#5527 ALDOSTERONE, CORTISOL AND URINE VOLUME CAN EXPLAIN DISCREPANCIES BETWEEN DIETARY AND URINARY NA/K RATIO

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Abstract Background and Aims Increased urinary sodium-to-potassium (Na/K) ratio has been associated with chronic kidney disease. However, we demonstrated that urinary Na/K ratio does not accurately reflect dietary Na/K ratio. Rhythmic patterns of sodium storage and release from the skin interstitium are associated with aldosterone and cortisol levels and previous studies linked tissue sodium accumulation to water conservation. Therefore, we investigated whether the discrepancy between urinary and dietary Na/K ratio could be explained by these factors. Method For this post-hoc analysis, we used data from the long-term sodium balance studies Mars105 and Mars520. These studies collected 24-hour urine samples and controlled dietary salt intake for 105 (4 men) and 205 days (6 men) at levels of 6, 9 and 12 grams per day. We calculated the difference between urinary and dietary Na/K ratio. We tested whether this difference varied across salt intake levels in a linear mixed-effects model. Furthermore, we fitted two linear mixed-effect models to explain discrepancies between urinary and dietary Na/K ratio. In the first model, sodium intake, potassium intake, urinary aldosterone and urinary cortisol were fixed effects and for each factor random slopes per participant were allowed. In the second model, sodium intake, potassium intake and urine volume were fixed effects and for each factor random slopes per participant were allowed. Each salt intake level was assessed separately. Results The median difference between 24-hour urinary and dietary Na/K ratio was −0.21 (IQR −0.47 to 0.09). At higher salt intake levels the underestimation was significantly larger (mean difference −0.11, −0.22 and −0.36 for 6, 9 and 12 grams salt intake, respectively; P<0.001). At each salt intake level, higher urinary aldosterone was associated with underestimation of the dietary Na/K ratio (Figure 1A). In contrast, higher urinary cortisol and higher urine volume were associated with relative overestimation of the dietary Na/K ratio (Figure 1B and C, respectively). Conclusion The discrepancy between dietary and urinary Na/K ratio can be explained by sodium intake, aldosterone, cortisol and urine volume. This suggests that tissue sodium accumulation contributes to the inaccuracy of a single 24-hour urine collection for estimation of dietary sodium and potassium intake.