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During the congress, E-Posters will be accessible to all participants on the congress website 24/7, as well as in the E-poster stations in the congress center.
Preparing your E-Poster
Please review the E-Poster format requirements carefully when preparing your E-Poster. Should your E-Poster not meet the mentioned requirements, it may not be displayed as described above.
E-Poster Submission Deadline
Please prepare and upload your E-Poster no later than March 14, 2026 11.59PM CET. After this date, you will no longer be able to prepare and upload your E-poster and it will not be displayed and accessible on the congress website.
Please follow the instructions below to input your abstract title.
Abstract titles should be brief and reflect the content of the abstract.
Diuretic response (DR) during hospitalization for acute heart failure (AHF) is a key determinant of decongestion and prognosis. In acute decompensated heart failure (ADHF), the relationship between plasma diuretic concentration and sodium chloride excretion shifts rightward, reducing natriuretic efficacy. In the PROTECT trial, DR was evaluated in hospitalized AHF patients, and lower DR was associated with reduced treatment success, highlighting its clinical relevance. Urinary biomarkers such as L-FABP and NGAL have been proposed as indicators of tubular stress, while adrenomedullin (tAM) reflects congestion biology. However, whether these biomarkers show a continuous association with DR remains unclear. We hypothesized that higher urinary biomarker levels would correlate with poorer DR.
We conducted a single-center observational study including 134 AHF patients. DR was defined as the body weight change over the first 3 days per 40 mg of loop diuretic administered, converted to furosemide equivalents. DR was multiplied by −1 to facilitate interpretation so that higher values indicate poorer responsiveness. Dose conversion was standardized: azosemide 60 mg = furosemide 40 mg, torasemide 8 mg = furosemide 40 mg; oral doses were adjusted using a bioavailability factor 0.5.
Urinary biomarkers (L-FABP, NGAL, and tAM) were collected within 3 days of admission, normalized to urinary creatinine, log10-transformed, and standardized (z-scores) using JMP software. Visualization included scatter plots with LOESS smoothing (span = 0.35) and boxplots across DR quartiles (Q1–Q4). Spearman correlation coefficients and p for trend were calculated.
Multivariable ordinary least squares (OLS) regression was performed to estimate standardized β (95% CI) for DR×−1. Three models were constructed:
Model 1: urinary biomarkers (log-transformed L-FABP, NGAL, tAM)
Model 2: Model 1 plus cardiac parameters (LVEF, TRPG)
Model 3: Model 2 plus clinical covariates (serum creatinine, BNP, systolic blood pressure)
Scatter plots and LOESS curves showed no monotonic trend between urinary biomarkers and DR×−1. Boxplots across DR quartiles revealed overlapping distributions without a significant trend (p for trend: L-FABP = 0.8013, NGAL = 0.5825, tAM = 0.064). Spearman correlation coefficients were weak: L-FABP (r = −0.0142, p = 0.8796), NGAL (r = 0.0203, p = 0.8703), tAM (r = −0.0189, p = 0.8395).
Multivariable regression results were as follows:
Model 1: L-FABP = 0.044 (95% CI −0.256 to 0.344), NGAL = −0.005 (−0.303 to 0.292), tAM = 0.057 (−0.206 to 0.319)
Model 2: L-FABP = 0.054 (−0.274 to 0.381), NGAL = −0.036 (−0.360 to 0.288), tAM = 0.105 (−0.195 to 0.405), LVEF = 0.074 (−0.235 to 0.382), TRPG = 0.179 (−0.179 to 0.537)
Model 3: L-FABP = 0.135 (−0.224 to 0.494), NGAL = 0.026 (−0.303 to 0.356), tAM = −0.109 (−0.491 to 0.409), TRPG = 0.247 (−0.115 to 0.609), BNP = −0.183 (−0.570 to 0.204)
Urinary biomarkers, including L-FABP, NGAL, and tAM, were not significantly associated with diuretic responsiveness during AHF hospitalization. We plan to construct an integrated prediction model using available parameters such as LVEF, TRPG, BNP, systolic blood pressure, and serum creatinine.
