TY - JOUR
T1 - Soluble TWEAK independently predicts atherosclerosis in renal transplant patients
AU - Turkmen, Kultigin
AU - Tonbul, Halil Zeki
AU - Erdur, Fatih Mehmet
AU - Toker, Aysun
AU - Biyik, Zeynep
AU - Ozbiner, Huseyin
AU - Gaipov, Abduzhappar
AU - Gul, Elvin Enes
AU - Kayrak, Mehmet
AU - Solak, Yalcin
AU - Ozbek, Orhan
AU - Turk, Suleyman
AU - Covic, Adrian
N1 - Copyright:
Copyright 2014 Elsevier B.V., All rights reserved.
PY - 2013/7/16
Y1 - 2013/7/16
N2 - Background: Cardiovascular risk is increased in the early stages of chronic kidney disease (CKD) and also found to be ongoing in renal transplant (Rtx) patients. As a sign of atherosclerosis, increased carotid intima-media thickness (CIMT) has been widely accepted as a strong predictor of cardiovascular disease (CVD) and mortality in CKD patients. A novel markers, soluble tumor necrosis factor-like weak inducer of apoptosis (sTWEAK) and neutrophil-to-lymphocyte ratio (NLR) were introduced as potential markers in inflammatory disorders including CKD. The role of Rtx in terms of atherogenesis is still unclear. We aimed to investigate the relationship between sTWEAK, NLR and CIMT in Rtx patients without overt CVD and to compare these results with those obtained from healthy subjects. Methods. Cross-sectional analysis in which CIMT measurements, NLR and serum TWEAK levels were assessed in 70 Rtx patients (29 females; mean age, 40.6 ± 12.4 years) and 25 healthy subjects (13 females, mean age; 37.4±8.8 years). Results: sTWEAK levels were significantly decreased (p=0.01) and hs-CRP, NLR and CIMT levels of Rtx patients were significantly increased compared to healthy subjects (p<0.0001, p=0.001, p<0.0001, respectively). sTWEAK was also found to be decreased when eGFR was decreased (p=0.04 between all groups). CIMT was positively correlated with sTWEAK and NLR in Rtx patients (r=0.81, p<0.0001 and r=0.33, p=0.006, respectively). sTWEAK was also positively correlated with NLR (r=0.37, p=0.002). In the multivariate analysis only sTWEAK was found to be an independent variable of increased CIMT. Conclusion: sTWEAK might have a role in the pathogenesis of ongoing atherosclerosis in Rtx patients.
AB - Background: Cardiovascular risk is increased in the early stages of chronic kidney disease (CKD) and also found to be ongoing in renal transplant (Rtx) patients. As a sign of atherosclerosis, increased carotid intima-media thickness (CIMT) has been widely accepted as a strong predictor of cardiovascular disease (CVD) and mortality in CKD patients. A novel markers, soluble tumor necrosis factor-like weak inducer of apoptosis (sTWEAK) and neutrophil-to-lymphocyte ratio (NLR) were introduced as potential markers in inflammatory disorders including CKD. The role of Rtx in terms of atherogenesis is still unclear. We aimed to investigate the relationship between sTWEAK, NLR and CIMT in Rtx patients without overt CVD and to compare these results with those obtained from healthy subjects. Methods. Cross-sectional analysis in which CIMT measurements, NLR and serum TWEAK levels were assessed in 70 Rtx patients (29 females; mean age, 40.6 ± 12.4 years) and 25 healthy subjects (13 females, mean age; 37.4±8.8 years). Results: sTWEAK levels were significantly decreased (p=0.01) and hs-CRP, NLR and CIMT levels of Rtx patients were significantly increased compared to healthy subjects (p<0.0001, p=0.001, p<0.0001, respectively). sTWEAK was also found to be decreased when eGFR was decreased (p=0.04 between all groups). CIMT was positively correlated with sTWEAK and NLR in Rtx patients (r=0.81, p<0.0001 and r=0.33, p=0.006, respectively). sTWEAK was also positively correlated with NLR (r=0.37, p=0.002). In the multivariate analysis only sTWEAK was found to be an independent variable of increased CIMT. Conclusion: sTWEAK might have a role in the pathogenesis of ongoing atherosclerosis in Rtx patients.
KW - Carotid intima-media thickness
KW - Neutrophil-to-lymphocyte ratio
KW - Renal transplantation
KW - sTWEAK
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U2 - 10.1186/1471-2369-14-144
DO - 10.1186/1471-2369-14-144
M3 - Article
C2 - 23849432
AN - SCOPUS:84880288779
VL - 14
JO - BMC Nephrology
JF - BMC Nephrology
SN - 1471-2369
IS - 1
M1 - 144
ER -