints at the population level.
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Shan et al. (2021) conducted a cohort in End-stage kidney disease and kidney-related death (n=444,086). 24-h urinary sodium excretion vs. Per 1-g increment was evaluated on Composite of incident end-stage kidney disease (ESKD) and death due to a kidney-related cause (HR 1.03, 95% CI 0.91-1.16). Estimated 24-h urinary sodium excretion was not associated with the incidence of a composite of end-stage kidney disease and kidney-related death (HR 1.03 per 1-g increment).
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