Background and objectives
High serum sodium concentration has been proven to boost T cell inflammatory responses, thus increasing the production of pro-inflammatory cytokines as well. We are not aware that the relationship between dietary salt intake and systemic inflammation has already been explored in population-based studies. The goal of this study was to explore the association between urinary sodium excretion, as a proxy for dietary salt intake and circulating inflammatory cytokines in the population based SKIPOGH cohort. Furthermore, we also explored the association of urinary potassium excretion with circulating inflammatory cytokines and its potential modifying effect on systemic inflammation.
Methods
For this study, we used data from SKIPOGH (Swiss Kidney Project on Genes in Hypertension), which is a family and population-based cohort study that examines the genetic determinants of BP.(1) SKIPOGH employs the same methodology as that implemented and validated in the EPOGH study. We explored through statistical analyses the association between urinary excretion of sodium and potassium and the various inflammatory cytokines that are IL6, IFNg, TNFα, IL10, IL1b and CRP.
Results
We have identified the relationship between urinary sodium and the different inflammatory cytokines, as well as for the urinary potassium. Overall, we observed significant negative associations of elevated IL10 and TNFα levels with 24-hour and daytime urinary sodium excretions in 1055 people aged 18 to 90 years randomly selected from the general population. The direction of the associations was similar for IL6 and IFNg but results were not statistically significant. By contrast, elevated IL1b levels tended to be associated positively with 24-hour and night-time urinary Na excretions. Elevated CRP levels were not associated with urinary Na excretions.
Conclusion
We observed a negative association between 24-hour and daytime urinary sodium and potassium excretion and IL6, IL10, IFNg and TNFα. However, it was only statistically significant for IL10 and TNFα. They also suggested a positive association for nighttime urinary excretion for IL6, IL10, IFNg and IL1b, but not statistically significant. A significant negative association between daytime urinary potassium excretion and IL6, CRP and IL1b was found. No association were found for TNFα and IL10 for both day and night potassium excretions, and a positive association for nighttime IL6, CRP, IL1B and IFNg, although only significant for IL6. Altogether, our results do not suggest that elevated sodium intake is associated with higher systemic inflammation in the general Swiss adult population.