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https://read.qxmd.com/read/38223338/real-world-usage-of-chronic-kidney-disease-mineral-bone-disorder-ckd-mbd-biomarkers-in-nephrology-practices
#1
JOURNAL ARTICLE
Maria Fusaro, Simona Barbuto, Maurizio Gallieni, Althea Cossettini, Giulia Vanessa Re Sartò, Laura Cosmai, Giuseppe Cianciolo, Gaetano La Manna, Thomas Nickolas, Serge Ferrari, Jordi Bover, Mathias Haarhaus, Carmela Marino, Maria Cristina Mereu, Maura Ravera, Mario Plebani, Martina Zaninotto, Mario Cozzolino, Stefano Bianchi, Piergiorgio Messa, Mariacristina Gregorini, Lorenzo Gasperoni, Caterina Agosto, Andrea Aghi, Giovanni Tripepi
BACKGROUND: Chronic kidney disease mineral bone disorder (CKD-MBD) is a condition characterized by alterations of calcium, phosphate, parathyroid hormone (PTH), and fibroblast growth factor 23 (FGF-23) metabolism that in turn promote bone disorders, vascular calcifications, and increase cardiovascular (CV) risk. Nephrologists' awareness of diagnostic, prognostic, and therapeutic tools to manage CKD-MBD plays a primary role in adequately preventing and managing this condition in clinical practice...
January 2024: Clinical Kidney Journal
https://read.qxmd.com/read/37963145/development-and-validation-of-a-quantitative-proximity-extension-assay-instrument-with-21-proteins-associated-with-cardiovascular-risk-cvd-21
#2
JOURNAL ARTICLE
Agneta Siegbahn, Niclas Eriksson, Erika Assarsson, Martin Lundberg, Andrea Ballagi, Claes Held, Ralph A H Stewart, Harvey D White, Mikael Åberg, Lars Wallentin
BACKGROUND: Treatment of cardiovascular diseases (CVD) is a substantial burden to healthcare systems worldwide. New tools are needed to improve precision of treatment by optimizing the balance between efficacy, safety, and cost. We developed a high-throughput multi-marker decision support instrument which simultaneously quantifies proteins associated with CVD. METHODS AND FINDINGS: Candidate proteins independently associated with different clinical outcomes were selected from clinical studies by the screening of 368 circulating biomarkers...
2023: PloS One
https://read.qxmd.com/read/35925260/long-term-use-of-burosumab-for-the-treatment-of-tumor-induced-osteomalacia
#3
JOURNAL ARTICLE
C Crotti, F Zucchi, C Alfieri, R Caporali, M Varenna
Tumor-induced osteomalacia (TIO) is a rare paraneoplastic syndrome caused by tumoral overproduction of FGF-23. Due to local recurrence, we describe the long-term efficacy and safety profile of burosumab, an anti-FGF-23 monoclonal antibody, in a TIO patient after three unsuccessfully surgical attempts. INTRODUCTION: TIO is a rare paraneoplastic syndrome caused by tumoral overproduction of fibroblast growth factor 23 (FGF23), resulting in hyperphospaturia, hypophosphatemia, and osteomalacia...
August 4, 2022: Osteoporosis International
https://read.qxmd.com/read/34901334/induction-of-fgf23-related-hypophosphatemic-osteomalacia-by-alcohol-consumption
#4
JOURNAL ARTICLE
Naoko Hidaka, Hajime Kato, Minae Koga, Masaki Katsura, Yuko Oyama, Yuka Kinoshita, Seiji Fukumoto, Noriko Makita, Masaomi Nangaku, Nobuaki Ito
CONTEXT: Fibroblast growth factor (FGF) 23 is a hormone that regulates serum phosphate levels, the excess action of which causes chronic hypophosphatemic rickets/osteomalacia. To date, there are only two identified causes of acquired FGF23-related hypophosphatemic osteomalacia: tumor-induced osteomalacia (TIO) and osteomalacia induced by the intravenous infusion of some forms of iron preparations. In the current study, two cases of FGF23-related hypophosphatemia probably induced by chronic alcohol consumption were first introduced...
