Background
The cause of early-accelerated atherosclerosis development observed in chronic kidney disease (CKD) is not fully understood. The determination of the relationship between the serum or blood levels of fibroblast growth factor 23 (FGF 23) and carotid artery intima media thicknesses (CIMT) and development of endothelial dysfunction lend support to the possibility that FGF-23 plays a role in the development of atherosclerosis in CKD.
 
Aim of Work 
To assess the circulating FGF23 as    a marker of vascular stiffness in children with CKD on conservative treatment regardless the etiology and to correlate its level with carotid artery intima media thickness as detected by ultrasonography.
 
Patients and Methods
 This is a prospective case control study was done on forty cases with CKD on conservative treatment (stage II - III and IV) regardless the etiology. Also twenty apparently healthy children age and sex matched with cases were included as a control group. After complete clinical evaluation of cases and controls including weight, height, body mass index, blood pressure and all body systems, FGF23 was measured in serum and carotid artery intima media thicknesses (CIMT) was measured as a marker of atherosclerosis using ultrasonography.
 
Results
CIMT measurements and FGF-23 levels were significantly higher in patients than controls. There was a positive correlation between FGF23 and both CIMT, CKD stage. On the other hand there was a negative correlation between FGF23 and the level of glomerular filtration rate (GFR).
 
Conclusion
FGF-23 may be used as a sensitive and non-invasive indicator of subclinical atherosclerosis in patients with chronic kidney disease where our results showed a positive correlation between FGF23 and CIMT.