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.