Background : Dysregulation of the FGF -23 – Klotho endocrine axis may be involved in the mechanism by which CKD patient's fail to maintain phosphate homeostasis. In fact serum FGF-23 Level are increased with advancing stages of CKD. Aim of Work :The study was to investigate FGF-23 Level in CKD patients who were under conservative treatment and ESRD Patient who were under hemodialysis.Patients and Methods: The study population included 22 patients with chronic kidney disease (CKD) and 48 patients with end stage renal disease (ESRD). Both sexes aged between 3 and 20 years, and 10 matached healthy controlers were studied.All our studied patients with ESRD were on renal replacement therapy by regular hemodialysis (HD). The patients were subjected to a thorough history and data was collected in the form of Age, sex, original disease, (duration of renal dialysis in ESRD Patients) and treatment they had received, and Blood Samples were collectedfor serum calcium, phosphorus, alkaline phosphatase, creatinine, and blood urea, nitrogen and fibroblast Growth Factor-23.Results: In Chronic Renal Failure Patients group (1) (CRF): The mean GFR for patients in group (1) was 35.51 + 16.57ml/min/1.73m2. Compared to control group, FGF-23 was significantly elevated in CKD patients (P<0.0001) FGF-23 was correlated negatively to GFR (P=0.045) and correlated positively to PTH (P-0.0001) but it was not correlated to other data (age, sex, duration of the disease) or laboratory (BUN, Ca, P, ALP) parameters. In End stage renal disease group (2) (ESRD): the mean Kt/v urea was 1.41 + 0.26 for ESRD patients under hemodialysis. Compared to control group. FGF-23 was significantly elevated in ESRD patients (P<0,0001) compared to CKD, FGF-23 was significantly elevated (P=0.002) .There were no statistically significant correlations between FGF-23 and Kt/v urea (which corresponds to dialysis adequacy). On the other hand, FGF-23 was positively correlated to serum PTH (P=0.001) and also correlated positively to PTH (P=0.0001).Conclusion: FGF-23 which plays an important role in phosphate homoeostasis, is increased in patients with CKD either who are under conservative treatment or under renal replacement therapy (heomdialysis). And it has become increasingly clear thatphosphate metabolism plays a critical role in the pathophysiology in CKD and that hyper phosphatemia should be aggressively treated to improve life expectancy of CKD patients.The klotho and FGF-23 axis is expected to be a novel target of therapeutic interventions in CKD