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Laboratory evaluation of parathyroid gland function
Published in Pallavi Iyer, Herbert Chen, Thyroid and Parathyroid Disorders in Children, 2020
Fibroblast growth factor-23 (FGF23) is a phosphatonin, a protein that impairs renal tubular reabsorption of phosphate, decreases renal synthesis of calcitriol and thereby depresses intestinal absorption of calcium and phosphate, and increases the synthesis and urinary excretion of water-soluble 1,24,25-trihydroxyvitamin D (9). FGF23 is expressed primarily by osteoblasts and osteocytes. FGF23 links to the “c” isoform of tyrosine kinase FGF receptors (FGFR) 1, 2, and 3. FGF23 binds to the dimeric co-receptor three-member complex—αKlotho/FGFR1(IIIc)/heparan sulfate—and depresses renal tubular reabsorption of phosphate, intestinal absorption of phosphate, synthesis of calcitriol, and secretion of PTH. Normal serum concentrations of FGF23 range between 5 and 210 U/mL and are increased in subjects with hypophosphatemia of diverse pathogenesis.
McCune−Albright Syndrome
Published in Dongyou Liu, Handbook of Tumor Syndromes, 2020
Cortisol (adrenal gland hormones) regulates metabolism of glucose and modulates stress. In MAS, cortisol levels are elevated and lead to Cushing syndrome (showing weight gain in the face and upper body, slowed growth in children, fragile skin, fatigue, and other health problems) before age 2. Certain individuals show elevated phosphate levels in blood, as renal absorption of phosphate is impaired. Fibrous dysplasia tissue produces a protein (fibroblast growth factor 23 [FGF 23]) that causes inability of the kidney to metabolize phosphate. Hypophosphatemia is seen likely in fibrous dysplasia individuals, leading to rickets (childhood) or osteomalacia (adults). Children with rickets have bowing deformity of the legs and short stature, while adults with osteomalacia suffer from softening of bone, fracture at younger age, and bone pain [1].
Osteoporosis
Published in Peter V. Giannoudis, Thomas A. Einhorn, Surgical and Medical Treatment of Osteoporosis, 2020
Ippokratis Pountos, Peter V. Giannoudis
Fibroblast growth factor 23 (FGF-23) is a circulating growth factor that regulates the serum levels of inorganic phosphorus and 1,25-dihydroxyvitamin D3. In a prospective 3-year study including 2868 elderly men, an increase in the baseline levels of FGF-23 was associated with an increased risk of fracture (42). Other similar studies contradict these results, with the role of FGF-23 in depicting low BMD remaining obscure (43).
Relationships between blood bone metabolic biomarkers and anemia in patients with chronic kidney disease
Published in Renal Failure, 2023
Fan Li, Xiaoxue Ye, Guang Yang, Hui Huang, Anning Bian, Changying Xing, Shaowen Tang, Jing Zhang, Yao Jiang, Huimin Chen, Caixia Yin, Lina Zhang, Jing Wang, Yaoyu Huang, Wenbin Zhou, Huiting Wan, Xiaoming Zha, Ming Zeng, Ningning Wang
Serum calcium (Ca) and phosphorus (P) are related to bone metabolism. Alkaline phosphatase (ALP) plays an important role in skeletal mineralization and is the most widely recognized biochemical marker for osteoblast activity [15]. Intact parathyroid hormone (iPTH) is a major mediator of bone remodeling and an essential regulator of Ca and P homeostasis [16]. Fibroblast growth factor 23 (FGF23), a hormone secreted by osteocytes and osteoblasts, is a potent regulator of vitamin D metabolism and phosphate homeostasis [13]. Finally, α-klotho is a membrane protein that is highly expressed in the kidney, especially in the distal tubular epithelial cells [17]. Patients with advanced CKD have a significant reduction in α-klotho levels and progressively lose the ability to prevent phosphate retention [18].
Past, present, and future of FGFR inhibitors in cholangiocarcinoma: from biological mechanisms to clinical applications
Published in Expert Review of Clinical Pharmacology, 2023
Elisabeth Amadeo, Federico Rossari, Francesco Vitiello, Valentina Burgio, Mara Persano, Stefano Cascinu, Andrea Casadei-Gardini, Margherita Rimini
Hyperphosphatemia is by far the most observed in all FGFR-I, thoroughly described in 55–81% of patients with CCA and FGFR alterations enrolled in clinical trials and in a lesser percentage in those with RLY-4008 administration [48]. A possible explanation for this phenomenon may lie in FGFR1 implication with a fibroblast growth factor 23 (FGF23), an important agent in phosphate homeostasis. Once the interaction between FGFR1 and FGF23 is disrupted by the FGFR inhibitor, FGF23 phosphate-lowering activity is impaired, especially at the intestinal and renal levels [55–58]. For correct management, dietary changes and phosphate lowering therapy, either phosphate binders and/or phophaturic agents, are advised, as well as dose adjustment. Available phosphate binders include magnesium hydroxide, calcium and iron-based regimes, lanthanum carbonate, and sevelamer. On the other hand, a frequently used phosphaturic agent is acetazolamide [59].
The pathophysiology and management of vascular calcification in chronic kidney disease patients
Published in Expert Review of Cardiovascular Therapy, 2023
Mehmet Kanbay, Sidar Copur, Cem Tanriover, Furkan Yavuz, Andrea Galassi, Paola Ciceri, Mario Cozzolino
High levels of fibroblast growth factor-23 (FGF-23) are related to mortality and cardiovascular events in patients with CKD [90]. Ok et al. have shown that in the prediction of coronary artery calcification in HD patients, plasma FGF-23 level is superior to phosphate, however it is not associated with carotid artery atherosclerosis [90]. In addition, soluble Klotho is associated with cardiovascular disease and mortality in CKD patients [91]. Cai et al. have reported that a decreased level of soluble Klotho can predict cardiovascular death in no or mild abdominal aortic calcification hemodialysis patients where lower soluble Klotho levels were associated with higher cardiovascular disease mortality rates [91]. One study assessed the role of Sclerostin, an osteocyte-derived inhibitor of the Wnt pathway and a key player in CKD-mineral and bone disorders [92]. They reported that sclerostin levels are increased in patients with CKD and are associated with VC and suggested that sclerostin could be used as a predictor of VC in the clinical setting [92].