Background and Objectives: Heart failure (HF) and chronic kidney disease (CKD) frequently coexist and are closely interrelated, significantly affecting clinical outcomes. Among CKD-related markers, albuminuria and estimated glomerular filtration rate (eGFR) have emerged as key prognostic indicators in HF. However, their specific predictive value across different HF phenotypes—namely HF with preserved ejection fraction (HFpEF) and HF with reduced ejection fraction (HFrEF)—remains incompletely understood. This systematic review aims to evaluate the prognostic significance of albuminuria and eGFR in patients with HF and to compare their predictive roles in HFpEF versus HFrEF populations. Materials and Methods: We conducted a systematic search of major databases to identify clinical studies evaluating the association between albuminuria, eGFR, and adverse outcomes in HF patients. Inclusion criteria encompassed studies reporting on cardiovascular events, all-cause mortality, or HF-related hospitalizations, with subgroup analyses based on ejection fraction. Data extraction and quality assessment were performed independently by two reviewers. Results: Twenty-one studies met the inclusion criteria, including diverse HF populations and various biomarker assessment methods. Both albuminuria and reduced eGFR were consistently associated with increased risk of mortality and hospitalization. In HFrEF populations, reduced eGFR demonstrated stronger prognostic associations, whereas albuminuria was predictive across both HF phenotypes. Heterogeneity in study design and outcome definitions limited comparability. Conclusions: Albuminuria and eGFR are valuable prognostic biomarkers in HF and may enhance risk stratification and clinical decision-making, particularly when integrated into clinical assessment models. Differential prognostic implications in HFpEF versus HFrEF highlight the need for phenotype-specific approaches. Further research is warranted to validate these findings and clarify their role in guiding personalized therapeutic strategies in HF populations. Limitations: The current evidence base consists primarily of observational studies with variable methodological quality and inconsistent reporting of effect estimates.

Background: Albuminuria reflects systemic endothelial dysfunction and cardiorenal interaction in heart failure (HF), yet its short-term prognostic value in acute decompensated HF (ADHF) remains incompletely characterized. Methods: We conducted a prospective observational cohort study including 144 patients with complete follow-up hospitalized for ADHF. Urinary albumin-to-creatinine ratio (ACR), NT-proBNP, and estimated glomerular filtration rate (eGFR) were measured within 24 h of admission. Prior HF hospitalization within 12 months was recorded. The primary endpoint was a 90-day post-discharge composite of all-cause mortality or HF rehospitalization. Associations were examined using logistic regression, and discrimination was assessed using ROC curves with AUC comparisons. Results: Twenty-six patients (18.1%) experienced the 90-day composite endpoint. In univariable analysis, log₁₀-transformed ACR was strongly associated with events (OR 3.90, 95% CI 1.92–7.91; p < 0.001). In multivariable analysis, ACR remained independently associated with the endpoint in Model 1 (ACR + prior HF hospitalization: OR 4.21, 95% CI 1.93–9.17; p < 0.001) and Model 2 (additional adjustment for log₁₀ NT-proBNP: OR 3.49, 95% CI 1.54–7.91; p = 0.003). NT-proBNP was not independently associated with outcome in the fully adjusted model (p = 0.080). Discrimination improved from AUC 0.724 for ACR alone to 0.821 for Model 1 and 0.836 for Model 2; the AUC difference between Model 1 and Model 2 was not statistically significant (p = 0.404). Conclusions: Urinary ACR independently predicts 90-day adverse outcomes after ADHF hospitalization and improves discrimination when combined with recent HF hospitalization history; NT-proBNP did not provide significant incremental discrimination beyond this model.

