Abstract
FGF23 is a bone-derived hormone that plays an important role in the regulation of phosphate and 1,25-dihydroxy vitamin D metabolism. FGF23 principally acts in the kidney to induce urinary phosphate excretion and suppress 1,25-dihydroxyvitamin D synthesis in the presence of FGF receptor 1 (FGFR1) and its coreceptor Klotho. In patients with chronic kidney disease (CKD), circulating FGF23 levels are progressively increased to compensate for persistent phosphate retention, but this results in reduced renal production of 1,25-dihydroxyvitamin D and leads to hypersecretion of parathyroid hormone. Furthermore, FGF23 is associated with vascular dysfunction, atherosclerosis, and left ventricular hypertrophy. This paper summarizes the role of FGF23 in the pathogenesis of mineral, bone, and cadiovascular disorders in CKD.
Highlights
Patients with chronic kidney disease (CKD) are at increased risk for cardiovascular events compared with individuals with normal kidney function [1]
Elevated serum phosphate, low calcitriol, and high PTH levels represent the classical triad that leads to secondary hyperparathyroidism, each factor being independently associated with cardiovascular events and mortality in patients with CKD [4, 5]
FGF-23 is a central regulator of phosphate homeostasis and calcitriol blood levels; FGF-19 inhibits the expression of enzyme cholesterol 7-ahydroxylase (CYP7A1), which is the first and rate-limiting step in bile acid synthesis [8]; FGF-21 stimulates insulinindependent glucose uptake in adipocytes and lowers triglycerides [9]
Summary
Patients with chronic kidney disease (CKD) are at increased risk for cardiovascular events compared with individuals with normal kidney function [1]. In addition to traditional cardiovascular risk factors, disturbances in calciumphosphate metabolism are regarded as strong contributing factors of higher cardiovascular mortality in CKD patients [2, 3]. Elevated serum phosphate, low calcitriol, and high PTH levels represent the classical triad that leads to secondary hyperparathyroidism, each factor being independently associated with cardiovascular events and mortality in patients with CKD [4, 5]. The phosphaturic hormone, fibroblast growth factor (FGF-23), is overpoweringly entered into the traditional pathophysiological scheme of secondary hyperparathyroidism
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