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Michael J Econs, Glenn W Irwin
No abstract text is available yet for this article.
October 13, 2016: Bone
Mark Hanudel, Harald Jüppner, Isidro B Salusky
In chronic kidney disease, systemic inflammation is common and associated with mortality. The present study demonstrates that fibroblast growth factor 23 (FGF23) contributes to uremic inflammation by increasing hepatic expression and secretion of inflammatory cytokines. FGF23 binds to hepatic FGFR4, inducing calcineurin/nuclear factor of activated T-cell signaling, resulting in increased expression of interleukin 6 and C-reactive protein. The proinflammatory effects of FGF23 are inhibited by an isoform-specific FGFR4 blocking antibody and by cyclosporine, a calcineurin inhibitor...
November 2016: Kidney International
Mark R Hanudel, Kristine Chua, Maxime Rappaport, Victoria Gabayan, Erika Valore, David Goltzman, Tomas Ganz, Elizabeta Nemeth, Isidro B Salusky
In the setting of normal kidney function, iron deficiency is associated with increased FGF23 production and cleavage, altering circulating FGF23 levels. Our objective was to determine how chronic kidney disease (CKD) and dietary iron intake affect FGF23 production and metabolism in wild type (WT) and hepcidin knockout (HKO) mice. For eight weeks, the mice were fed diets that contained adenine (to induce CKD) or no adenine (control group), with either low iron (4 ppm) or standard iron (335 ppm) concentrations...
October 12, 2016: American Journal of Physiology. Renal Physiology
Christian Faul
Fibroblast growth factors (FGF) are mitogenic signal mediators that induce cell proliferation and survival. Although cardiac myocytes are post-mitotic, they have been shown to be able to respond to local and circulating FGFs. While precise molecular mechanisms are not well characterized, some FGF family members have been shown to induce cardiac remodeling under physiologic conditions by mediating hypertrophic growth in cardiac myocytes and by promoting angiogenesis, both events leading to increased cardiac function and output...
October 7, 2016: Bone
Shih-Yu Huang, Yao-Chang Chen, Yu-Hsun Kao, Ming-Hsiung Hsieh, Yung-Kuo Lin, Cheng-Chih Chung, Ting-I Lee, Wen-Chin Tsai, Shih-Ann Chen, Yi-Jen Chen
Fibroblast growth factor 23 (FGF23), elevated in chronic renal failure, increases atrial arrhythmogenesis and dysregulates calcium homeostasis. Late sodium currents (INa-Late) critically induces ectopic activity of pulmoanry vein (the most important atrial fibrillation trigger). This study was to investigate whether FGF23 activates the INa-Late leading to calcium dysregulation and increases PV arrhythmogenesis. Patch clamp, western blot, and confocal microscopy were used to evaluate the electrical activities, calcium homeostasis, and mitochondrial reactive oxygen species (ROS) in PV cardiomyocytes with or without FGF23 (0...
October 4, 2016: Oncotarget
Dieter Haffner, Maren Leifheit-Nestler
Chronic kidney disease (CKD) is associated with an increased risk of cardiovascular mortality, infections, and impaired cognitive function. It is characterized by excessively increased levels of the phosphaturic hormone fibroblast growth factor 23 (FGF23) and a deficiency of its co-receptor Klotho. Despite the important physiological effect of FGF23 in maintaining phosphate homeostasis, there is increasing evidence that higher FGF23 levels are a risk factor for mortality and cardiovascular disease. FGF23 directly induces left ventricular hypertrophy via activation of the FGF receptor 4/calcineurin/nuclear factor of activated T cells signaling pathway...
October 4, 2016: Pediatric Nephrology: Journal of the International Pediatric Nephrology Association
Xiang Hu, Xiaojing Ma, Yuqi Luo, Yiting Xu, Qin Xiong, Xiaoping Pan, Yuqian Bao, Weiping Jia
Accumulating evidence supported an association between diabetes and fibroblast growth factor 23 (FGF23). The goal of the present study was to explore alteration in serum FGF23 levels and to assess its value for identifying subclinical atherosclerosis in normoglycemic individuals with a first-degree family history of diabetes (FHD). The study enrolled 312 subjects with a first-degree FHD and 1407 subjects without an FHD. Serum FGF23 levels were detected by a sandwich enzyme-linked immunosorbent assay. Serum FGF23 levels were much higher in subjects with a first-degree FHD than in those without an FHD (P = 0...
