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Plasma endocan levels associate with inflammation, vascular abnormalities, cardiovascular events, and survival in chronic kidney disease
Author(s) -
Mahmut İlker Yılmaz,
Dimitrie Siriopol,
Mutlu Sağlam,
Yasemin Gülcan Kurt,
Hilmi Umut Ünal,
Tayfun Eyıleten,
Mahmut Gök,
Hakkı Çetinkaya,
Yusuf Oğuz,
Sebahattin Sarı,
Abdülgaffar Vural,
Irina Mititiuc,
Adrian Covic,
Mehmet Kanbay
Publication year - 2014
Publication title -
kidney international
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 3.499
H-Index - 276
eISSN - 1523-1755
pISSN - 0085-2538
DOI - 10.1038/ki.2014.227
Subject(s) - kidney disease , inflammation , medicine , disease , kidney , vascular disease , pathology , cardiology
Plasma endocan levels are elevated in a large number of diseases, and may reflect endothelial cell dysfunction. There are currently no data on endocan in patients with chronic kidney disease (CKD). Therefore, we measured plasma endocan in 251 patients with CKD (stage 1-5) and 60 control individuals. Plasma endocan concentrations correlated with estimated glomerular filtration rate (eGFR), different markers of inflammation (pentraxin 3 and high-sensitivity C-reactive protein), and vascular abnormalities (flow-mediated vasodilation (FMV) and carotid intima media thickness (CIMT)). All-cause mortality and cardiovascular events (CVE) were also analyzed with respect to plasma endocan. Patients with CKD showed significantly increased plasma endocan (4.7 [IQR 1.9-9.4] compared with controls [IQR 1.1-1.5] ng/ml), with values progressively higher across stages of CKD. On univariate analysis, plasma endocan concentrations correlated negatively with eGFR and FMV, but positively with both markers of inflammation and CIMT. However, on multivariate analysis only high-sensitivity C-reactive protein, FMV, and CIMT remained significantly associated with plasma endocan. On Cox survival analysis, endocan levels were associated with all-cause mortality and CVE in these patients. Thus, plasma endocan increases in the presence of decreasing eGFR and influences all-cause mortality and CVE in patients with CKD independent of traditional and nontraditional risk factors.

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