RESUMEN
Background: Fetuin-A is a circulating calcium- regulatory glycoprotein that inhibits vascular calcification. In end stage renal disease [ESRD], fetuin -A has been demonstrated to be reduced and inversely related to cardiovascular mortality. The present study aimed to determine the effect of renal function on serum levels of fetuin-A in patients with chronic kidney disease [CKD] and to investigate the relationship between fetuin-A serum level and vascular calcification which represents a risk factor for the development of endothelial dysfunction[ED]
Methods: 20 CKD patients on conservative treatment, 20 ESRD patients on regular hemodialysis [HD] treatment, as well as 40 apparently healthy controls of matchable age and sex were enrolled in the study. All the patients and controls were subjected to the following investigations: estimation of serum levels of fetuin-A, high sensitivity-CRP [hs-CRP], creatinine, calcium [Ca], phosphorus [Po4], alkaline phosphatase [ALP], and parathormone [PTH]. In addition, glomerular filtration rate was estimated for cases and controls
Results: There was significant reduction in fetuin-A serum levels in CKD and ESRD patients compared to controls. A significant decrease was also detected in ESRD group when compared to CKD group. The inflammation marker hs-CRP was significantly increased in CKD and ESRD patients in comparison to controls. The increase was also significant on comparing ESRD group with CKD group. A strong inverse correlation was found between serum fetuin-A and hs-CRP, Significantly increased serum levels of ALP and PTH were found in CKD and ESRD patients compared with controls. The increase was also significant in ESRD patients compared with CKD patients. In ESRD patients, Serum levels of fetuin-A showed significant inverse correlations with each of: duration of igalysis, ALP and PTH serum levels, while hs-CRP serum levels showed significant positive corelations with CaxPo4 ratio and PTH serum levels
Conclusion: Results of the present study demonstrate that inflammatory processes are increased among CKD and ESRD patients and linked to low fetuin-A serum levels and vascular calcification which represents a risk factor for the development of ED. The interaction of these incidents may be responsible for the development and progression of thrombogenesis in such cases