Background: Risk stratification for acute decompensated heart failure (ADHF) at admission remains clinically challenging, particularly in patients with concomitant renal dysfunction. Although B-type natriuretic peptide (BNP) is a well-established biomarker in ADHF, its prognostic dominance in prespecified multivariable analyses of cohorts with frequent cardiorenal dysfunction remains incompletely characterized. Methods: We conducted a single-center retrospective cohort study of 220 index admissions for ADHF. A prespecified multivariable logistic regression model was developed to estimate in-hospital mortality using admission variables, including age, sex, heart failure phenotype, systolic blood pressure, estimated glomerular filtration rate, serum albumin, and log-transformed BNP. Model performance was evaluated using discrimination (AUC), bootstrap optimism correction (200 iterations), calibration assessment, and decision curve analysis, in accordance with the TRIPOD guidelines. Results: In-hospital mortality occurred in 7.7% of patients (n = 17). In multivariable analysis, ln(BNP) was the only variable that reached statistical significance as an independent predictor of in-hospital mortality (OR 2.39 per unit increase; 95% CI 1.25–4.59; p = 0.009), representing the dominant prognostic signal in this dataset. Albumin and eGFR showed consistent but non-significant associations. The exploratory model demonstrated apparent discrimination (AUC 0.81), which decreased to 0.73 after optimism correction. A prespecified simplified model including albumin and ln(BNP) yielded an AUC of 0.77. Conclusions: In this exploratory multivariable analysis, admission BNP emerged as the primary prognostic factor for in-hospital mortality in an ADHF cohort with a high prevalence of renal dysfunction. The small number of outcome events limits confidence in model stability and precludes clinical deployment. These findings are hypothesis-generating and support BNP as the strongest prognostic signal observed in this cohort. External validation in larger cohorts is required before any clinical application.

Background: Admission-based risk stratification in acute decompensated heart failure (ADHF) remains challenging, particularly in cohorts enriched for cardiorenal syndrome type 1 (CRS1). B-type natriuretic peptide (BNP) is the most extensively validated admission biomarker in ADHF, yet its independent contribution alongside heart failure (HF) phenotype and serum albumin within a prespecified multivariable mortality prediction model has not been formally established in CRS-enriched populations. Methods: In a retrospective cohort of consecutive index ADHF admissions (N=220 complete cases) at a single center enriched for CRS1, we developed a prespecified multivariable logistic regression model to predict in-hospital death using: age, sex, HF phenotype (HFpEF/HFmrEF/HFrEF), systolic blood pressure (SBP), estimated glomerular filtration rate (eGFR), serum albumin, and log-transformed BNP [ln(BNP)]. Discrimination was assessed by the area under the receiver operating characteristic curve (AUC) with 200-iteration bootstrap optimism correction. Calibration was assessed across risk deciles, and clinical utility was evaluated by decision curve analysis. Reporting followed the TRIPOD statement. Results: Seventeen patients (7.7%) died during the index hospitalization. ln(BNP) was the sole statistically significant independent predictor of in-hospital mortality (OR 2.39 per ln-unit; 95% CI 1.25–4.59; p=0.009). Albumin and eGFR showed consistent directional associations with mortality. The model demonstrated good apparent discrimination (AUC 0.81), with an optimism-corrected AUC of 0.73. Decision curve analysis indicated net benefit at threshold probabilities of 5–30%. A prespecified two-variable sensitivity model (albumin + ln[BNP]) yielded AUC 0.77, confirming the robustness of these two markers. Conclusions: This exploratory, internally validated model incorporating BNP, albumin, eGFR, and HF phenotype demonstrated promising discrimination for in-hospital mortality in a CRS-enriched ADHF cohort. The principal contribution is the application of a formally prespecified, TRIPOD-reported admission model in a CRS-enriched population, rather than identifying BNP as a novel prognostic marker. ln(BNP) was the sole statistically significant independent predictor. These findings are hypothesis-generating and require external validation before any clinical deployment.

