الفهرس 
IntroductionOnly 14 pages are availabe for public view
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Abstract
CKD is a worldwide health problem, affects 8% to 16% of the population worldwide and clinical outcomes including mortality and cardiovascular events are strongly affected by the kidney involvement. Cardiovascular disease is the leading cause of death among patients with CKD. Vascular calcification is one of the independent risk factors associated with cardiovascular disease and mortality. Endothelial dysfunction one of the first steps in the development and progression of atherosclerosis, is a non-traditional CV risk factor in CKD. CKD-MBD and the subsequent vascular calcification, starts developing very early in the course of CKD. FGF-23 at very high serum concentrations in CKD exerts adverse effects through low-affinity and Klotho-independent binding to FGF-R, on endothelial cells. FGF23 hinders NO bioavailability in the endothelium and impair endothelium-dependent vasorelaxation. Hence, we studied the markers of atherosclerosis and endothelial dysfunction in relation to mineral bone disorders in our CKD patients. We found the following results: In our study, we were in line with other previous studies that reported that atherosclerotic changes in CKD patients showed increase cIMT with CKD progression. To study endothelial dysfunction, we assessed flow mediated dilatation, Percent FMD was significantly lower in stage V CKD. In the current study, the serum FGF-23 levels increased in parallel with the progressive reductions in GFR, and its levels showed significant positive correlation with FMD. Nephron index showed significant positive correlation with FMD, Ph, serum bicarbonate, blood hemoglobin, and measured GFR. At a multivariable linear regression analysis of selected independent variables, FGF-23 was a statistically significant independent predictor of FEP. We failed to find a statistically significant correlation between 24-hour urinary phosphorus excretion and indicator of endothelial dysfunction (FMD). The present study adds to the evidence that endothelial dysfunction and structural vascular damage, which are markers of atherosclerosis, originate in pre-dialysis stages of CKD, as indicated by significantly reduced brachial artery FMD and increased CIMT respectively.