Soluble TWEAK level: is it a marker for cardiovascular disease in long-term hemodialysis patients?
Makaleler > Tam Makale · 2012
Yazarlar: Ozkan GUNGOR, Fatih KIRCELLI, Gülay AŞCI, Juan Jesus Carrero, Erhan TATAR, Meltem SEZİŞ, Süha Süreyya ÖZBEK, Naim CEYLAN, Hüseyin TÖZ, Mehmet ÖZKAHYA, Ercan OK
Journal of Nephrology, SCI Expanded İndekslerine Giren Dergi, Uluslararası, Wos, 2012, cilt 26, ss 136-143
DOI: 10.5301/jn.5000121
Özet
BACKGROUND: Reduced soluble tumor necrosis factor-like weak inducer of apoptosis (sTWEAK) levels follow declining renal function, are strongly associated with endothelial dysfunction and predict cardiovascular events in nondialyzed chronic kidney disease patients. In contrast, elevated levels of sTWEAK predict poor survival in hemodialysis (HD) patients. Recent evidence suggests a role for sTWEAK in the pathophysiology of vascular calcification. The aim of the study was to investigate plausible links between sTWEAK, atherosclerosis, arterial stiffness and vascular calcification in HD patients. METHODS: Coronary artery calcification score (CACs) determined by multislice computed tomography, arterial stiffness by pulse wave velocity (PWV) and carotid artery intima-media thickness (CA-IMT) by carotid Doppler ultrasonography were assessed in 131 long-term prevalent HD patients. sTWEAK levels were measured by ELISA (Bender MedSystems, Vienna, Austria). RESULTS: Mean serum sTWEAK level was 237.0 ± 147.5 pg/mL (range 78-937). sTWEAK level was inversely correlated with CA-IMT at a borderline significance (r=-0.168, p=0.05). Neither carotid-radial PWV nor carotid-femoral PWV values correlated with sTWEAK. sTWEAK level was higher in patients with severe vascular calcification (CACs ≥400) compared to patients with CACs <400 (264.5 ± 146.8 pg/mL vs. 205.04 ± 122.4 pg/mL, p=0.02).The association between sTWEAK and vascular calcification persisted after multivariate adjustment. CONCLUSIONS: There exists a weak inverse correlation between sTWEAK and carotid atherosclerosis and a positive correlation with coronary artery calcification in long-term HD patients. Our data give support for a role for sTWEAK in the pathogenesis of vascular injury in HD patients.