scholarly journals Interorgan handling of fibroblast growth factor-23 in humans

2017 ◽  
Vol 312 (2) ◽  
pp. F254-F258 ◽  
Author(s):  
Daniela Verzola ◽  
Francesca Ansaldo ◽  
Samantha Milanesi ◽  
Emanuele Luigi Parodi ◽  
Gian Marco Rosa ◽  
...  
Keyword(s):  
Growth Factor ◽  
Glomerular Filtration ◽  
Fibroblast Growth Factor ◽  
Fibroblast Growth Factor 23 ◽  
Human Kidney ◽  
Cardiovascular Complications ◽  
Fibroblast Growth ◽  
Early Increase ◽  
Cardiac Catheterizations ◽  
Fgf 23

Fibroblast growth factor-23 (FGF-23) accumulates in blood of patients with chronic kidney disease (CKD) and is associated both with cardiovascular complications and disease progression. However, our knowledge of the sites and mechanisms that regulate plasma FGF-23 is still incomplete. We measured plasma intact FGF-23 across the kidney, splanchnic organs, and lung in 11 patients [estimated glomerular filtration rate (eGFR) 60 ± 6 ml/min] during elective diagnostic cardiac catheterizations. In these patients FGF-23 was removed by the kidney, with a fractional extraction (FE) of ∼22%. The FE of FGF-23 across the kidney was similar to that of creatinine (∼17%, P = NS). In addition, the FGF-23 FE by the kidney was significantly directly related to eGFR ( r = 0.709 P = 0.018) and to kidney creatinine FE ( r = 0.736 P = 0.013) but only as a trend to plasma phosphate levels (r = 0.55, P = 0.18). There was no difference in FGF-23 levels in blood perfusing splanchnic organs and cardiopulmonary bed. However, the arterial-venous difference of FGF-23 across the lung was directly related to FGF-23 pulmonary artery levels, suggesting that the lung, and possibly the heart, participate in the homeostasis of plasma FGF-23 when its systemic levels are increased. Our data show that the human kidney is the only site for FGF-23 removal from blood and suggest that FGF-23 is predominantly removed by glomerular filtration. The kidney ability to remove FGF-23 from the circulation likely accounts for the early increase in blood of FGF-23 in patients with CKD.

The significance of Fibroblast growth factor 23 (FGF-23) in humans

2021 ◽  
Vol 7-8 (217-218) ◽  
pp. 37-43
Author(s):  
Altynay Balmukhanova ◽  
◽  
Assiya Kanatbayeva ◽  
Kairat Kabulbayev ◽  
Maxsot Karasayev ◽  
...  
Keyword(s):  
Growth Factor ◽  
Left Ventricular Hypertrophy ◽  
Fibroblast Growth Factor ◽  
Ventricular Hypertrophy ◽  
Fibroblast Growth Factor 23 ◽  
Physiological Role ◽  
Cardiovascular Complications ◽  
Left Ventricular ◽  
Fibroblast Growth ◽  
Fgf 23

Nowadays chronic kidney disease (CKD) is one of the leading chronic non-communicable diseases in terms of morbidity and mortality. One of the most serious complications is mineral-bone disorder, which worsen the clinical course and prognosis of patients. Fibroblast growth factor 23 (FGF-23) is a new biomarker that regulates phosphate metabolism and plays an important role in the pathogenesis of many complications in CKD. Purpose. To study the physiological role of FGF-23, as well as its potential clinical significance in the progression of CKD and its complications. Material and methods. A 20-year-deep literature search was conducted in the international scientific databases PubMed / Medline, Web of Science and Google Scholar for the following keywords: "Fibroblast growth factor 23", "FGF-23", "phosphate homeostasis", "chronic kidney disease", "Mineral and bone disorders", "left ventricular hypertrophy". Results and discussion. FGF-23 is a protein secreted by bone cells and its primary physiological role is to regulate urinary excretion of phosphate to maintain a stable level in serum. Moreover, FGF-23 decreases calcitriol levels and inhibits parathyroid hormone secretion. In CKD, there is a gradual increase in FGF-23 levels as renal function declines, which can be regarded as physiological compensation to stabilize serum phosphate levels. According to the several studies, FGF-23 might be associated with cardiovascular complications, such as left ventricular hypertrophy and heart failure. Conclusion. Thus, FGF-23 is not only a marker of mineral-bone disorders in CKD, but also a key link in the pathogenesis of the development of secondary hyperparathyroidism and cardiovascular complications. With this in mind, FGF-23 may represent a multifunctional therapeutic target that may improve the prognosis of patients with CKD. Keywords: fibroblast growth factor-23, phosphate, parathyroid hormone, left ventricular hypertrophy, mineral-bone disorder.

