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

Pieter Martens, Matthias Dupont, Frederik Hendrik Verbrugge, Kevin Damman, Nicolas Degryse, Petra Nijst, Carmen Reynders, Joris Penders, W. H. Wilson Tang, Jeffrey Testani, Wilfried Mullens*

*Corresponding author for this work

Research output: Contribution to journalArticleAcademicpeer-review

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OBJECTIVES This study sought to determine the relationship between urinary sodium (U-na) 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-na 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-na samples for 30 consecutive weeks. Linear mixed modeling was used to assess the longitudinal changes in U-na 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-na samples for 30 weeks. A total of 1,970 U-na samples were collected, with mean U-na 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-na [n = 39]) and low (73 mmol/l U-na [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-na concentrations (F-[1.80] = 24.063; p <0.001). The discriminating capacity of U-na 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-na concentration dropped (U-na = 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-na = 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-na 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-na concentration and exhibited a further drop in U-na concentration during the week preceding hospitalization. Ambulatory U-na sample collection is feasible and may offer additional prognostic and therapeutic information. (C) 2019 by the American College of Cardiology Foundation.

Original languageEnglish
Pages (from-to)404-414
Number of pages11
JournalJACC. Heart failure
Issue number5
Publication statusPublished - May-2019


  • heart failure
  • outcome
  • salt
  • sodium
  • urinary sodium

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