December 2021: Bone Reports
https://read.qxmd.com/read/34351500/performance-evaluation-of-the-new-chemiluminescent-intact-fgf23-assay-relative-to-the-existing-assay-system
#5
JOURNAL ARTICLE
Hajime Kato, Naoko Hidaka, Minae Koga, Noriyuki Ogawa, Shichihiro Takahashi, Hiromi Miyazaki, Masaomi Nangaku, Noriko Makita, Nobuaki Ito
INTRODUCTION: This study assessed the performance of a new fully automated immunoassay for fibroblast growth factor (FGF) 23 (Determinar CL FGF23 CL) among healthy individuals and those with chronic hypophosphatemia compared with the previous assay (Kainos FGF23 KI). MATERIALS AND METHODS: A total of 380 serum samples from healthy participants were collected to determine the reference range of FGF23 levels with CL. A total of 200 serum samples from 22 hypophosphatemic patients were collected simultaneously to compare the difference in FGF23 levels between CL and KI...
January 2022: Journal of Bone and Mineral Metabolism
https://read.qxmd.com/read/31238301/gfr-specific-versus-gfr-agnostic-cutoffs-for-parathyroid-hormone-and-fibroblast-growth-factor-23-in-advanced-chronic-kidney-disease
#6
JOURNAL ARTICLE
Mark Canney, Ognjenka Djurdjev, Mila Tang, Claudia Zierold, Frank Blocki, Myles Wolf, Adeera Levin
BACKGROUND: In the majority of patients with advanced chronic kidney disease (CKD), values of parathyroid hormone (PTH1-84) and fibroblast growth factor 23 (FGF-23) exceed the normal reference range, potentially as an appropriate adaptation to reduced glomerular filtration rate (GFR). We tested whether GFR-specific cutoffs for PTH1-84 and FGF-23 could better identify patients with inappropriately high PTH1-84 and FGF-23 for their degree of CKD and thereby improve prognostication of clinical outcomes compared to a uniform threshold...
2019: American Journal of Nephrology
https://read.qxmd.com/read/19929273/a-prospective-study-of-fibroblast-growth-factor-23-in-children-with-chronic-kidney-disease
#7
JOURNAL ARTICLE
Per Magnusson, Sverker Hansson, Diana Swolin-Eide
BACKGROUND: Fibroblast growth factor-23 (FGF-23) is a novel regulator of phosphate metabolism; however, the clinical knowledge is limited in children with chronic kidney disease (CKD) who are at risk of developing mineral bone disorder. METHODS: This prospective study over 2 years investigated the development of bone mass and bone turnover in relation to serum FGF-23 in children with CKD. Thirteen patients, 4-15 years, were included with a median corrected glomerular filtration rate (GFR) of 38 (range 7-74) mL/min/1...
February 2010: Scandinavian Journal of Clinical and Laboratory Investigation
https://read.qxmd.com/read/15121023/resolution-of-severe-adolescent-onset-hypophosphatemic-rickets-following-resection-of-an-fgf-23-producing-tumour-of-the-distal-ulna
#8
JOURNAL ARTICLE
L M Ward, F Rauch, K E White, G Filler, M A Matzinger, M Letts, R Travers, M J Econs, F H Glorieux
Oncogenic hypophosphatemic osteomalacia (OHO) is an uncommon hypophosphatemic syndrome characterized by bone pain, proximal muscle weakness and rickets. It has been postulated that OHO results from overproduction of a humoral phosphaturic factor by an occult tumour. Recently, some OHO tumours have been shown to elaborate fibroblast growth factor-23 (FGF-23), which causes renal phosphate wasting when administered to mice. The purpose of this study was to undertake detailed investigations to confirm the diagnosis of OHO in a pediatric patient and to document the biochemical, radiographic and bone histological phenotype before and after tumour removal...
May 2004: Bone
https://read.qxmd.com/read/12711740/fibroblast-growth-factor-23-in-oncogenic-osteomalacia-and-x-linked-hypophosphatemia
#9
JOURNAL ARTICLE
Kenneth B Jonsson, Richard Zahradnik, Tobias Larsson, Kenneth E White, Toshitsugu Sugimoto, Yasuo Imanishi, Takehisa Yamamoto, Geeta Hampson, Hiroyuki Koshiyama, Osten Ljunggren, Koichi Oba, In Myung Yang, Akimitsu Miyauchi, Michael J Econs, Jeffrey Lavigne, Harald Jüppner
BACKGROUND: Mutations in fibroblast growth factor 23 (FGF-23) cause autosomal dominant hypophosphatemic rickets. Clinical and laboratory findings in this disorder are similar to those in oncogenic osteomalacia, in which tumors abundantly express FGF-23 messenger RNA, and to those in X-linked hypophosphatemia, which is caused by inactivating mutations in a phosphate-regulating endopeptidase called PHEX. Recombinant FGF-23 induces phosphaturia and hypophosphatemia in vivo, suggesting that it has a role in phosphate regulation...
April 24, 2003: New England Journal of Medicine
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