Background: Cardiorenal syndrome type 1 (CRS1) is an important complication of acute decompensated heart failure (ADHF). Admission hyperglycemia may reflect chronic dysglycemia, acute stress physiology, or both, but its relationship to CRS1 remains incompletely characterized. The primary objective was to assess the association between admission RBS and CRS1 in patients with ADHF. Secondary objectives were to compare RBS by CRS1 status and to explore its relationships with renal function, diabetes, and length of hospitalization. Methods: The study included 314 records (non-CRS1, n = 153; CRS1, n = 161), and admission random blood sugar (RBS) was available in 312. Cluster-robust logistic regression accounted for repeated admissions within patients and evaluated the association between CRS1 status and continuous RBS, with sequential adjustment for age, sex, diabetes, hypertension, prior acute kidney injury (AKI), chronic kidney disease (CKD), chronic obstructive pulmonary disease (COPD), estimated glomerular filtration rate (eGFR), and glycated hemoglobin (HbA1c). Exploratory analyses evaluated RBS categories, diabetes interaction, RBS–eGFR correlation, discrimination, and hospitalization duration. Results: Admission RBS was higher in CRS1 than in non-CRS1 records (11.02 ± 6.07 vs. 9.74 ± 5.04 mmol/L; Welch p = 0.044; Mann–Whitney p = 0.049). Each 1 mmol/L RBS increase was associated with CRS1 in the unadjusted model (OR = 1.042, 95% CI = 1.004–1.082; p = 0.030), but not after adjustment for age, sex, and diabetes (OR = 1.034, 95% CI = 0.993–1.076; p = 0.103) or the expanded clinical model (OR = 1.049, 95% CI = 0.989–1.112; p = 0.111). Adding eGFR or HbA1c did not yield a significant association. RBS showed poor discrimination (AUC = 0.564, 95% level bootstrap CI = 0.501–0.627, 3000 resamples of 198 unique patients). Prolonged hospitalization (>7 days) was not associated with CRS1 or admission RBS. Conclusions: In this retrospective study, admission RBS was higher in ADHF records classified as CRS1; however, after adjusting for clinical risk factors, the association attenuated, and RBS showed limited discriminatory ability. No significant correlation between RBS and eGFR was observed within the CRS1 group. These findings do not establish a causal relationship between admission glycemia and CRS1, nor do they support using RBS alone to identify CRS1. The LOS findings should be interpreted cautiously because of substantial missing data and the potential for selection bias. Prospective studies incorporating standardized and longitudinal glycemic measures, HbA1c, and established cardiorenal markers are warranted to determine whether comprehensive glycemic assessment improves CRS1 risk stratification.

Background: BNP is widely used for risk stratification in acute decompensated heart failure (ADHF), but its prognostic meaning may differ across clinical phenotypes, particularly cardiorenal syndrome type 1 (CRS1). Hypothesis: We hypothesized that serum albumin modifies the association between BNP and adverse in‐hospital course in ADHF. Methods: In this retrospective cohort study, adults hospitalized with ADHF were classified as CRS1 or control. The primary endpoint was adverse in‐hospital course, defined as in‐hospital death and/or prolonged length of stay (≥ 75th percentile). BNP was analyzed on the natural log scale. Multivariable logistic regression included albumin, ln(BNP), and an albumin × ln(BNP) interaction term, adjusted for age, sex, systolic blood pressure, eGFR, ejection fraction, CRS status, body mass index, and diabetes mellitus. Results: In the complete‐case cohort ( N = 292; events = 77), albumin significantly modified the BNP‐risk association (interaction β = −0.236 per 5 g/L; Wald p = 0.045; likelihood‐ratio test p = 0.050). The adjusted odds ratio for a 1‐unit increase in ln(BNP) was 1.81 at albumin 30 g/L, 1.42 at 35 g/L, and 1.12 at 40 g/L. Discrimination improved modestly with the interaction (AUC 0.714 vs. 0.726), and the high‐BNP/low‐albumin stratum showed the highest observed event risk. Conclusions: Serum albumin modifies the prognostic meaning of BNP in ADHF. Integrating albumin into BNP interpretation identifies a high‐risk “congestion plus vulnerability” phenotype and may support pragmatic triage and discharge planning in CRS‐enriched ADHF populations.