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https://www.readbyqxmd.com/read/28448530/response-of-npt2a-knockout-mice-to-dietary-calcium-and-phosphorus
#1
Yuwen Li, Daniel Caballero, Julian Ponsetto, Alyssa Chen, Chuanlong Zhu, Jun Guo, Marie Demay, Harald Jüppner, Clemens Bergwitz
Mutations in the renal sodium-dependent phosphate co-transporters NPT2a and NPT2c have been reported in patients with renal stone disease and nephrocalcinosis, but the relative contribution of genotype, dietary calcium and phosphate to the formation of renal mineral deposits is unclear. We previously reported that renal calcium phosphate deposits persist and/or reappear in older Npt2a-/- mice supplemented with phosphate despite resolution of hypercalciuria while no deposits are seen in wild-type (WT) mice on the same diet...
2017: PloS One
https://www.readbyqxmd.com/read/28429545/do-the-benefits-of-using-calcitriol-and-other-vitamin-d-receptor-activators-in-patients-with-chronic-kidney-disease-outweigh-the-harms
#2
Nigel D Toussaint, Matthew J Damasiewicz
The primary indication for administration of calcitriol or other vitamin D receptor activators (VDRA) in chronic kidney disease (CKD) is secondary hyperparathyroidism (SHPT). Prevention and treatment of SHPT appears important, as imbalances in mineral metabolism are associated with renal osteodystrophy, and higher parathyroid hormone (PTH) levels are associated with increased rates of mortality and morbidity in CKD patients. There is, however, a lack of controlled trial data that show lowering PTH with calcitriol/VDRA equates to improved clinical outcomes...
March 2017: Nephrology
https://www.readbyqxmd.com/read/28425622/targeted-disruption-of-nf1-in-osteocyte-increases-fgf23-and-osteoid-with-osteomalacia-like-bone-phenotype
#3
Nobuhiro Kamiya, Ryosuke Yamaguchi, Olumide Aruwajoye, Audrey Kim, Gen Kuroyanagi, Matthew Phipps, Naga Suresh Adapala, Jian Q Feng, Harry K W Kim
Neurofibromatosis type 1 (NF1, OMIM 162200), caused by NF1 gene mutations, exhibits multi-system abnormalities including skeletal deformities in humans. Osteocytes play critical roles in controlling bone modeling and remodeling. However, the role of neurofibromin, the protein product of the NF1 gene, in osteocytes is largely unknown. This study investigated the role of neurofibromin in osteocytes by disrupting Nf1 under the Dmp1-promoter. The conditional knockout (Nf1 cKO) mice displayed serum profile of a metabolic bone disorder with an osteomalacia-like bone phenotype...
April 20, 2017: Journal of Bone and Mineral Research: the Official Journal of the American Society for Bone and Mineral Research
https://www.readbyqxmd.com/read/28415155/letter-to-the-editor-regarding-dounousi-e-et%C3%A2-al-intact-fgf23-and-%C3%AE-klotho-during-acute-inflammation-sepsis-in-ckd-patients-eur-j-clin-invest-2016-46-234-41
#4
Axel Schlitt, Urban Sester, Martina Sester, Sarah Seiler-Mussler, Vincent Brandenburg, Elke Schäffner, Gunnar H Heine
With interest we read the recent European Journal of Clinical Investigation paper entitled "Intact FGF23 and α-Klotho during acute inflammation/sepsis in CKD patients" by E. Dounousi and coworkers (1). In their article, the authors analyse the association between acute infection and plasma levels of the phosphaturic hormone fibroblast growth factor 23 (FGF-23). The physiological regulation of FGF-23 is not fully understood so far, and hence novel pathophysiological data are of importance. Particularly the link between FGF23 and inflammation is a growing field...
