Urinary Sodium Profiling in Chronic Heart Failure to Detect Development of Acute Decompensated Heart Failure.

Objectives: This study sought to determine the relationship between urinary sodium (U) concentration and the pathophysiologic interaction with the development of acute heart failure (AHF) hospitalization.

Background: No data are available on the longitudinal dynamics of U concentration in patients with chronic heart failure (HF), including its temporal relationship with AHF hospitalization.

Methods: Stable, chronic HF patients with either reduced or preserved ejection fraction were prospectively included to undergo prospective collection of morning spot U samples for 30 consecutive weeks. Linear mixed modeling was used to assess the longitudinal changes in U concentration. Patients were followed for the development of the clinical endpoint of AHF.

Results: A total of 80 chronic HF patients (71 ± 11 years of age; an N-terminal pro-B-type natriuretic peptide [NT-proBNP] concentration of 771 [interquartile range: 221 to 1,906] ng/l; left ventricular ejection fraction [LVEF] 33 ± 7%) prospectively submitted weekly pre-diuretic first void morning U samples for 30 weeks. A total of 1,970 U samples were collected, with mean U concentration of 81.6 ± 41 mmol/l. Sodium excretion remained stable over time on a population level (time effect p = 0.663). However, interindividual differences revealed the presence of high (88 mmol/l U [n = 39]) and low (73 mmol/l U [n = 41]) sodium excreters. Only younger age was an independent predictor of high sodium excretion (odds ratio [OR]: 0.91; 95% confidence interval [CI]: 0.83 to 1.00; p = 0.045 per year). During 587 ± 54 days of follow-up, 21 patients were admitted for AHF. Patients who developed AHF had significantly lower U concentrations (F = 24.063; p < 0.001). The discriminating capacity of U concentration to detect AHF persisted after inclusion of NT-proBNP and estimated glomerular filtration rate (eGFR) measurements as random effects (p = 0.041). Furthermore, U concentration dropped (U = 46 ± 16 mmol/l vs. 70 ± 32 mmol/l, respectively; p = 0.003) in the week preceding the hospitalization and returned to the individual's baseline (U = 71 ± 22 mmol/l; p = 0.002) following recompensation, while such early longitudinal changes in weight and dyspnea scores were not apparent in the week preceding decompensation.

Conclusions: Overall, U concentration remained relatively stable over time, but large interindividual differences existed in stable, chronic HF patients. Patients who developed AHF exhibited a chronically lower U concentration and exhibited a further drop in U concentration during the week preceding hospitalization. Ambulatory U sample collection is feasible and may offer additional prognostic and therapeutic information.