#1429 Daily urinary potassium excretion is not a fixed percentage of daily potassium intake

Abstract

Abstract Background and Aims High potassium intake is associated with a lower blood pressure and lower incidence of chronic kidney disease. Since a significant amount of potassium is lost via stool, the World Health Organization advices to multiply 24-hour renal potassium excretion by 1.3 for estimation of dietary intake. We analyzed whether this 1.3 factor for potassium intake varies in healthy volunteers and evaluated whether factors associated with tissue cation storage, namely sodium intake, aldosterone, cortisol and urine volume, affect the renal potassium excretion. Method We performed a post-hoc analysis of the long-term sodium balance studies Mars105 and Mars520. Ten healthy male participants consumed a fixed amount of salt (6, 9 and 12 grams/day for >29 days) and potassium (4 grams/day) for 105 (n = 4) and 205 days (n = 6). During the entire study period all urine was collected in 24-hour aliquots. We calculated the percentage of potassium intake that was excreted in the corresponding 24-hour urine collection during steady-state. We assessed whether this percentage was associated with sodium intake, potassium intake, urinary aldosterone, urinary cortisol and urine volume using a multivariable mixed-effects model. Results Overall, the median renal potassium excretion was 80% of potassium intake (IQR 65-97%; range 24-304%). This corresponds to a conversion factor of 1.25 (IQR 1.03-1.54). Within individual subjects we also observed a marked day-to-day variation in the percentage of renal potassium excretion: the average intraperson width of the IQR was 25%. A higher sodium intake was associated with an increased percentage of renal potassium excretion, whereas a higher potassium intake was associated with a decreased percentage of renal potassium excretion. A significant positive interaction between the effects of sodium and potassium intake was present (P < .001; Fig. A). Furthermore, urinary aldosterone (Fig. B), urinary cortisol (Fig. C) and urine volume (Fig. D) were positively associated with the percentage of renal potassium excretion. Conclusion The percentage of consumed potassium that is excreted via urine shows considerable intra- and inter-subject variability. During steady-state this percentage is independently affected by sodium intake, potassium intake, urinary aldosterone, urinary cortisol, and urine volume. Our results suggest that the WHO's fixed 1.3 conversion factor may lead to inaccurate estimations of potassium intake.