April 17, 2017: European Journal of Clinical Investigation
https://www.readbyqxmd.com/read/28411494/fibroblast-growth-factor-23-as-a-predictor-of-cardiovascular-and-all-cause-mortality-in-prospective-studies
#5
Zhexue Qin, Xi Liu, Mingbao Song, Quan Zhou, Jie Yu, Baoshang Zhou, Yazhou Wu, Yongming He, Lan Huang
BACKGROUND AND AIMS: The prognostic value of fibroblast growth factor 23 (FGF23) for mortality remains controversial. We performed a meta-analysis of cohort studies to examine the controversial relationship between FGF23 and mortality. METHODS: PubMed, EMBASE, the Cochrane Library databases and reference bibliographies were searched through September 2016 to identify prospective cohort studies with relative risks (RRs) and 95% confidence intervals (CIs) for FGF23 and mortality...
April 1, 2017: Atherosclerosis
https://www.readbyqxmd.com/read/28406928/fibroblast-growth-factor-23-promotes-terminal-differentiation-of-atdc5-cells
#6
Mathilde Guibert, Adeline Gasser, Hervé Kempf, Arnaud Bianchi
OBJECTIVES: Fibroblast Growth Factor 23 (FGF23) is well documented as a crucial player in the systemic regulation of phosphate homeostasis. Moreover, loss-of-function experiments have revealed that FGF23 also has a phosphate-independent and local impact on skeletogenesis. Here, we used ATDC5 cell line to investigate the expression of FGF23 and the role it may play locally during the differentiation of these cells. METHODS: ATDC5 cells were differentiated in the presence of insulin, and treated with recombinant FGF23 (rFGF23), inorganic phosphate (Pi) and/or PD173074, an inhibitor of FGF receptors (FGFRs)...
2017: PloS One
https://www.readbyqxmd.com/read/28405606/changes-in-markers-of-mineral-metabolism-after-living-kidney-donation
#7
Sven-Jean Tan, Tim D Hewitson, Peter D Hughes, Stephen G Holt, Nigel D Toussaint
BACKGROUND: Living kidney donors (LKDs) experience reduction in kidney function, however serum phosphate (sPi) levels are lower compared to patients with chronic kidney disease matched for reduced kidney function. Mineral metabolism adaptations that occur in LKDs have not been adequately investigated. To evaluate the effect of nephrectomy on markers of mineral metabolism in LKDs compared to healthy volunteers (HV) over 12 months. METHODS: Mineral parameters were evaluated in twenty-one adult LKDs and twenty HVs...
April 2017: Transplantation Direct
https://www.readbyqxmd.com/read/28401422/acetate-free-biofiltration-to-remove-fibroblast-growth-factor-23-in-hemodialysis-patients-a-pilot-study
#8
Valeria Cernaro, Silvia Lucisano, Valeria Canale, Annamaria Bruzzese, Daniela Caccamo, Giuseppe Costantino, Michele Buemi, Domenico Santoro
AIM: Serum levels of 32 kDa-phosphaturic hormone fibroblast growth factor 23 (FGF23) rise early in renal failure in order to keep phosphatemia within the normal range; however, this compensatory mechanism itself contributes to chronic kidney disease-mineral bone disorder. High FGF23 is also associated to left ventricular hypertrophy, vascular calcifications and thus increased cardiovascular risk. The aim of this pilot pre-post study was to evaluate the effects of a single hemodiafiltration session with acetate-free biofiltration (AFB) on FGF23 serum levels...
April 11, 2017: Journal of Nephrology
https://www.readbyqxmd.com/read/28399017/iron-induced-hypophosphatemia-an-emerging-complication
#9
Heinz Zoller, Benedikt Schaefer, Bernhard Glodny
PURPOSE OF REVIEW: Iron-induced hypophosphatemia is a well documented side-effect but associated complications are largely neglected, because the results from single dosing studies suggest that transient decreases in plasma phosphate concentrations are asymptomatic and fully reversible. However, an increasing number of case reports and case series suggest that some patients develop severe and symptomatic hypophosphatemia. Long-term complications from hypophosphatemia include osteomalacia and bone fractures, which can result from repeated intravenous administration of certain high-dose iron preparations...