Background and Objectives: Post-stroke spasticity is a frequent complication that contributes to impaired mobility, reduced functional independence, and decreased exercise tolerance. While botulinum toxin A (BoNT-A) is widely used to improve muscle tone, its effects on cardiopulmonary exercise capacity remain insufficiently characterized. This study aimed to evaluate the impact of BoNT-A treatment on cardiopulmonary performance and functional outcomes in patients with post-stroke spasticity. Materials and Methods: A prospective before–after study was conducted including 50 patients with post-stroke spasticity. Cardiopulmonary exercise testing was performed before and after BoNT-A administration. The primary outcome was peak oxygen consumption (VO₂ peak), while secondary outcomes included anaerobic threshold (AT), exercise duration, maximal workload, 10 m walk test time, Barthel Index, and modified Rankin Scale (mRS). Paired comparisons and multivariable linear regression analyses were performed to assess changes and associated factors. Results: VO₂ peak increased significantly following treatment (12.96 ± 2.70 vs. 13.55 ± 2.85 mL/kg/min; mean change 0.59 mL/kg/min, 95% CI 0.36–0.82; p < 0.001). Similar improvements were observed for AT (10.47 ± 2.77 vs. 10.97 ± 2.97 mL/kg/min; p < 0.001), exercise duration (6.70 ± 1.48 vs. 7.11 ± 1.55 min; p < 0.001), and maximal workload (44.70 ± 10.97 vs. 48.06 ± 12.60 W; p < 0.001). Functional performance improved, as indicated by reduced 10 m walk time (18.33 ± 4.67 vs. 17.36 ± 4.82 s; p < 0.001) and increased Barthel Index (57.62 ± 19.18 vs. 61.92 ± 21.10; p < 0.001). A modest but significant reduction in disability was observed on the mRS (p = 0.003). Baseline values were the strongest predictors of post-treatment outcomes, while smoking status was associated with worse walking performance. Conclusions: BoNT-A treatment was associated with modest but consistent improvements in cardiopulmonary exercise capacity and functional performance in patients with post-stroke spasticity. These findings suggest that spasticity management may be associated with functional and exercise-related benefits extending beyond local neuromuscular effects, although causal relationships cannot be established based on the present study design. Further controlled studies are needed to confirm these findings and evaluate their long-term clinical significance.

Background: Renal dysfunction is common in patients hospitalized with acute decompensated heart failure (ADHF) and represents a key component of cardiorenal syndrome. However, the relationships between renal impairment, cardiorenal biomarkers, and echocardiographic markers of myocardial function remain incompletely characterized in ADHF populations. Methods: We conducted a cross-sectional analysis of 144 consecutive patients hospitalized with ADHF. Renal dysfunction was defined as an estimated glomerular filtration rate (eGFR) < 60 mL/min/1.73 m². Clinical, laboratory, and echocardiographic parameters were compared according to renal function. Correlation analyses, multivariable logistic regression, and receiver operating characteristic (ROC) curve analyses were performed to evaluate associations between renal dysfunction, cardiorenal biomarkers, and myocardial functional indices. Results: Patients with renal dysfunction were older (p = 0.002) and more frequently had diabetes mellitus (p = 0.006). Echocardiographic evaluation demonstrated significantly lower systolic mitral annular velocity (S′) (p < 0.001) and higher E/e′ ratios (p < 0.001) in patients with renal dysfunction, whereas left ventricular ejection fraction (p = 0.133) and global longitudinal strain (GLS) (p = 0.121) were similar between groups. Log-transformed NT-proBNP and albuminuria were significantly correlated with S′, GLS, and E/e′ (all p < 0.001). In multivariable analysis adjusted for clinically relevant confounders, chronic kidney disease (OR 8.16, 95% CI 2.13–31.34; p = 0.002) and the E/e′ ratio (OR 2.01, 95% CI 1.52–2.66; p < 0.001) remained independently associated with renal dysfunction. ROC analysis showed that E/e′ had the strongest ability to distinguish between patients with and without renal dysfunction (AUC 0.887, 95% CI 0.834–0.941; p < 0.001). Conclusions: Renal dysfunction in ADHF is associated with echocardiographic markers reflecting impaired longitudinal myocardial function and elevated filling pressure, with E/e′ emerging as the strongest echocardiographic correlate. The integration of echocardiographic parameters with cardiorenal biomarkers may improve the characterization of the cardiorenal profile in patients hospitalized with ADHF.