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fibroblast growth factor 23

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https://www.readbyqxmd.com/read/28346348/vitamin-d-in-chronic-kidney-disease-and-dialysis-patients
#1
REVIEW
Guillaume Jean, Jean Claude Souberbielle, Charles Chazot
Vitamin D deficiency (<20 ng/mL) and insufficiency (20-29 ng/mL) are common among patients with chronic kidney disease (CKD) or undergoing dialysis. In addition to nutritional and sunlight exposure deficits, factors that affect vitamin D deficiency include race, sex, age, obesity and impaired vitamin D synthesis and metabolism. Serum 1,25(OH)₂D levels also decrease progressively because of 25(OH)D deficiency, together with impaired availability of 25(OH)D by renal proximal tubular cells, high fibroblast growth factor (FGF)-23 and decreased functional renal tissue...
March 25, 2017: Nutrients
https://www.readbyqxmd.com/read/28341900/tumor-induced-osteomalacia-experience-from-a-south-american-academic-center
#2
G González, R Baudrand, M F Sepúlveda, N Vucetich, F J Guarda, P Villanueva, O Contreras, A Villa, F Salech, L Toro, L Michea, P Florenzano
The majority of tumor-induced osteomalacia cases have been reported in the Northern Hemisphere and Asia. In this first series of South American patients, we show that the clinical presentation and sensitivity of plasmatic fibroblast growth factor 23 and somatostatin analog-based imaging are similar to those described in other populations. INTRODUCTION: Describe the experience of clinical presentation, diagnostic study, and treatment of patients with tumor-induced osteomalacia (TIO) in a South American academic center in comparison to literature...
March 25, 2017: Osteoporosis International
https://www.readbyqxmd.com/read/28341272/kidney-fibroblast-growth-factor-23-does-not-contribute-to-elevation-of-its-circulating-levels-in-uremia
#3
Maria L Mace, Eva Gravesen, Anders Nordholm, Jacob Hofman-Bang, Thomas Secher, Klaus Olgaard, Ewa Lewin
Fibroblast growth factor 23 (FGF23) secreted by osteocytes is a circulating factor essential for phosphate homeostasis. High plasma FGF23 levels are associated with cardiovascular complications and mortality. Increases of plasma FGF23 in uremia antedate high levels of phosphate, suggesting a disrupted feedback regulatory loop or an extra-skeletal source of this phosphatonin. Since induction of FGF23 expression in injured organs has been reported we decided to examine the regulation of FGF23 gene and protein expressions in the kidney and whether kidney-derived FGF23 contributes to the high plasma levels of FGF23 in uremia...
March 21, 2017: Kidney International
https://www.readbyqxmd.com/read/28339837/vitamin-d-treatment-attenuates-cardiac-fgf23-fgfr4-signaling-and-hypertrophy-in-uremic-rats
#4
Maren Leifheit-Nestler, Alexander Grabner, Laura Hermann, Beatrice Richter, Karin Schmitz, Dagmar-Christiane Fischer, Christopher Yanucil, Christian Faul, Dieter Haffner
Background.: Vitamin D deficiency and excess of circulating fibroblast growth factor 23 (FGF23) contribute to cardiovascular mortality in patients with chronic kidney disease (CKD). FGF23 activates FGF receptor 4 and (FGFR4) calcineurin/nuclear factor of activated T cells (NFAT) signaling in cardiac myocytes, thereby causing left ventricular hypertrophy (LVH). Here, we determined if 1,25-dihydroxyvitamin D (calcitriol) inhibits FGF23-induced cardiac signaling and LVH. Methods...
February 23, 2017: Nephrology, Dialysis, Transplantation
https://www.readbyqxmd.com/read/28339804/intra-cardiac-and-peripheral-levels-of-biochemical-markers-of-fibrosis-in-patients-undergoing-catheter-ablation-for-atrial-fibrillation
#5
Gordon A Begg, Rashed Karim, Tobias Oesterlein, Lee N Graham, Andrew J Hogarth, Stephen P Page, Christopher B Pepper, Kawal Rhode, Gregory Y H Lip, Arun V Holden, Sven Plein, Muzahir H Tayebjee
Aims: Measurement of circulating biomarkers of fibrosis may have a role in selecting patients and treatment strategy for catheter ablation. Pro-collagen type III N-terminal pro-peptide (PIIINP), C-telopeptide of type I collagen (ICTP), fibroblast growth factor 23 (FGF-23), and galectin 3 (gal-3) have all been suggested as possible biomarkers for this indication, but studies assessing whether peripheral levels reflect intra-cardiac levels are scarce. Methods and results: We studied 93 patients undergoing ablation for paroxysmal atrial fibrillation (AF) (n = 63) or non-paroxysmal AF (n = 30)...
