Background and Hypothesis: Mortality in hemodialysis (HD) remains high and is not fully explained by traditional risk factors. Biomarkers reflecting myocardial stress and fibrosis, together with measures of vascular stiffness, may provide additional prognostic information in this population. Methods: We conducted a retrospective study evaluating 173 HD patients who were clinically stable and asymptomatic at baseline over a follow-up period of over 10 years. Patients were classified into four groups based on median baseline values of NT-proBNP and galectin-3 (4234 pg/mL and 28.1 ng/mL, respectively). Primary outcomes were all-cause mortality and major adverse cardiovascular events (MACE). Pulse wave velocity (PWV) was evaluated as an additional prognostic marker. Results: During follow-up, 76.9% of patients died. Higher NT-proBNP levels were associated with increased all-cause mortality, irrespective of galectin-3 levels, with adjusted hazard ratios of 2.58 and 1.93 compared with the reference group (p < 0.05). Age and PWV were independently associated with mortality risk, corresponding to a 4% increase in risk per year of age and a 6% increase per 1 m/s increase in PWV. MACE occurred in 26.8% of patients and did not differ significantly between biomarker-defined groups. Conclusions: In this long-term HD cohort, elevated NT-proBNP and increased arterial stiffness were independently associated with higher all-cause mortality. These findings support the complementary prognostic value of markers of cardiac stress and vascular stiffness in chronic hemodialysis patients.

Background: Chronic kidney disease (CKD) is associated with a high burden of cardiovascular remodeling and increased risk of heart failure with preserved ejection fraction (HFpEF). However, the interpretation of natriuretic peptide-based HFpEF diagnostic remains challenging in CKD populations, where structural cardiac abnormalities and elevated NT-proBNP levels frequently coexist. Methods: We conducted a cross-sectional study including ambulatory patients with CKD stages G3–G4 and NYHA II dyspnea. Clinical, metabolic, vascular, and echocardiographic assessments were performed. HFpEF was assessed using a modified HFA-PEFF-based approach derived from the ESC-recommended diagnostic algorithm. We evaluated the impact of NT-proBNP thresholds on HFpEF classification and explored the relationship between NT-proBNP, echocardiographic diastolic dysfunction, and structural cardiac abnormalities. Results: The cohort displayed a high cardiometabolic burden (74.9%), and structural cardiac abnormalities were highly prevalent. Using a modified HFA-PEFF diagnostic algorithm, HFpEF was identified in 52.9% of patients. However, when the biomarker domain was excluded, 86.7% of patients remained within the intermediate-probability range. In an exploratory analysis, a cutoff of 700 pg/mL was identified as the cohort-adapted threshold with the best diagnostic balance and identified 19.8% patients as having HFpEF. Conclusions: Patients with CKD G3–G4 exhibited substantial structural and functional cardiovascular abnormalities despite no prior diagnosis of heart failure. HFpEF classification varied according to the NT-proBNP threshold applied, while NT-proBNP demonstrated limited discriminatory performance for echocardiographic diastolic dysfunction. These findings support the need for more refined and CKD-sensitive approaches for HFpEF characterization in this population.