October 4, 2016: Scientific Reports
Pamela L Lutsey, Christina M Parrinello, Jeffrey R Misialek, Andy N Hoofnagle, Clark M Henderson, Thomas J Laha, Erin D Michos, John H Eckfeldt, Elizabeth Selvin
BACKGROUND: Quantifying the variability of biomarkers is important, as high within-person variability can lead to misclassification of individuals. Short-term variability of important markers of vitamin D metabolism is relatively unknown. METHODS: A repeatability study was conducted in 160 Atherosclerosis Risk in Communities study participants (60% female, 28% black, mean age 76 years). Fasting serum was drawn at 2 time points, a median of 6 (range 3-13) weeks apart...
September 30, 2016: Clinical Chemistry
Miki Imazu, Hiroyuki Takahama, Makoto Amaki, Yasuo Sugano, Takahiro Ohara, Takuya Hasegawa, Hideaki Kanzaki, Toshihisa Anzai, Naoki Mochizuki, Hiroshi Asanuma, Masanori Asakura, Masafumi Kitakaze
Recently, fibroblast growth factor 23 (FGF23), a phosphate-regulating hormone, has been linked to the pathophysiology of heart failure (HF), thus encouraging us to examine which hemodynamic abnormalities of HF are linked to either serum FGF23 or plasma B-type natriuretic peptide (BNP) levels. We measured both the serum FGF23 and plasma BNP levels in 154 consecutive prospectively enrolled hospitalized HF patients, with an estimated glomerular filtration rate >40 ml min(-1) 1.73 m(-2), who underwent heart catheterizations and an echocardiogram...
September 29, 2016: Hypertension Research: Official Journal of the Japanese Society of Hypertension
Shunsuke Goto, Hideki Fujii, Keiji Kono, Kentaro Watanabe, Kentaro Nakai, Shinichi Nishi
Fibroblast growth factor 23 (FGF23) is regulated by sustained phosphate supplementation and restriction. However, few studies have investigated FGF23 levels in patients with Fanconi syndrome. Therefore, we evaluated intact and C-terminal FGF23 and FGF23-associated parameters in four patients with Fanconi syndrome. Serum intact and C-terminal FGF23 levels were extremely low. Although serum phosphate and 1,25-dihydroxyvitamin D levels improved to or above the normal range within 1 year of treatment with oral phosphate and calcitriol, serum FGF23 levels remained low...
October 2016: Clinical Kidney Journal
Narayan Prasad, Akhilesh Jaiswal, Vikas Agarwal, Shashi Kumar, Saurabh Chaturvedi, Subhash Yadav, Amit Gupta, Raj K Sharma, Dharmendra Bhadauria, Anupama Kaul
BACKGROUND: We aimed to longitudinally analyse changes in the levels of serum fibroblast growth factor 23 (FGF23), intact parathyroid hormone (iPTH) and associated minerals in patients undergoing renal transplantation. METHODS: Sixty-three patients with end-stage renal disease (ESRD) who underwent living donor transplantation were recruited. Serum FGF23, iPTH, uric acid, inorganic phosphorous (iP), blood urea nitrogen and serum creatinine were measured pre-transplant and at 1 (M1), 3 (M3) and 12 months (M12) post-transplantation...
October 2016: Clinical Kidney Journal
Giuseppe Cianciolo, Mario Cozzolino
During the last decade, a new view into the molecular mechanisms of chronic kidney disease-mineral bone disorder (CKD-MBD) has been proposed, with fibroblast growth factor 23 (FGF23) as a novel player in the field. Enhanced serum FGF23 levels cause a reduction in serum phosphate, together with calcitriol suppression and consequent hyperparathyroidism (HPT). In contrast, reduced serum FGF23 levels are associated with hyperphosphatemia, higher calcitriol levels and parathyroid hormone (PTH) suppression. In addition, serum FGF23 levels are greatly increased and positively correlated with serum phosphate levels in CKD patients...
October 2016: Clinical Kidney Journal
Stuart M Sprague, Paul W Crawford, Joel Z Melnick, Stephen A Strugnell, Shaukat Ali, Roberto Mangoo-Karim, Sungchun Lee, P Martin Petkovich, Charles W Bishop
BACKGROUND/AIMS: Vitamin D insufficiency and secondary hyperparathyroidism (SHPT) are associated with increased morbidity and mortality in chronic kidney disease (CKD) and are poorly addressed by current treatments. The present clinical studies evaluated extended-release (ER) calcifediol, a novel vitamin D prohormone repletion therapy designed to gradually correct low serum total 25-hydroxyvitamin D, improve SHPT control and minimize the induction of CYP24A1 and FGF23. METHODS: Two identical multicenter, randomized, double-blind, placebo-controlled studies enrolled subjects from 89 US sites...