February 27, 2017: Europace: European Pacing, Arrhythmias, and Cardiac Electrophysiology
https://www.readbyqxmd.com/read/28337344/is-fibroblast-growth-factor-23-the-leading-cause-of-increased-mortality-among-chronic-kidney-disease-patients-a-narrative-review
#6
REVIEW
Usama A Sharaf El Din, Mona M Salem, Dina O Abdulazim
The death rate among chronic kidney disease patients is the highest compared to other chronic diseases. 60% of these fatalities are cardiovascular. Cardiovascular calcifications and chronic inflammation affect almost all chronic kidney disease patients and are associated with cardiovascular mortality. Fibroblast growth factor 23 is associated with vascular calcification. Systemic inflammation in chronic kidney disease patients is multifactorial. The role of systemic inflammation in the pathogenesis of vascular calcification was recently reappraised...
May 2017: Journal of Advanced Research
https://www.readbyqxmd.com/read/28329057/coronary-artery-calcification-and-risk-of-cardiovascular-disease-and-death-among-patients-with-chronic-kidney-disease
#7
Jing Chen, Matthew J Budoff, Muredach P Reilly, Wei Yang, Sylvia E Rosas, Mahboob Rahman, Xiaoming Zhang, Jason A Roy, Eva Lustigova, Lisa Nessel, Virginia Ford, Dominic Raj, Anna C Porter, Elsayed Z Soliman, Jackson T Wright, Myles Wolf, Jiang He
Importance: Coronary artery calcification (CAC) is highly prevalent in dialysis-naive patients with chronic kidney disease (CKD). However, there are sparse data on the association of CAC with subsequent risk of cardiovascular disease and all-cause mortality in this population. Objective: To study the prospective association of CAC with risk of cardiovascular disease and all-cause mortality among dialysis-naive patients with CKD. Design, Setting, and Participants: The prospective Chronic Renal Insufficiency Cohort study recruited adults with an estimated glomerular filtration rate of 20 to 70 mL/min/1...
March 22, 2017: JAMA Cardiology
https://www.readbyqxmd.com/read/28326356/effect-of-four-monthly-doses-of-a-human-monoclonal-anti-fgf23-antibody-krn23-on-quality-of-life-in-x-linked-hypophosphatemia
#8
Mary D Ruppe, Xiaoping Zhang, Erik A Imel, Thomas J Weber, Mark A Klausner, Takahiro Ito, Maria Vergeire, Jeffrey S Humphrey, Francis H Glorieux, Anthony A Portale, Karl Insogna, Munro Peacock, Thomas O Carpenter
X-linked hypophosphatemia (XLH) is characterized by lower extremity deformities that lead to bone and/or joint pain that result from decreased renal tubular reabsorption leading to hypophosphatemia caused by elevated levels of fibroblast growth factor 23 (FGF23). OBJECTIVE: Validate the use of SF-36v2 Health Survey (SF-36v2) and the Western Ontario and McMaster Osteoarthritis Index (WOMAC) to measure previously unstudied health-related quality of life (HRQoL) in XLH patients and determine the change in HRQoL before and after treatment with KRN23, a human monoclonal anti-FGF23 antibody...
December 2016: Bone Reports
https://www.readbyqxmd.com/read/28326350/tumor-induced-osteomalacia-secondary-to-anaplastic-thyroid-carcinoma-a-case-report-and-review-of-the-literature
#9
Ejigayehu G Abate, Victor Bernet, Cherise Cortese, Hillary W Garner
CONTEXT: Tumor induced osteomalacia related to anaplastic thyroid cancer has never been reported. OBJECTIVE: We describe a case of tumor induced osteomalacia (TIO) in a patient with a fibroblast growth factor 23 (FGF-23) secreting anaplastic thyroid carcinoma. The current imaging modalities are reviewed. DESIGN AND INTERVENTION: Clinical, biochemical, and radiological assessments were done, including computer tomography (CT) of the neck and skull to thigh positron emission tomography (PET)/CT...
December 2016: Bone Reports
https://www.readbyqxmd.com/read/28324013/acute-parathyroid-hormone-injection-increases-c-terminal-but-not-intact-fibroblast-growth-factor-23-levels
#10
V M Knab, B Corbin, O Andrukhova, J M Hum, P Ni, S Rabadi, A Maeda, K E White, R G Erben, H Jüppner, M Christov
The acute effects of PTH on FGF23 in vivo are not well understood. After a single s.c. PTH(1-34) injection (50nmol/kg) in mice, FGF23 levels were assessed in plasma using assays that measure either intact alone (iFGF23) or intact/C-terminal FGF23 (cFGF23). Furthermore, FGF23 mRNA and protein levels were assessed in bone. In addition, we examined the effects of PTH treatment on FGF23 production in vitro using differentiated calvarial osteocyte-like cells. cFGF23 levels increased by 3-5-fold within two hours following PTH injection, which returned to baseline by 4 hours...