April 8, 2017: Current Opinion in Nephrology and Hypertension
https://www.readbyqxmd.com/read/28383812/mutational-analysis-of-phex-fgf23-and-clcn5-in-patients-with-hypophosphataemic-rickets
#10
Ayla Guven, Roua A Al-Rijjal, Huda BinEssa, Durmuş Dogan, Yılmaz Kor, Minjing Zou, Namik Kaya, Anwar F Al-Enazi, Suna Hancili, Ömer Tarım, Essa Y Baitei, Walaa E Kattan, Brian F Meyer, Yufei Shi
CONTEXT: Hypophosphataemic rickets (HR) is a group of rare hereditary renal phosphate wasting disorders caused by mutations in PHEX, FGF23, DMP1, ENPP1, CLCN5, or SLC34A3. OBJECTIVE: To investigate underlying genetic defects in patients with hypophosphataemic rickets. METHODS: We analyzed genomic DNA from 9 unrelated families for mutations in the entire coding region of PHEX, FGF23, DMP1, ENPP1, CLCN5, or SLC34A3 by PCR-sequencing and copy number analysis...
April 6, 2017: Clinical Endocrinology
https://www.readbyqxmd.com/read/28382624/cinacalcet-as-an-alternative-to-phosphate-therapy-in-x-linked-hypophosphataemic-rickets
#11
Uri S Alon, Dale Jarka, Penny J Monachino, Judith Sebestyen VanSickle, Tarak Srivastava
X-linked hypophosphataemic rickets (XLH), caused by mutations in the PHEX gene, has traditionally been treated with a combination of high doses of oral phosphate and active vitamin D metabolites with the goal of normalizing serum phosphate concentration to a degree sufficient to heal the rickets while avoiding iatrogenic complications. Although XLH is caused by elevated serum levels of fibroblast growth factor 23 (FGF23), parathyroid hormone (PTH) still plays a role through its independent effect on the tubular threshold for phosphate per glomerular filtration rate (TP/GFR), which influences serum phosphate concentration...
April 6, 2017: Clinical Endocrinology
https://www.readbyqxmd.com/read/28379384/osteocyte-protein-expression-is-altered-in-low-turnover-osteoporosis-caused-by-mutations-in-wnt1-and-pls3
#12
Katherine Wesseling-Perry, Riikka E Mäkitie, Ville-Valtteri Välimäki, Tero Laine, Christine M Laine, Matti J Välimäki, Renata C Pereira, Outi Mäkitie
Context: Osteocytes express proteins that regulate bone remodeling and mineralization as well as osteoblast and adipocyte differentiation. Objective: To evaluate the relationship between osteocyte-specific protein expression and bone histology in patients with monogenic osteoporosis due to WNT1 or PLS3 mutations. Design and Setting: Cross-sectional cohort study at a University Hospital. Participants: 6 patients (4 males, age range 14-72 years) with a heterozygous WNT1 mutation and 5 patients (4 males, age 9-70 years) with a hetero-/hemizygous PLS3 mutation...
April 3, 2017: Journal of Clinical Endocrinology and Metabolism
https://www.readbyqxmd.com/read/28378123/secondary-hyperparthyroidism-pathogenesis-diagnosis-preventive-and-therapeutic-strategies
#13
REVIEW
Mariano Rodríguez Portillo, María E Rodríguez-Ortiz
Uremic secondary hyperparathyroidism is a multifactorial and complex disease often present in advanced stages of chronic kidney disease. The accumulation of phosphate, the increased FGF23 levels, the reduction in active vitamin D production, and the tendency to hypocalcemia are persistent stimuli for the development and progression of parathyroid hyperplasia with increased secretion of PTH. Parathyroid proliferation may become nodular mainly in cases of advanced hyperparathyroidism. The alterations in the regulation of mineral metabolism, the development of bone disease and extraosseous calcifications are essential components of chronic kidney disease-mineral and bone disorder and have been associated with negative outcomes...
