الفهرس 
INTRODUCTIONOnly 14 pages are availabe for public view
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Abstract
ID-HTN is a common (prevalence 15%) complication in the dialysis population. This complication predicts a high death risk. It has a complex mechanistic background and is multifactorial in nature. Volume and sodium overload, endothelial dysfunction, over activity of the RAS and SNS all play a role.
FGF-23 is a novel marker in CKD and HD patients implicated in abnormal phosphate and vitamin D metabolism. FGF-23 concentration progressively increases in CKD patients. Increased FGF-23 levels is related to accelerated atherosclerosis and endothelial dysfunction, and accepted as a predictor of mortality.
During HD, hypovolemia causes stimulation of RAAS and Sympathetic Nervous System to increase COP and increase peripheral vascular resistance as BP = COP × PVR. But in patients with atherosclerosis and arterial stiffening, this may cause exaggerated vascular response to increased sympathetic discharge and increased cardiac output which may lead to ID-HTN.
Our study aimed to evaluate the association between the occurrence of ID-HTN episodes in maintenance hemodialysis patients and FGF-23 and other biochemical markers of MBD including serum levels of Ca, P, and Ca x P product, ALP, iPTH and FGF-23.
Our study included sixty patients from the Haemodialysis Unit in Alexandria Medical Research Institute. The patients were divided into 2 groups: Hypertensive prone patients (HP group) including 45 patients, and stable patients (S group) including 15 patients.
Compared with haemodynamically stable patients, maintenance HD patients who are prone for recurrent intradialytic hypertensive episodes had significantly longer duration of dialysis, higher abdominal aortic calcification score and lower pre-dialysis serum sodium, while there was no statistically significant difference between the two groups regarding atherosclerosis score, mean CIMT and S.FGF-23.