January 23, 2017: Endocrinology
https://www.readbyqxmd.com/read/28323996/molecular-physiology-of-the-hypocalcemic-action-of-fibroblast-growth-factor-23-in-zebrafish-danio-rerio
#11
Chia-Hao Lin, Huei-Jyun Hu, Pung-Pung Hwang
Fibroblast growth factor 23 (FGF23), a hormone required for phosphorus metabolism, was recently proposed to act on Ca2+ uptake; however, the available evidences of how FGF23 controls the body fluid Ca2+ homeostasis needs to be further clarified. The use of zebrafish as a model system revealed that FGF23 is specifically expressed in the corpuscles of Stannius (CS), an organ involved in Ca2+ homeostasis in fish, and its expression is stimulated by ambient water with a high Ca2+ level. The overexpression of FGF23 inhibited Ca2+ uptake by downregulating the mRNA expression of epithelium calcium channel (ECaC)...
March 1, 2017: Endocrinology
https://www.readbyqxmd.com/read/28323987/fibroblast-growth-factor-23-mineral-metabolism-and-adiposity-in-normal-kidney-function
#12
Sarah Zaheer, Ian H de Boer, Matthew Allison, Jenifer M Brown, Bruce M Psaty, Cassianne Robinson-Cohen, Erin D Michos, Joachim H Ix, Bryan Kestenbaum, David Siscovick, Anand Vaidya
Context: Obesity is associated with poor bone mineralization and quality. Fibroblast growth factor 23 (FGF23) plays an important role in calcium, phosphate, and skeletal physiology. Objective: To test the hypothesis that greater adiposity results in higher FGF23 levels among individuals with normal estimated glomerular filtration rate (eGFR). Design, Setting, Participants: Cross-sectional analyses among participants of the Multi-Ethnic Study of Atherosclerosis with eGFR ≥60 mL/min/1...
January 17, 2017: Journal of Clinical Endocrinology and Metabolism
https://www.readbyqxmd.com/read/28323960/fgf23-is-not-associated-with-age-related-changes-in-phosphate-but-enhances-renal-calcium-reabsorption-in-girls
#13
Deborah M Mitchell, Harald Jüppner, Sherri-Ann M Burnett-Bowie
Context: Fibroblast growth factor 23 (FGF23) is a critical determinant of phosphate homeostasis. The role of FGF23, however, in regulating physiologic changes in serum phosphate and renal phosphate handling across childhood is not well-described. In addition, animal models have suggested a role for FGF23 in regulating renal calcium excretion. Objective: To assess changes in FGF23 concentrations across childhood in relation to changes in mineral ions and hormones of mineral ion homeostasis...
January 31, 2017: Journal of Clinical Endocrinology and Metabolism
https://www.readbyqxmd.com/read/28323144/tissue-expression-and-source-of-circulating-%C3%AE-klotho
#14
REVIEW
Hannes Olauson, Rik Mencke, Jan-Luuk Hillebrands, Tobias E Larsson
αKlotho (Klotho), a type I transmembrane protein and a coreceptor for Fibroblast growth factor-23, was initially thought to be expressed only in a limited number of tissues, most importantly the kidney, parathyroid gland and choroid plexus. Emerging data may suggest a more ubiquitous Klotho expression pattern which has prompted reevaluation of the restricted Klotho paradigm. Herein we systematically review the evidence for Klotho expression in various tissues and cell types in humans and other mammals, and discuss potential reasons behind existing conflicting data...
March 17, 2017: Bone
https://www.readbyqxmd.com/read/28321399/renocardiovascular-biomarkers-from-the-perspective-of-managing-chronic-kidney-disease-and-cardiovascular-disease
#15
REVIEW
Shinichiro Niizuma, Yoshitaka Iwanaga, Takaharu Yahata, Shunichi Miyazaki
Mortality among the patients with chronic kidney disease (CKD) and end-stage renal disease (ESRD) remains high because of the very high incidence of cardiovascular disease (CVD) such as coronary artery disease, cardiac hypertrophy, and heart failure. Identifying CVD in patients with CKD/ESRD remains a significant hurdle and the early diagnosis and therapy for CVD is crucial in these patients. Therefore, it is necessary for the better management to identify and utilize cardiovascular (CV) biomarkers in profiling CVD risk and enabling stratification of early mortality...
