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DOI 10.3390/biom16010102

Медицинская библиотека · Biomolecules · 2026

Inflammation and Dysregulated Bone Turnover Confound Serum ICAM-1 as a Cardiovascular Marker in Hemodialysis.

Divani Maria, Katsanaki Aikaterini, Makri Panagiota, Poulianiti Christina, Lykotsetas Evangelos, Balatsouka Andriani, Tziastoudi Maria, Stefanidis Ioannis, Eleftheriadis Theodoros

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Аннотация

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.

Для цитирования: Divani Maria, Katsanaki Aikaterini, Makri Panagiota, Poulianiti Christina, Lykotsetas Evangelos, Balatsouka Andriani, Tziastoudi Maria, Stefanidis Ioannis, Eleftheriadis Theodoros. Inflammation and Dysregulated Bone Turnover Confound Serum ICAM-1 as a Cardiovascular Marker in Hemodialysis.. Biomolecules. 2026. DOI: 10.3390/biom16010102.

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