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Urinary Sodium Profiling in Chronic HF to Detect Development of Acute HF
Study Questions:
What is the relationship between spot urinary sodium (UNa) concentration and the risk of developing acute heart failure (AHF) resulting in hospitalization?
Methods:
The study cohort was comprised of stable chronic HF patients (both HF with reduced ejection fraction [HFrEF] and HF with preserved EF [HFpEF]) who underwent prospective collection of weekly prediuretic first void morning spot UNa samples for 30 weeks. During this period, patients were followed prospectively for the development of AHF or mortality. The study authors utilized linear mixed modeling to assess the longitudinal changes in UNa concentration.
Results:
The final study cohort was comprised of 80 chronic HF patients (71 ± 11 years of age; N-terminal pro–B-type natriuretic peptide [NT-proBNP] concentration of 771 [interquartile range, 221-1,906] ng/L; left ventricular EF [LVEF] 33 ± 7%). A total of 1,970 UNa samples were collected, with mean UNa concentration of 81.6 ± 41 mmol/L. Sodium excretion remained stable over time on a population level (time effect, p = 0.663). Interindividual differences revealed the presence of high (88 mmol/L UNa [n = 39]) and low (73 mmol/L UNa [n = 41]) sodium excreters. Only younger age was an independent predictor of high sodium excretion (odds ratio [OR], 0.91; 95% confidence interval [CI], 0.83-1.00; p = 0.045 per year).
During 587 ± 54 days of follow-up, 21 patients were admitted for AHF. Patients who had AHF hospitalization during follow-up had lower blood pressure, a lower level of hemoglobin, lower estimated glomerular filtration rate (eGFR), higher NT-proBNP, and poorer right and left ventricular systolic function, and indices of higher filling pressures (E/e’ and right ventricular systolic pressure). The median time to the first AHF hospitalization was 129 days (range, 71-248 days). Patients who developed AHF had significantly lower UNa concentrations (F[1.80] = 24.063; p < 0.001). The discriminating capacity of UNa concentration to detect AHF persisted after inclusion of NT-proBNP and eGFR measurements as random effects (p = 0.041). UNa concentration dropped (UNa = 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 (UNa = 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. The median duration between the collection of the spot sample of the week of HF hospitalization and presentation to the hospital was 5 days (range, 4-7 days).
The sensitivity analysis revealed that patients with AHF hospitalization also had a significantly lower UNa concentration (F[1.46] = 5.071; p = 0.027). An additional sensitivity analysis restricted to HFrEF patients indicated similar results (F[1.218] = 20; p < 0.001), as did a sensitivity analysis restricted to patients not taking loop diuretics at baseline (F[1.203] = 11; p < 0.001).
Conclusions:
The study authors concluded that: 1) alterations in the renal pathway (e.g., loss of natriuretic capacity) probably contribute to and precede the development of AHF, and 2) spot UNa may offer additional prognostic and therapeutic information in HF patients.
Perspective:
Although the sample population was small, the findings of this study are important, and if substantiated, may help better manage HF. Spot UNa, a test that can be done like home blood sugar, may help predict HF decompensation. Large multicenter studies are now needed to validate the findings of this study and whether indeed spot UNa continues to be of value as a predictor in patients with accompanying renal dysfunction, which is not uncommon in HF patients.
Clinical Topics: Anticoagulation Management, Geriatric Cardiology, Heart Failure and Cardiomyopathies, Prevention, Acute Heart Failure, Heart Failure and Cardiac Biomarkers
Keywords: Blood Pressure, Dyspnea, Geriatrics, Glomerular Filtration Rate, Heart Failure, Hemoglobins, Natriuretic Peptide, Brain, Peptide Fragments, Secondary Prevention, Sodium, Sodium Potassium Chloride Symporter Inhibitors, Stroke Volume, Systole, Ventricular Function, Left, Ventricular Function, Right
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