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Association of Sodium with Obstructive Sleep Apnea: The ELSA-Brasil Study.

RATIONALE
Excessive sodium may have a role in the pathogenesis of obstructive sleep apnea (OSA) for patients with hypervolemic conditions, but it is unclear whether this is valid for all patients with OSA, including those with no significant comorbidities.


OBJECTIVES
To test the association of urinary sodium and OSA in a large sample of participants from the ELSA-Brasil Study. In addition, we stratified the analysis participants according to the presence of hypertension.


METHODS
In this cross-sectional study, OSA was defined by an apnea-hypopnea index, AHI, ≥15 events/h. A validated 12-hour urine collection as representative of the 24-hour period was obtained from all participants to measure sodium excretion. We performed a logistic regression analysis to test the association of urinary sodium excretion with OSA (dependent variable) adjusting for age, sex, race and income, glomerular filtration rate, diabetes, physical activity, and anti-hypertensive classes related to sodium excretion. To address potential residual factors that may influence sodium excretion, we performed additional analysis replacing sodium excretion for salt intake (food frequency questionnaire) using the same models.


RESULTS
We studied 1,946 participants (age 49±8 years; 43.4% men). A third of them had OSA. Compared to no OSA, OSA participants presented with higher sodium excretion (1.66 [1.19-2.29] vs. 1.99 [1.44-2.69] g/12h; p<0.001). After adjustments for confounding factors, we found no overall significant associations of sodium excretion with OSA (OR 1.09; 95% CI 0.97-1.23; p=0.150). Regardless of the OSA status, the sodium excretion was higher in hypertensive than in normotensives participants (1.93 [1.35-2.64] vs. 1.71 [1.22-2.37] g/12h). An independent association of sodium excretion with OSA was observed in patients with hypertension only (OR 1.326; 95% IC 1.067-1.648; p=0.011) but the interaction of urinary sodium with hypertension was not significant (p=0.37). The analysis of salt intake revealed consistent findings.


CONCLUSION
The potential role of sodium in the pathogenesis of OSA seems to be modest and limited for those with higher salt intake and consequently, higher fluid retention such as observed in patients with hypertension.