March 2017: Reviews in Endocrine & Metabolic Disorders
https://www.readbyqxmd.com/read/28377980/the-metabolic-bone-disease-associated-with-the-hyp-mutation-is-independent-of-osteoblastic-hif1%C3%AE-expression
#14
Julia M Hum, Erica L Clinkenbeard, Colin Ip, Taryn A Cass, Matt Allen, Kenneth E White
Fibroblast growth factor-23 (FGF23) controls key responses to systemic phosphate increases through its phosphaturic actions on the kidney. In addition to stimulation by phosphate, FGF23 positively responds to iron deficiency anemia and hypoxia in rodent models and in humans. The disorder X-linked hypophosphatemia (XLH) is characterized by elevated FGF23 in concert with an intrinsic bone mineralization defect. Indeed, the Hyp mouse XLH model has disturbed osteoblast to osteocyte differentiation with altered expression of a wide variety of genes, including FGF23...
June 2017: Bone Reports
https://www.readbyqxmd.com/read/28376076/effects-of-growth-hormone-treatment-on-growth-plate-bone-and-mineral-metabolism-of-young-rats-with-uremia-induced-by-adenine
#15
Débora Claramunt, Helena Gil-Peña, Rocío Fuente, Enrique García-López, Olaya Hernández Frías, Flor A Ordoñez, Julián Rodríguez-Suárez, Fernando Santos
BACKGROUND: In a model of growth retardation secondary to chronic kidney disease (CKD) induced by adenine, this study explores the effects of growth hormone (GH) therapy on growth plate and mineral metabolism. METHODS: Weaning female rats receiving 0.5% adenine diet during 21 days, untreated (AD) or treated with GH (ADGH) for one-week, were compared with control rats receiving normal diet, either ad libitum or pair-fed with AD animals. AD and ADGH rats had similarly elevated serum concentrations of urea nitrogen, parathyroid hormone (PTH) and fibroblast growth factor 23 (FGF23)...
April 4, 2017: Pediatric Research
https://www.readbyqxmd.com/read/28362263/inhibitor-of-ppgalnac-t3-mediated-o-glycosylation-blocks-cancer-cell-invasiveness-and-lowers-fgf23-levels
#16
Lina Song, Adam Linstedt
Small molecule inhibitors of site-specific O-glycosylation by the polypeptide N-acetylgalactosaminyltransferase (ppGalNAc-T) family are currently unavailable but hold promise as therapeutics, especially if selective against individual ppGalNAc-T isozymes. To identify a compound targeting the ppGalNAc-T3 isozyme, we screened libraries to find compounds that act on a cell-based fluorescence sensor of ppGalNAc-T3 but not on a sensor of ppGalNAc-T2. This identified a hit that subsequent in vitro analysis showed directly binds and inhibits purified ppGalNAc-T3 with no detectable activity against either ppGalNAc-T2 or ppGalNAc-T6...
March 31, 2017: ELife
https://www.readbyqxmd.com/read/28345861/identification-of-gene-transcription-start-sites-and-enhancers-responding-to-pulmonary-carbon-nanotube-exposure-in-vivo
#17
Jette Bornholdt, Anne Thoustrup Saber, Berit Lilje, Mette Boyd, Mette Jørgensen, Yun Chen, Morana Vitezic, Nicklas Raun Jacobsen, Sarah Søs Poulsen, Trine Berthing, Simon Bressendorff, Kristoffer Vitting-Seerup, Robin Andersson, Karin Sørig Hougaard, Carole L Yauk, Sabina Halappanavar, Håkan Wallin, Ulla Vogel, Albin Sandelin
Increased use of nanomaterials in industry, medicine, and consumer products has raised concerns over their toxicity. To ensure safe use of nanomaterials, understanding their biological effects at the molecular level is crucial. In particular, the regulatory mechanisms responsible for the cascade of genes activated by nanomaterial exposure are not well-characterized. To this end, we profiled the genome-wide usage of gene transcription start sites and linked active enhancer regions in lungs of C57BL/6 mice 24 h after intratracheal instillation of a single dose of the multiwalled carbon nanotube (MWCNT) Mitsui-7...
April 25, 2017: ACS Nano
https://www.readbyqxmd.com/read/28341900/tumor-induced-osteomalacia-experience-from-a-south-american-academic-center
#18
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
#19
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
#20
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
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