Chronic Kidney Disease and Hypertensive-Related Complications of Elevated Fibroblast Growth Factor 23
Journal Title: Journal of Advances in Medicine and Medical Research - Year 2017, Vol 24, Issue 4
Abstract
Chronic Kidney Disease (CKD) affects more than 10% of the world population. Treatment methods such as dialysis or transplantation are expensive. Among different factors responsible for the cause and progression of CKD are diabetes mellitus and hypertension. Hypertension is also a consequence of CKD. According to studies, hypertension is highly prevalent among patients with CKD and becomes more severe as the disease progresses. Fibroblast growth factor 23 (FGF-23) is an hormone which is a major regulator of phosphate balance. Vascular dysfunction and hypertension are among the various cardiovascular diseases (CVDs) associated with CKD. Reports suggest that the development of vascular dysfunction and hypertension is mediated by elevated FGF-23 levels in CKD. FGF-23 causes: renin-angiotensin-aldosterone system (RAAS) activation, plasma volume expansion due to aldosterone activities and increased expression of Na+Cl- Co-transporter (NCC) in the renal distal tubule, increased vascular resistance due to the vascular effects of angiotensin II and free radicals. All of which independently result in the development of hypertension in CKD. In opposition, RAAS inhibition prevents vascular smooth muscle contraction. It has been found in both experimental and human studies that RAAS inhibition may restore renal klotho, which may directly and indirectly improve kidney function and protect the cardiovascular system during CKD. Also, chlorothiazide, an inhibitor of NCC function, decreases blood volume and consequently prevents volume-induced hypertension. Furthermore, treatment with antioxidant agents to scavenge and reduce reactive oxygen species (ROS) or superoxide decreases vascular reactivity, hence, reduces or prevent oxidative stress. Also, oxidative stress is reduced or prevented through caloric restriction and calorie-restriction mimetics which reduce the generation of ROS by stabilizing mitochondrial energy production and efficiency. This review focuses on the role of elevated FGF-23 complications in the development of hypertension in CKD, and how these complications could be ameliorated. In conclusion, this review recommends treatment of hypertension that targets reduction or prevention of elevated FGF-23 complications in CKD and increased klotho expression to prevent CKD progression.
Authors and Affiliations
O. O. Omodara, P. P. Mshelia, M. I. A. Saleh, A. A. Madaki
Keywords
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- EP ID EP312461
- DOI 10.9734/JAMMR/2017/36967
- Views 57
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