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Assessment of Vascular Function in Patients With Chronic Kidney Disease
Published on: June 16, 2014
Markers of increased cardiovascular risk in patients with chronic kidney disease
Anna Gluba-Brzózka1, Marta Michalska-Kasiczak, Beata Franczyk-Skóra
1Department of Nephrology, Hypertension and Family Medicine, WAM University Hospital of Lodz, Medical University of Lodz, Zeromskiego 113, 90-549 Lodz, Poland. aniagluba@yahoo.pl.
Insights
Chronic kidney disease (CKD) is linked to atherosclerosis. This study found decreased fetuin A and increased osteocalcin, renalase, MMP-2, and TIMP-2 in CKD patients, suggesting their role in cardiovascular disease development.
Area of Science:
- Nephrology
- Cardiology
- Biochemistry
Background:
- Chronic kidney disease (CKD) is a significant risk factor for atherosclerosis and cardiovascular disease (CAD).
- Understanding the specific agents involved in atherosclerosis progression within CKD patients is crucial for risk stratification and management.
Purpose of the Study:
- To identify novel biomarkers associated with an elevated risk of CAD in patients with CKD.
- To elucidate the role of specific proteins and enzymes in the development of atherosclerosis in the context of CKD.
Main Methods:
- Enzyme-linked immunosorbent assay (ELISA) was employed to measure the concentrations of various biomarkers.
- Key markers included osteoprotegerin, osteopontin, osteocalcin, matrix γ-carboxyglutamic acid (Gla) protein (MGP), fetuin A, matrix metalloproteinases (MMP-2, MMP-9), tissue inhibitors of metalloproteinases (TIMP-1, TIMP-2), ATP binding cassette transporters (ABCA1, ABCG1), and renalase.
- A cohort of 139 CKD patients was compared with 45 healthy controls.
Main Results:
- CKD patients exhibited significantly lower levels of fetuin A compared to controls.
- Elevated concentrations of osteocalcin, matrix metalloproteinase-2 (MMP-2), tissue inhibitor of metalloproteinase-2 (TIMP-2), and renalase were observed in the CKD group.
- Patients with CKD showed a higher prevalence of aortic valve calcification and impaired left ventricle ejection fraction.
Conclusions:
- Reduced fetuin A and elevated osteocalcin, renalase, MMP-2, and TIMP-2 are implicated in the pathogenesis of CAD in CKD.
- Increased indicators of cardiac hypertrophy and dysfunction in CKD patients highlight pathological cardiovascular changes.
- These findings underscore the complex interplay between CKD and cardiovascular complications.
Background:
Epidemiological studies have shown that chronic kidney disease (CKD) is an important risk factor for atherosclerosis and cardiovascular disease (CAD). The aim of the study was to determine markers of increased risk of CAD and to achieve a better understanding of agents implicated in the process of atherosclerosis in CKD patients.
Methods:
The study group consisted of a total of 139 patients with CKD while the control group comprised 45 healthy volunteers. Concentrations of osteoprotegerin, osteopontin, osteocalcin, matrix γ-carboxyglutamic acid (Gla) protein (MGP), fetuin A, matrix metalloproteinase-2 (MMP-2), matrix metalloproteinase-9 (MMP-9), tissue inhibitor of metalloproteinase-1 (TIMP-1), tissue inhibitor of metalloproteinase-2 (TIMP-2), ATP binding cassette transporter A1 (ABCA1), ATP binding cassette transporter G1 (ABCG1) and renalase were measured by the ELISA method.
Results:
We observed decreased levels of fetuin A (control vs. CKD group: 37.5 vs. 33.2 ng/ml, p = 0.018), and increased concentrations of osteocalcin (control vs. CKD group: 9.1 ± 6.0 vs. 13.6 ± 10.3 ng/ml, p = 0.05), MMP-2 (113.1 ± 75.0 vs. 166.0 ± 129.9 ng/ml, p = 0.045), TIMP-2 (22.1 ± 5.1 vs. 25.4 ± 7,0 ng/ml, p = 0.005) and renalase (251.0 ± 157 vs. 316.1 ± 155.3 ng/ml, p = 0.026). In patients with CKD (in comparison to control group), left ventricle ejection fraction: 53.0 ± 3,5% vs. 48.5%, p = 0.012) and calcification of the aortic valve (9.5% vs. 39.8%, p = 0.008) were observed more frequently.
Conclusions:
Decreased levels of fetuin A and increased concentration of osteocalcin, renalase, MMP-2 and TIMP-2 suggest that these factors may be involved in the pathogenesis of CAD in patients with CKD. Significantly increased indices of cardiac hypertrophy and its dysfunction in patients with CKD are indicators of pathological mechanisms occurring in cardiovascular system in this group of patients.
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