Background: N-terminal pro-B-type natriuretic peptide (NT-proBNP) is released in response to increased cardiac wall stress and is used as a biomarker for volume overload and heart failure (HF). It is also elevated in atrial fibrillation (AF) and inflammation. However, in hemodialysis (HD) patients, its interpretation is complicated by reduced renal clearance, large fluid shifts between dialysis sessions, and chronic inflammation. Methods: In 123 HD patients, we examined the relationship between NT-proBNP and interdialytic weight gain, HF with preserved ejection fraction (HFpEF), left ventricular systolic dysfunction (LVSD), and AF, as well as the impact of inflammation. Clinical characteristics, laboratory data, and echocardiography (within three months) were evaluated, while serum NT-proBNP and calprotectin levels were measured by ELISA. Results: NT-proBNP showed no association with interdialytic weight gain and did not identify HFpEF. Inflammatory markers (C-reactive protein and calprotectin) correlated positively with NT-proBNP. Multivariable analysis demonstrated that LVSD, AF, and inflammation remained independent predictors of NT-proBNP levels. Although NT-proBNP levels were higher in LVSD, its diagnostic performance was poor (AUC 0.627). In contrast, NT-proBNP was significantly elevated in patients with AF and showed good diagnostic performance (AUC 0.801). Conclusions: In HD patients, NT-proBNP is not correlated with interdialytic weight gain, performs poorly as a marker of LVSD, but may serve as a useful marker of AF.

Cardiovascular disease (CVD) remains the leading cause of mortality among hemodialysis (HD) patients, underscoring the need for reliable biomarkers for early diagnosis and management. Serum intercellular adhesion molecule-1 (ICAM-1) has been investigated for years as a potential CVD marker but has yet to establish clinical utility. In a cohort of 142 HD patients, we examined the potential of serum ICAM-1 as a CVD biomarker and evaluated whether confounding factors, including low-grade inflammation and chronic kidney disease–mineral bone disorder (CKD-MBD), limit its diagnostic value. In addition to serum ICAM-1, routine biochemical parameters, bone alkaline phosphatase (bALP), and nitric oxide (NO) were measured. Serum levels of ICAM-1, bALP, and NO did not differ between patients with and without CVD, defined by a positive history of coronary heart disease, stroke, or peripheral arterial disease. Serum ICAM-1 concentrations were higher in HD patients with inflammation, as indicated by C-reactive protein levels >1 mg/dL. ICAM-1 showed no correlation with NO, a marker of endothelial dysfunction, but was positively correlated with bALP, a marker of CKD-MBD. In conclusion, serum ICAM-1 is not a reliable biomarker of CVD in HD patients. Its diagnostic utility appears confounded by inflammation and disturbances in bone turnover.