September 28, 2016: American Journal of Nephrology
María Luisa Ceballos Osorio, Francisco Cano Schuffeneger
: Growth failure is one of the most relevant complications in children with chronic kidney disease (CKD). Among others, growth hormone (GH) resistance and bone mineral disorders have been identified as the most important causes of growth retardation. OBJECTIVES: 1. To characterize bone mineral metabolism and growth hormone bio-markers in CKD children treated with chronic peritoneal dialysis (PD). 2. To evaluate height change with rhGH treatment. PATIENTS AND METHOD: A longitudinal 12-month follow-up in prepuberal PD children...
September 19, 2016: Revista Chilena de Pediatría
Jan Rossaint, Mark Unruh, Alexander Zarbock
During chronic kidney disease (CKD), bone mineral metabolism is disturbed owing in part to the endogenous hormone fibroblast growth factor 23 (FGF23). Elevated FGF23 levels are seen in CKD patients. Current research has demonstrated that FGF23 directly modulates the immune response and host defense to bacterial infections. FGF23 also impairs the activation and recruitment of neutrophils, which are the main immune effector cells required for host defense against bacterial infections. In addition, while FGF23 levels reduce leukocyte recruitment and functions, inflammatory conditions may also-in a reverse fashion-contribute to elevated FGF23 levels in the circulation...
September 22, 2016: Nephrology, Dialysis, Transplantation
Hiroshi Matsuzaki, Shinichi Katsumata, Yoshiaki Maeda, Yasutaka Kajita
Fibroblast growth factor 23 (FGF23) is a potent regulator of phosphorus (P) and vitamin D metabolism. Long-term dietary magnesium (Mg) deficiency increases circulating levels of FGF23, whereas the effects of short-term dietary Mg deficiency are unclear. Thus, the present study investigated whether short-term dietary Mg deficiency affects circulating levels of FGF23. We also assessed changes in renal mRNA expression of vitamin D metabolizing enzymes and type II sodium-phosphate (Na/Pi) cotransporters, since these are regulated by FGF23...
June 1, 2016: Magnesium Research: Official Organ of the International Society for the Development of Research on Magnesium
Reinhold G Erben, Olena Andrukhova
Fibroblast growth factor-23 (FGF23) is a bone-derived hormone protecting against the potentially deleterious effects of hyperphosphatemia by suppression of phosphate reabsorption and of active vitamin D hormone synthesis in the kidney. The kidney is one of the main target organs of FGF23 signaling. The purpose of this review is to highlight the recent advances in the area of FGF23-Klotho signaling in the kidney. During recent years, it has become clear that FGF23 acts independently on proximal and distal tubular epithelium...
September 10, 2016: Bone
Teppei Sakoh, Masaru Nakayama, Takuya Tsuchihashi, Ryota Yoshitomi, Shigeru Tanaka, Eisuke Katafuchi, Akiko Fukui, Yui Shikuwa, Naohiko Anzai, Takanari Kitazono, Kazuhiko Tsuruya
OBJECTIVE: In patients with preserved kidney function, a positive association of fibroblast growth factor 23 (FGF23) with serum uric acid (SUA) has been reported; however, the relationship in overall chronic kidney disease (CKD) patients has not been investigated. No report has examined the relationship between FGF23 and uric acid clearance (CUA). The aim of the present study was to determine whether FGF23 is independently associated with urate metabolism in patients with CKD stages 1-5...
October 2016: Metabolism: Clinical and Experimental
Takehiro Nakahara, Keiko Kawai-Kowase, Hiroki Matsui, Hiroaki Sunaga, Toshihiro Utsugi, Tatsuya Iso, Masashi Arai, Shouichi Tomono, Masahiko Kurabayashi
BACKGROUND AND AIMS: Elevated fibroblast growth factor 23 (FGF23) levels are associated with cardiovascular mortality in patients with chronic kidney disease. However, both clinical and basic research have demonstrated conflicting evidence regarding the pathophysiological role of FGF23 in vascular calcification. The aim of this study was to determine the role of FGF23 in the osteoblastic gene expression in vascular smooth muscle cells (SMCs). METHODS AND RESULTS: We transduce human aortic SMCs (HASMCs) expressing klotho and FGF receptors with the adenovirus expressing human FGF23 (Ad-FGF23)...
October 2016: Atherosclerosis
Valentin David, Connor Francis, Jodie L Babitt
The bone-secreted hormone fibroblast growth factor 23 (FGF23) has an essential role in phosphate homeostasis by regulating expression of the kidney proximal tubule sodium-phosphate co-transporters as well as parathyroid hormone levels. Induction of FGF23 early in chronic kidney disease (CKD) helps to maintain normal phosphorous levels. However, high FGF23 levels become pathologic as kidney disease progresses and are associated with an increased risk of CKD progression, cardiovascular events, and death. The factors responsible for increasing FGF23 levels early in CKD are unknown, but recent work has proposed a role for inflammation and disordered iron homeostasis...
August 31, 2016: American Journal of Physiology. Renal Physiology
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