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.
Abstract

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