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Deeper insight into chronic kidney disease-related atherosclerosis: comparative proteomic studies of blood plasma
Magdalena Luczak1,2, Dorota Formanowicz3, Łukasz Marczak4
1Institute of Bioorganic Chemistry, Polish Academy of Sciences, Noskowskiego 12/14, 61-704, Poznan, Poland. magdalu@ibch.poznan.pl.
Insights
This study used proteomics to investigate accelerated atherosclerosis in chronic kidney disease (CKD). Findings suggest distinct molecular mechanisms and inflammation play key roles in CKD-related cardiovascular disease.
Area of Science:
- Proteomics
- Cardiovascular Science
- Nephrology
Background:
- Atherosclerosis is a primary driver of cardiac events and mortality in chronic kidney disease (CKD) patients.
- Cardiovascular disease (CVD) risk escalates with declining kidney function, yet specific mechanisms remain unclear.
- Comparative proteomic analysis was conducted on plasma from CKD patients, advanced CVD patients, and healthy controls.
Purpose of the Study:
- To elucidate the molecular mechanisms underlying accelerated atherosclerosis in patients with CKD.
- To identify specific risk factors and protein differences contributing to CVD in CKD.
- To compare proteomic profiles across different stages of CKD and CVD.
Main Methods:
- Plasma samples underwent affinity chromatography and fractionation (high-abundant, low-abundant, low-molecular weight proteins).
- Proteomic analysis utilized two-dimensional gel electrophoresis and mass spectrometry (MS/MS).
- Differential protein expression was confirmed via selected reaction monitoring (SRM) and analyzed for Gene Ontology (GO) functions and interaction networks.
Main Results:
- Forty-nine proteins exhibited altered accumulation levels, with 11 confirmed by SRM.
- Identified proteins were linked to blood coagulation, lipoprotein metabolism, and inflammatory processes.
- Distinct molecular mechanisms were observed in CKD-related atherosclerosis compared to classical CVD.
Conclusions:
- The study provides evidence for different molecular mechanisms in CKD- and CVD-related atherosclerosis.
- Anti-atherogenic factors in CKD patients do not appear to mitigate atherosclerosis progression as in classical CVD.
- Mechanisms of CVD acceleration may vary across CKD stages, with pronounced inflammation in advanced CKD.
Background:
Atherosclerosis is a major cause of cardiac events and mortality in patients suffering from chronic kidney disease (CKD). Moreover, the risk of cardiovascular disease (CVD) development in patients with CKD increases as kidney function declines. Although the close connection between atherosclerosis and kidney dysfunction is undeniable, particular risk factors and specific mechanisms that promote CVD in patients with CKD remain unclear. To gain insight into better recognition of the mechanisms of accelerated atherosclerosis in patients with CKD, we performed a comparative proteomic analysis of blood plasma from patients in various stages of CKD and thus distinct progression of atherosclerosis (n = 90), patients with advanced CVD and normal renal function (n = 30) and healthy volunteers (n = 30).
Methods:
Plasma samples were depleted using affinity chromatography and divided into three fractions: high-abundant, low-abundant and low-molecular weight proteins. The first two fractions were analyzed by two-dimensional gel electrophoresis and mass spectrometry, the last one has been subjected to direct MS/MS analysis. A proteomic profiles for high-abundant, low-abundant and low-molecular weight proteins fractions were obtained. Differential accumulated proteins were confirmed by selected reaction monitoring analysis (SRM). The Gene Ontology (GO) function and the interaction networks of differentially expressed proteins were then analyzed.
Results:
Forty-nine proteins (13 high- and 36 low-molecular mass) showed differences in accumulation levels. For eleven of them differential expression were confirmed by selected reaction monitoring analysis. Bioinformatic analysis showed that identified differential proteins were related to three different processes: the blood coagulation cascade, the transport, binding and metabolism of lipoproteins and inflammatory processes.
Conclusions:
Obtained data provide an additional line of evidence that different molecular mechanisms are involved in the development of CKD- and CVD-related atherosclerosis. The abundance of some anti-atherogenic factors revealed in patients with CKD suggests that these factors are not associated with the reduction of atherosclerosis progression in CKD that is typically observed in "classical" CVD. Moreover, obtained data also suggest that mechanism of CVD acceleration may be different in initial and advanced stages of CKD. Undoubtedly, in advanced stages of CKD inflammation is highly pronounced.
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