iTRAQ-based proteomic analysis of plasma reveals abnormalities in lipid metabolism proteins in chronic kidney disease-related atherosclerosis.
Patients with chronic kidney disease (CKD) have a considerably higher risk of death due to cardiovascular causes. Using an iTRAQ MS/MS approach, we investigated the alterations in plasma protein accumulation in patients with CKD and classical cardiovascular disease (CVD) without CKD. The proteomic analysis led to the identification of 130 differentially expressed proteins among CVD and CKD patients and healthy volunteers. Bioinformatics analysis revealed that 29 differentially expressed proteins were involved in lipid metabolism and atherosclerosis, 20 of which were apolipoproteins and constituents of high-density lipoprotein (HDL) and low-density lipoprotein (LDL). Although dyslipidemia is common in CKD patients, we found that significant changes in apolipoproteins were not strictly associated with changes in plasma lipid levels. A lack of correlation between apoB and LDL concentration and an inverse relationship of some proteins with the HDL level were revealed. An increased level of apolipoprotein AIV, adiponectin, or apolipoprotein C, despite their anti-atherogenic properties, was not associated with a decrease in cardiovascular event risk in CKD patients. The presence of the distinctive pattern of apolipoproteins demonstrated in this study may suggest that lipid abnormalities in CKD are characterized by more qualitative abnormalities and may be related to HDL function rather than HDL deficiency.
European Centre for Bioinformatics and Genomics, Institute of Bioorganic Chemistry, Poznan, 61-138, Poland.|Institute of Chemical Technology and Engineering, Poznan University of Technology, Poznan, 60-965, Poland.
Magdalena
M
Luczak
Department of Clinical Biochemistry and Laboratory Medicine, Poznan University of Medical Sciences, Poznan, 60-780, Poland.
Dorota
D
Formanowicz
European Centre for Bioinformatics and Genomics, Institute of Bioorganic Chemistry, Poznan, 61-138, Poland.
Łukasz
Ł
Marczak
Department of Biochemistry and Biotechnology, Poznan University of Life Sciences, Poznan, 60-632, Poland.
Joanna
J
Suszyńska-Zajczyk
Department of Nephrology, Transplantology and Internal Medicine, Poznan University of Medical Sciences, Poznan, 60-355, Poland.
Elżbieta
E
Pawliczak
Department of Nephrology, Transplantology and Internal Medicine, Poznan University of Medical Sciences, Poznan, 60-355, Poland.
Maria
M
Wanic-Kossowska
European Centre for Bioinformatics and Genomics, Institute of Bioorganic Chemistry, Poznan, 61-138, Poland.
Maciej
M
Stobiecki
D000368:Aged; D001053:Apolipoproteins / Q000097:blood; D050197:Atherosclerosis / Q000097:blood* / Q000150:complications / Q000235:genetics / Q000473:pathology; D001798:Blood Proteins / Q000235:genetics*; D005260:Female; D006801:Humans; D050356:Lipid Metabolism / Q000235:genetics*; D008075:Lipoproteins, HDL / Q000097:blood; D008077:Lipoproteins, LDL / Q000097:blood; D008297:Male; D008875:Middle Aged; D040901:Proteomics; D051436:Renal Insufficiency, Chronic / Q000097:blood* / Q000150:complications / Q000235:genetics / Q000473:pathology
D001053:Apolipoproteins; D001798:Blood Proteins; D008075:Lipoproteins, HDL; D008077:Lipoproteins, LDL