P1072 - Association of Urine Na:K with Renin and Aldosterone at Baseline in Pediatric Hypertension

Background/Purpose: Pediatric hypertension is increasingly prevalent and increases the risk of organ injury. Increased sodium (Na) and decreased potassium (K) consumption likely contribute to hypertension, but data are limited in children. The urine Na-to-K ratio (UNaK) correlates with Na and K intake in adults, but again the data in children are limited. The renin-angiotensin-aldosterone system (RAAS) controls BP by regulating Na excretion, but the clinical correlation between UNaK and RAAS measurements is incompletely described. We hypothesized that UNaK negatively correlates with circulating RAAS levels.

Methods: Cross-sectional analysis was of baseline data from the Pediatric Hypertension Registry, a retrospective and prospective cohort of children with hypertensive disorders at a single tertiary care center. We recorded urine Na and K and calculated UNaK. We recorded serum creatinine, plasma renin activity (PRA), and serum aldosterone and calculated the aldosterone-to-renin ratio (ARR) and estimated glomerular filtration rate (eGFR). Variables were ln transformed when indicated to improve distributional characteristics. We used multivariable generalized linear regression models, adjusting for the potentially confounding factors race, body mass index z-score, and eGFR identified using directed acyclic graphs.

Results: Of 47 subjects, mean urine Na was 159.8 mmol/l (SD 60.2) and mean urine K was 66.2 mmol/l (SD 32.8); the median UNaK was 2.62 [IQR 1.77, 3.58]. After adjustment for confounding factors, UNaK (ln) was inversely associated with PRA (ln) (β: -0.62, 95% CI -1.14 to -0.11), and UNa was inversely associated with PRA (β: -0.08 pmol/l/h, -0.16 to -0.003). UNa (ln) and UNa were positively associated with ARR (ln) when adjusting for race and body mass index z-score (β: 1.06, 0.05 to 2.08; β: 0.02, 0.008 to 0.03, respectively), but adding eGFR to the models attenuated these results.

Conclusion: Urine Na:K excretion was inversely associated with PRA but positively associated with ARR, suggesting that increased dietary Na consumption may suppress the RAAS proximally in children with hypertension. The lack of a corresponding suppression of aldosterone may indicate that the downstream RAAS is dysregulated in children with hypertension. Further studies could help guide treatment for pediatric hypertension patients.