Document Type : Original Article
Authors
1
Nephrology Department, Theodor Bilharz Research Institute, Giza, Egypt
2
Nephrology Department, Theodor Bilharz Research Institute, Giza, Egypt, Giza, Egypt
3
heodor Bilharz Research Institute Biochemistry and Molecular Biology Department, Giza, Egypt
4
Intensive Care Unit Theodor Bilharz Research Institute, Giza, Egypt
Abstract
Patients with chronic kidney disease (CKD) exhibit an increased cardiovascular (CV) complications including vascular and valve calcification, coronary artery disease, heart failure, arrhythmias, and sudden cardiac death. The incidence and prevalence of cardiovascular events is significantly higher in patients with early CKD stages compared with the general population, however patients with advanced CKD stages and those on dialysis exhibit a markedly elevated cardiovascular risk. Cardiovascular rather than end-stage kidney disease (CKD stage 5) is the leading cause of death in this high-risk population. CKD causes a systemic, chronic proinflammatory state contributing to vascular and myocardial remodeling resulting in vascular calcification, and vascular senescence as well as myocardial fibrosis and calcification of cardiac valves mainly aortic and mitral valves. In addition, conventional hemodialysis (HD) itself leads to myocardial stress and injury on the already compromised cardiovascular system in uremic patients. Inflammation, low serum fetuin-A levels and high serum ferritin levels are implicated for increase morbidity and mortality in this group of population. So, the current study aims to assess the function of fetuin-A in combination with inflammatory markers; TNF-α, hs-CRP and ferritin in the progression of CV complications in dialysis patients.
A total of (60) chronic hemodialysis patients and (30) healthy volunteers were participated in this study at Theodor Bilharz Research Institute’s Nephrology Department. Laboratory parameters were measured; serum Calcium, phosphorus, parathormone, calcium-phosphate, inflammatory markers; Serum levels of fetuin-A, tumor necrosis factor alfa (TNF-α), and highly sensitive C-reactive protein (hs-CRP). The common carotid arteries' intima-media thicknesses (CIMT) and the calcification of the mitral and aortic annuli were performed.
The results indicated that fetuin-A levels showed statistically significant low levels in HD group in contrast to control group (p˂.0001), while there were statistically significant rise in hs-CRP (p˂.0001), TNF-α (p˂ .0001), serum ferritin (p˂ .0001) in HD group compared to control group. In addition, there was a negative connection between fetuin-A and CIMT, SBP, DBP, while there was a positive connection between hs-CRP, TNF-α and CIMT.
In conclusion determination of fetuin-A is a useful tool to assess inflammation and CV risk in HD patients.
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