A higher urinary sodium-to-potassium ratio was significantly associated with elevated BNP levels, with the highest tertile showing a 2.24-fold higher prevalence of BNP ≥35 pg/mL compared to the lowest tertile.
Cross-Sectional (n=436)
No
Does a higher urinary sodium-to-potassium ratio associate with elevated BNP levels in a general population without cardiovascular disease or antihypertensive treatment?
A higher urinary sodium-to-potassium ratio is independently associated with elevated BNP levels in a general population without cardiovascular disease, suggesting its utility as an early marker for cardiac burden.
Relative Risk: 2.24 (95% CI 1.35–3.72)
p-value: p=0.0005
The urinary sodium-to-potassium (Na/K) ratio is associated with blood pressure (BP) and cardiovascular risk. We examined the association between the urinary Na/K ratio and brain natriuretic peptide (BNP), a biomarker indicative of cardiac stress levels within the general population. This cross-sectional study included 436 participants (mean age: 65.4 ± 6.9 years; 73.2% women) without antihypertensive medications or cardiovascular diseases (including atrial fibrillation) from the Ohasama Study. The urinary Na/K ratio was calculated using casual daytime spot urine samples. Analyses of covariance and multiple linear and Poisson regression models were conducted. The median BNP value was 18.6 pg/mL (interquartile range: 11.4-31.2 pg/mL). Participants in the first (≤2.19), second (2.19-3.27), and third (≥3.28) tertiles of the urinary Na/K ratio had adjusted mean natural log-transformed (ln)BNP of 2.74, 2.88, and 3.06 (converted BNP values: 15.50, 17.81, and 21.37 pg/mL), respectively, after adjusting for covariates including estimated glomerular filtration rate, home systolic BP, and Sokolow-Lyon voltage (P for trend = 0.0005). The adjusted prevalence ratios (95% confidence intervals) for BNP ≥35 pg/mL were 1.27 (0.76-2.14) and 2.24 (1.35-3.72) in the second and third tertiles, respectively, compared with the lowest tertile. The highest standardized regression coefficient for lnBNP was observed for the urinary Na/K ratio ( | 0.24 | ), surpassing estimated 24-h urinary sodium ( | 0.16 | ) or potassium ( | 0.09 | ) excretion. In conclusion, urinary Na/K ratio was associated with elevated BNP levels in individuals without antihypertensive treatment and cardiovascular disease history. This urinary marker may be valuable for early prevention of organ damage and cardiac burden.
Muroya et al. (Thu,) conducted a cross-sectional in General population without antihypertensive treatment and cardiovascular diseases (n=436). Urinary sodium-to-potassium ratio vs. Lowest tertile of urinary sodium-to-potassium ratio (≤2.19) was evaluated on Prevalence of BNP ≥35 pg/mL (PR 2.24, 95% CI 1.35-3.72, p=0.0005). A higher urinary sodium-to-potassium ratio was significantly associated with elevated BNP levels, with the highest tertile showing a 2.24-fold higher prevalence of BNP ≥35 pg/mL compared to the lowest tertile.