2017: Frontiers in Cardiovascular Medicine
https://www.readbyqxmd.com/read/28318623/the-complexity-of-chronic-kidney-disease-mineral-and-bone-disorder-across-stages-of-chronic-kidney%C3%A2-disease
#16
Fabiana G Graciolli, Katia R Neves, Fellype Barreto, Daniela V Barreto, Luciene M Dos Reis, Maria E Canziani, Yves Sabbagh, Aluizio B Carvalho, Vanda Jorgetti, Rosilene M Elias, Susan Schiavi, Rosa M A Moysés
Chronic Kidney Disease (CKD)-Mineral and Bone Disorder (CKD-MBD) is a complex disease that is not completely understood. However, some factors secreted by the osteocytes might play an important role in its pathophysiology. Therefore, we evaluated the bone expression of proteins in a group of patients with CKD 2-3, CKD 4, and CKD 5 on dialysis and healthy individuals. We also tested several bone remodeling markers, and correlated these levels with bone biopsy findings. As expected, as serum calcium decreased, serum phosphate, alkaline phosphatase, fibroblast growth factor-23 (FGF-23), parathyroid hormone, and osteoprotegerin increased, as CKD progressed...
March 15, 2017: Kidney International
https://www.readbyqxmd.com/read/28298956/phosphorus-regulation-in-chronic-kidney-disease
#17
Wadi N Suki, Linda W Moore
Serum phosphorus levels stay relatively constant through the influence of multiple factors-such as parathyroid hormone, fibroblast growth factor 23, and vitamin D-on the kidney, bone, and digestive system. Whereas normal serum phosphorus ranges between 3 mg/dL to 4.5 mg/dL, large cross-sectional studies have shown that even people with normal kidney function are sometimes found to have levels ranging between 1.6 mg/dL and 6.2 mg/dL. While this may partially be due to diet and the factors mentioned above, total understanding of these atypical ranges of serum phosphorus remains uncertain...
October 2016: Methodist DeBakey Cardiovascular Journal
https://www.readbyqxmd.com/read/28298360/stimulation-of-fibroblast-growth-factor-23-by-metabolic-acidosis-requires-osteoblastic-intracellular-calcium-signaling-and-prostaglandin-synthesis
#18
Nancy S Krieger, David A Bushinsky
Serum fibroblast growth factor 23 (FGF23) increases progressively in chronic kidney disease (CKD) and is associated with increased mortality. FGF23 is synthesized in osteoblasts and osteocytes; however, the factors regulating its production are not clear. Patients with CKD have decreased renal acid excretion leading to metabolic acidosis (MET). During MET, acid is buffered by bone with release of mineral calcium (Ca) and phosphate (P). MET increases intracellular Ca signaling and cyclooxygenase 2 (COX2)-induced prostaglandin production in the osteoblast leading to decreased bone formation and increased bone resorption...
March 15, 2017: American Journal of Physiology. Renal Physiology
https://www.readbyqxmd.com/read/28294047/klotho-fgf23-cardiovascular-disease-and-vascular-calcification-black-or-white
#19
Giuseppe Cianciolo, Andrea Galassi, Irene Capelli, Roberto Schillaci, Gaetano La Manna, Mario Cozzolino
Patients affected by Chronic Kidney Disease and Mineral Bone Disorder (CKD-MBD) have a high risk of cardiovascular (CV) mortality that is poorly explained by traditional risk factors. The newest medical treatments for CKD-MBD have been associated with encouraging, but still inconsistent, improvement in CV disease complications and patient survival. A better understanding of the biomarkers and mechanisms of left ventricular hypertrophy (LVH), atherosclerosis, and vascular calcification (VC) may help with diagnosis and treatment of the organ damage that occurs secondary to CKD-MBD, thus improving survival...
March 9, 2017: Current Vascular Pharmacology
https://www.readbyqxmd.com/read/28276325/ferric-carboxymaltose-induced-hypophosphataemia-after-kidney-transplantation
#20
V Sari, R Atiqi, E J Hoorn, A C Heijboer, T van Gelder, D A Hesselink
BACKGROUND: Ferric carboxymaltose (FCM) can induce hypophosphataemia in the general population and patients with chronic kidney disease (CKD). Less is known about the effect of FCM in the kidney transplant population. It has been suggested that fibroblast growth factor 23 (FGF-23)-mediated renal phosphate wasting may be the most likely cause of this phenomenon. In the current study, the effects of FCM on phosphate metabolism were studied in a cohort of kidney transplant recipients. METHODS: Two index patients receiving FCM are described...
March 2017: Netherlands Journal of Medicine
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