scholarly journals Increased Levels of sRAGE in Diabetic CKD-G5D Patients: A Potential Protective Mechanism against AGE-Related Upregulation of Fibroblast Growth Factor 23 and Inflammation

2017 ◽  
Vol 2017 ◽  
pp. 1-9 ◽  
Author(s):  
Elena Dozio ◽  
Valentina Corradi ◽  
Elena Vianello ◽  
Elisa Scalzotto ◽  
Massimo de Cal ◽  
...  
Keyword(s):  
Cardiovascular Risk ◽  
Growth Factor ◽  
Fibroblast Growth Factor ◽  
Cardiac Remodeling ◽  
Glycated Albumin ◽  
Fibroblast Growth Factor 23 ◽  
Protective Mechanism ◽  
Fibroblast Growth ◽  
Increased Risk ◽  
Fgf 23

Advanced glycation end products (AGEs) may induce cardiac remodeling in kidney disease by promoting fibroblast growth factor 23 (FGF-23) expression. Since AGEs are increased in diabetes mellitus (DM), our first aim was to evaluate the existence of any potential association between AGEs, FGF-23, inflammation, and increased cardiovascular risk in DM patients on dialysis (CKD-G5D). Secondarily, we explored the potential role of the soluble receptor for AGEs (sRAGE) as a marker of heart failure. Levels of glycated albumin (GA), sRAGE, c-terminal FGF-23 (cFGF-23), brain natriuretic peptide (BNP), and inflammatory mediators were compared between DM and non-DM CKD-G5D patients. The levels of sRAGE, cFGF-23, BNP, and proinflammatory markers were over the ranges of normality in both DM and non-DM groups. Only GA and sRAGE levels were increased in DM compared to non-DM patients. Plasma levels of sRAGE and CRP were the only independent predictors of BNP concentration. In conclusion, in DM CKD-G5D patients, sRAGE appeared to be a marker of cardiac remodeling. Indeed, its increase could be a potential protective mechanism against the increased risk of cardiovascular complications related to AGEs and inflammation. The causal relationship between sRAGE and cardiovascular risk in these patients needs to be further confirmed by mechanistic studies.

scholarly journals MP594THE RELATIONSHIP BETWEEN FIBROBLAST GROWTH FACTOR-23 (FGF-23) AND SELECTED CLINICAL AND LABORATORY PARAMETERS

2017 ◽  
Vol 32 (suppl_3) ◽  
pp. iii648-iii649
Author(s):  
Danuta Fedak ◽  
Marek Kużniewski ◽  
Marcin Krzanowski ◽  
Paulina Dumnicka ◽  
Wladyslaw Sulowicz
Keyword(s):  
Growth Factor ◽  
Fibroblast Growth Factor ◽  
Fibroblast Growth Factor 23 ◽  
Fibroblast Growth ◽  
Laboratory Parameters ◽  
Fgf 23

Serum fibroblast growth factor-23 (FGF-23) and fracture risk in elderly men

2011 ◽  
Vol 26 (4) ◽  
pp. 857-864 ◽  
Author(s):  
Majd AI Mirza ◽  
Magnus K Karlsson ◽  
Dan Mellström ◽  
Eric Orwoll ◽  
Claes Ohlsson ◽  
...  
Keyword(s):  
Growth Factor ◽  
Fracture Risk ◽  
Fibroblast Growth Factor ◽  
Fibroblast Growth Factor 23 ◽  
Fibroblast Growth ◽  
Elderly Men ◽  
Fgf 23

scholarly journals Fibroblast Growth Factor 23-Producing Phosphaturic Mesenchymal Tumor with Extraordinary Morphology Causing Oncogenic Osteomalacia

