Title:
Pentraxin 3 (PTX3) is elevated in hemodialysis (HD)- but not peritoneal dialysis (PD) patients and is associated with cardiovascular disease
M. Boehme
1 ;M. Boehme
1 ;M. Boehme
1 ;M. Boehme
2 ;M. Boehme
2 ;M. Boehme
2 ;M. Boehme
2 ;M. Boehme
3 ;M. Boehme
1
Berlin' ne ''
; 2. KfH Dialysis Clinics Nordgraben/Bismarckstr.
Berlin' ne ''
E-mail address corresponding author:
ralf.schindler@charite.de
Background:
Pentraxins are mediators of inflammation as well as markers of the acute-phase-reaction. Pentraxins are produced during inflammatory diseases, the short pentraxin C-reactive protein (CRP) is produced by hepatocytes while the long pentraxin PTX3 is produced by monocytes, macrophages and cells of the vessel wall. Elevated levels of PTX3 were reported in septic patients and those after myocardial infarction. PTX3 expression was observed in atherosclerotic plaques suggesting a role for PTX3 in atherosclerosis. While elevation of CRP in patients with chronic renal failure (CRF) and its association with cardiovascular disease is well described, there are no data on PTX3 in this population. We investigated whether plasma levels of PTX3 are increased in HD-patients and whether there is an increase in PTX3 levels during HD
Methods:
Plasma was obtained from 44 chronic HD-patients, in 38 PD patients, in 37 patients with CRF and 18 age-matched normal subjects. PTX3 plasma levels were measured by ELISA (Alexis, USA), CRP by immunoturbidimetry and IL-6 by high-sensitivity ELISA (R&D systems). PTX3 production in whole blood was also investigated in samples taken before and after HD.
Results:
Levels of PTX3 were significantly elevated in HD- (5.8±0.6 ng/ml) compared to PD- (1.5±0.4) and CRF-patients (1.5±0.3) and normal subjects (0.76±0.2). Levels of CRP and IL-6 were similar in all three groups with renal failure and higher compared to normals. The difference in PTX3 levels was not caused by differences in residual renal function. PTX3 levels were significantly higher in patients with coronary artery disease and with peripheral artery occlusive disease (p<0.01). In HD patients, PTX3 levels correlated highly significantly with the time on HD therapy and with erythropoietin dosage. During a single HD session, PTX3 production was higher in whole blood samples taken after 3 h HD compared to samples taken before HD. Neither CRP- nor IL-6-levels increased during HD. There was no correlation between CRP and PTX3.
Conclusion:
PTX3-levels are exclusively elevated in HD-patients compared to PD- and CRF-patients. The increase in PTX3 production during HD indicates that the HD procedure itself contributes to PTX3 levels in HD-patients. The association between PTX3 and cardiovascular morbidity possibly suggests a contribution of circulating PTX3 in the pathogenesis of atherosclerosis and cardiovascular disease in HD-patients.
Subject:
Complications
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