Document Detail

Soluble TWEAK and PTX3 in nondialysis CKD patients: impact on endothelial dysfunction and cardiovascular outcomes.
MedLine Citation:
PMID:  21330486     Owner:  NLM     Status:  MEDLINE    
BACKGROUND AND OBJECTIVES: Chronic kidney disease (CKD) conveys high mortality rates. Soluble TNF-like weak inducer of apoptosis (sTWEAK) and long pentraxin 3 (PTX3) are predictors of mortality in dialysis patients and determinants of endothelial dysfunction. Now, we hypothesize that both sTWEAK and PTX3 act as biomarkers of cardiovascular outcomes in nondialysis CKD patients.
DESIGN, SETTING, PARTICIPANTS, & MEASUREMENTS: Cross-sectional analysis in which flow-mediated dilation (FMD) and intima-media thickness (IMT) were assessed in 257 nondialysis stage 1 to 5 CKD patients (mean age, 52 ± 12 years; 130 men), together with biochemical measurements and sTWEAK and PTX3 assessments. Patients were followed for cardiovascular outcomes.
RESULTS: PTX3 and IMT increased, whereas FMD and sTWEAK decreased across CKD stages (P<0.001 for all). Both PTX3 and sTWEAK appeared as strong determinants of FMD in multivariate analysis. The univariate associations of sTWEAK and PTX3 with IMT were dependent on estimated GFR. After a median of 39 months (range, 2 to 43 months), 22 fatal and 57 nonfatal cardiovascular events occurred. In a Cox model excluding PTX3, decreasing sTWEAK concentration was associated with increased risk of cardiovascular events independently of basic confounders (age, gender, estimated GFR, C reactive protein, diabetes, and cardiovascular comorbidity) and FMD. In a model excluding sTWEAK, circulating levels of PTX3 were directly associated with cardiovascular outcomes independently of basic confounders, but this association was lost after adjustment for FMD.
CONCLUSIONS: Both PTX3 and sTWEAK levels associated with the endothelial dysfunction observed with progressive kidney failure. Additionally, both biomarkers impacted the predictability of cardiovascular outcomes.
Mahmut Ilker Yilmaz; Alper Sonmez; Alberto Ortiz; Mutlu Saglam; Selim Kilic; Tayfun Eyileten; Kayser Caglar; Yusuf Oguz; Abdulgaffar Vural; Mustafa Çakar; Jesus Egido; Battal Altun; Mujdat Yenicesu; Luis Miguel Blanco-Colio; Juan Jesús Carrero
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Publication Detail:
Type:  Journal Article; Research Support, Non-U.S. Gov't     Date:  2011-02-17
Journal Detail:
Title:  Clinical journal of the American Society of Nephrology : CJASN     Volume:  6     ISSN:  1555-905X     ISO Abbreviation:  Clin J Am Soc Nephrol     Publication Date:  2011 Apr 
Date Detail:
Created Date:  2011-04-08     Completed Date:  2011-08-18     Revised Date:  2013-06-30    
Medline Journal Info:
Nlm Unique ID:  101271570     Medline TA:  Clin J Am Soc Nephrol     Country:  United States    
Other Details:
Languages:  eng     Pagination:  785-92     Citation Subset:  IM    
Copyright Information:
© 2011 by the American Society of Nephrology
Department of Nephrology, Gu¨lhane School of Medicine, Ankara, Turkey.
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MeSH Terms
C-Reactive Protein / analysis*,  physiology
Cardiovascular Diseases / blood,  etiology*
Chronic Disease
Cross-Sectional Studies
Endothelium, Vascular / physiopathology*
Glomerular Filtration Rate
Kidney Diseases / blood*,  complications,  physiopathology
Middle Aged
Serum Amyloid P-Component / analysis*,  physiology
Tumor Necrosis Factors / blood*,  physiology
Tunica Intima / pathology
Tunica Media / pathology
Reg. No./Substance:
0/Serum Amyloid P-Component; 0/TNFSF12 protein, human; 0/Tumor Necrosis Factors; 148591-49-5/PTX3 protein; 9007-41-4/C-Reactive Protein
Comment In:
Clin J Am Soc Nephrol. 2011 Apr;6(4):697-9   [PMID:  21441127 ]

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