Medicina ◽  
2020 ◽  
Vol 56 (1) ◽  
pp. 34
Author(s):  
Cornelia Then ◽  
Evelyn Asbach ◽  
Harald Bartsch ◽  
Niklas Thon ◽  
Christian Betz ◽  
...  
Keyword(s):  
Growth Factor ◽  
Fibroblast Growth Factor ◽  
Fibroblast Growth Factor 23 ◽  
Olfactory Neuroblastoma ◽  
Mesenchymal Tumor ◽  
Fibroblast Growth ◽  
Phosphaturic Mesenchymal Tumor ◽  
Oncogenic Osteomalacia ◽  
Pet Ct ◽  
Fgf 23

A possible cause of hypophosphatemia is paraneoplastic secretion of fibroblast growth factor 23 (FGF-23). Tumors secreting FGF-23 are rare, mostly of mesenchymal origin, usually benign, and may be located anywhere in the body, including hands and feet, which are often not represented in conventional imaging. A 50-year-old woman presented with diffuse musculoskeletal pain and several fractures. Secondary causes of osteoporosis were excluded. Laboratory analysis revealed hypophosphatemia and elevated alkaline phosphatase, parathyroid hormone, and FGF-23. Thus, oncogenic osteomalacia due to neoplastic FGF-23 secretion was suspected. FDG-PET-CT and DOTATATE-PET-CT imaging demonstrated no tumor. Cranial MRI revealed a tumorous mass in the left cellulae ethmoidales. The tumor was resected and histopathological examination showed a cell-rich tumor with round to ovoid nuclei, sparse cytoplasm, and sparse matrix, resembling an olfactory neuroblastoma. Immunohistochemical analysis first led to diagnosis of olfactory neuroblastoma, which was later revised to phosphaturic mesenchymal tumor. Following the resection, FGF-23 and phosphate levels normalized. In conclusion, we here describe a patient with an FGF-23-secreting phosphaturic mesenchymal tumor with an unusual morphology. Furthermore, we emphasize diagnostic pitfalls when dealing with FGF-23-induced hypophosphatemia.

scholarly journals Fibroblast growth factor-23 is associated with imaging markers of diabetic cardiomyopathy and anti-diabetic therapeutics

2020 ◽  
Vol 19 (1) ◽  
Author(s):  
Martin H. Sørensen ◽  
Annemie S. Bojer ◽  
Niklas R. Jørgensen ◽  
David A. Broadbent ◽  
Sven Plein ◽  
...  
Keyword(s):  
Type 2 Diabetes ◽  
Growth Factor ◽  
Fibroblast Growth Factor ◽  
Kidney Function ◽  
Fibroblast Growth Factor 23 ◽  
Left Ventricular ◽  
Fibroblast Growth ◽  
Cardiovascular Morbidity And Mortality ◽  
Fgf 23

