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Open Access Highly Accessed Research

Chronic kidney disease-related atherosclerosis - proteomic studies of blood plasma

Magdalena Luczak1, Dorota Formanowicz2, Elzbieta Pawliczak3, Maria Wanic-Kossowska3, Andrzej Wykretowicz4 and Marek Figlerowicz15*

Author Affiliations

1 Institute of Bioorganic Chemistry, Polish Academy of Sciences, Noskowskiego 12/14, 61-704 Poznan, Poland

2 Department of Clinical Biochemistry, Poznan University of Medical Sciences, Grunwaldzka 6, 60-780 Poznan, Poland

3 Department of Nephrology, Transplantology and Internal Medicine, Poznan University of Medical Sciences, Przybyszewskiego 49, 60-355 Poznan, Poland

4 Department of Internal Medicine, Division of Cardiology - Intensive Therapy, Poznan University of Medical Sciences, Przybyszewskiego 49, 60-355 Poznan, Poland

5 Institute of Computing Science, Poznan University of Technology, Piotrowo 3A, 60-965 Poznan, Poland

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Proteome Science 2011, 9:25  doi:10.1186/1477-5956-9-25

Published: 13 May 2011

Abstract

Background

Atherosclerosis is considered the major cause of the dramatic increase in cardiovascular mortality among patients suffering from chronic kidney disease (CKD). Although the close connection between atherosclerosis and kidney dysfunction is undeniable, factors enhancing CKD-mediated plaque formation are still not well recognized.

Results

To increase our knowledge of this process we carried out a comparative proteomic analysis of blood plasma proteins isolated from 75 patients in various stages of renal dysfunction (CKD group), 25 patients with advanced cardiovascular disease (CVD group) and 25 healthy volunteers (HV group). The collected samples were subjected to 2D electrophoresis. Then, individual proteins were identified by mass spectrometry. The comparative analysis involving CKD and HV groups showed a differential accumulation of α-1-microglobulin, apolipoprotein A-IV, γ-fibrinogen and haptoglobin in patients with kidney disease. Exactly the same proteins were identified as differentially expressed when proteomes of CVD patients and HV were compared. However, a direct comparison of CKD and CVD groups revealed significant differences in the accumulation of two proteins: α-1-microglobulin and apolipoprotein A-IV.

Conclusions

The obtained results indicate that at least two processes differentially contribute to the plaque formation in CKD- and CVD-mediated atherosclerosis. It seems that the inflammatory process is more intense in CKD patients. On the other hand, the down- and up-regulation of apolipoprotein A-IV in CVD and CKD groups, respectively, suggests that substantial differences exist in the efficacy of cholesterol transport in both groups of patients.