Abstract Background The biomarker fibroblast growth factor-23 (FGF-23) has been associated with increased cardiovascular morbidity and mortality in both patients with and without type 2 diabetes. The aim of this study was to evaluate the relationship between FGF-23 and cardiac structure, function and perfusion in patients with type 2 diabetes and normal or mildly impaired kidney function. Furthermore, to investigate the association between FGF-23, anti-diabetes therapy and the classic complications and risk factors associated with type 2 diabetes. Methods In this cross-sectional study, 246 patients with type 2 diabetes underwent echocardiography and advanced cardiac magnetic resonance imaging to assess left ventricular (LV) structure and function. In addition, myocardial blood flow (MBF) during rest and pharmacological stress (adenosine 140 µg/kg/min) were evaluated in 183 of the patients. Patients with eGFR < 60 ml/min/1.73 m2 were excluded. Results Median (Q1–Q3) FGF-23 was 74 (58–91) ng/L. Patients with FGF-23 above the median had lower MBF during stress (2.3 ± 0.9 vs. 2.7 ± 0.9 ml/min/g, P = 0.001) and lower overall myocardial perfusion reserve (MPR) (2.7 ± 0.8 vs. 3.3 ± 1.1, P < 0.001). LV mass (143 ± 40 vs. 138 ± 36 g, P = 0.04) and E/e* (8.5 ± 3.2 vs. 7.6 ± 2.7, P = 0.04) were higher in patients with FGF-23 above the median. In a linear model adjusted for age, sex, eGFR and hypertension, increasing FGF-23 was associated with decreased MPR (P < 0.01, R2 = 0.11) and increased E/e* (P < 0.01, R2 = 0.07). FGF-23 was lower in patients receiving glucagon like peptide-1 (GLP-1) analogues (71 (57–86) vs. 80 (60–98) ng/L, P = 0.01) than in those who did not receive GLP-1 analogues. Conclusions In patients with type 2 diabetes and normal or mildly impaired kidney function, increased levels of FGF-23 are associated with impaired cardiac diastolic function and decreased MPR, caused by a decrease in maximal MBF during stress. Use of GLP-1 analogues is associated with decreased levels of FGF-23. Clinical trial registrationhttps://www.clinicaltrials.gov. Unique identifier: NCT02684331. Date of registration: February 18, 2016

scholarly journals Fibroblast Growth Factor 23 is Associated with a Frequent Exacerbator Phenotype in COPD: A Cross-Sectional Pilot Study

2019 ◽  
Vol 20 (9) ◽  
pp. 2292 ◽  
Author(s):  
Swati Gulati ◽  
J. Michael Wells ◽  
Gisel P. Urdaneta ◽  
Kira Balestrini ◽  
Isabel Vital ◽  
...  
Keyword(s):  
Growth Factor ◽  
Lung Function ◽  
Fibroblast Growth Factor ◽  
Fibroblast Growth Factor 23 ◽  
Airway Disease ◽  
Cross Sectional Study ◽  
Chronic Obstructive ◽  
Fibroblast Growth ◽  
Cross Sectional ◽  
Fgf 23

Chronic Obstructive Pulmonary Disease (COPD) is a chronic inflammatory airway disease punctuated by exacerbations (AECOPD). Subjects with frequent AECOPD, defined by having at least two exacerbations per year, experience accelerated loss of lung function, deterioration in quality of life and increase in mortality. Fibroblast growth factor (FGF)23, a hormone associated with systemic inflammation and altered metabolism is elevated in COPD. However, associations between FGF23 and AECOPD are unknown. In this cross-sectional study, individuals with COPD were enrolled between June 2016 and December 2016. Plasma samples were analyzed for intact FGF23 levels. Logistic regression analyses were used to measure associations between clinical variables, FGF23, and the frequent exacerbator phenotype. Our results showed that FGF23 levels were higher in frequent exacerbators as compared to patients without frequent exacerbations. FGF23 was also independently associated with frequent exacerbations (OR 1.02; 95%CI 1.004–1.04; p = 0.017), after adjusting for age, lung function, smoking, and oxygen use. In summary, FGF23 was associated with the frequent exacerbator phenotype and correlated with number of exacerbations recorded retrospectively and prospectively. Further studies are needed to explore the role of FGF 23 as a possible biomarker for AECOPD to better understand the pathobiology of COPD and to help develop therapeutic targets.

scholarly journals Fibroblast growth factor-23 (FGF-23) is independently correlated to aortic calcification in haemodialysis patients

2010 ◽  
Vol 25 (8) ◽  
pp. 2679-2685 ◽  
Author(s):  
M. M. Nasrallah ◽  
A. R. El-Shehaby ◽  
M. M. Salem ◽  
N. A. Osman ◽  
E. El Sheikh ◽  
...  
Keyword(s):  
Growth Factor ◽  
Fibroblast Growth Factor ◽  
Fibroblast Growth Factor 23 ◽  
Aortic Calcification ◽  
Fibroblast Growth ◽  
Fgf 23
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