scholarly journals Calcitriol, calcidiol, parathyroid hormone, and fibroblast growth factor‐23 interactions in chronic kidney disease

2013 ◽  
Vol 23 (2) ◽  
pp. 134-162 ◽  
Author(s):  
Joao F. Brito Galvao ◽  
Larry A. Nagode ◽  
Patricia A. Schenck ◽  
Dennis J. Chew
Keyword(s):  
Chronic Kidney Disease ◽  
Parathyroid Hormone ◽  
Growth Factor ◽  
Kidney Disease ◽  
Fibroblast Growth Factor ◽  
Fibroblast Growth Factor 23 ◽  
Fibroblast Growth

scholarly journals Fibroblast growth factor 23 is elevated before parathyroid hormone and phosphate in chronic kidney disease

2011 ◽  
Vol 79 (12) ◽  
pp. 1370-1378 ◽  
Author(s):  
Tamara Isakova ◽  
◽  
Patricia Wahl ◽  
Gabriela S. Vargas ◽  
Orlando M. Gutiérrez ◽  
...  
Keyword(s):  
Chronic Kidney Disease ◽  
Parathyroid Hormone ◽  
Growth Factor ◽  
Kidney Disease ◽  
Fibroblast Growth Factor ◽  
Fibroblast Growth Factor 23 ◽  
Fibroblast Growth

scholarly journals Fibroblast growth factor 23 and parathyroid hormone predict extent of aortic valve calcifications in patients with mild to moderate chronic kidney disease

2015 ◽  
Vol 8 (6) ◽  
pp. 732-736 ◽  
Author(s):  
Luca Di Lullo ◽  
Antonio Gorini ◽  
Antonio Bellasi ◽  
Luigi F. Morrone ◽  
Rodolfo Rivera ◽  
...  
Keyword(s):  
Chronic Kidney Disease ◽  
Parathyroid Hormone ◽  
Growth Factor ◽  
Kidney Disease ◽  
Aortic Valve ◽  
Fibroblast Growth Factor ◽  
Fibroblast Growth Factor 23 ◽  
Fibroblast Growth ◽  
Moderate Chronic Kidney Disease

Phosphate homeostasis, parathyroid hormone, and fibroblast growth factor 23 in stages 3 and 4 chronic kidney disease

2016 ◽  
Vol 85 (2016) (05) ◽  
pp. 251-261 ◽  
Author(s):  
Kenneth R. Phelps ◽  
Darius L. Mason ◽  
Kim S. Stote
Keyword(s):  
Chronic Kidney Disease ◽  
Parathyroid Hormone ◽  
Growth Factor ◽  
Kidney Disease ◽  
Fibroblast Growth Factor ◽  
Fibroblast Growth Factor 23 ◽  
Fibroblast Growth ◽  
Phosphate Homeostasis

scholarly journals GFR-Specific versus GFR-Agnostic Cutoffs for Parathyroid Hormone and Fibroblast Growth Factor-23 in Advanced Chronic Kidney Disease

2019 ◽  
Vol 50 (2) ◽  
pp. 105-114
Author(s):  
Mark Canney ◽  
Ognjenka Djurdjev ◽  
Mila Tang ◽  
Claudia Zierold ◽  
Frank Blocki ◽  
...  
Keyword(s):  
Chronic Kidney Disease ◽  
Parathyroid Hormone ◽  
Growth Factor ◽  
Kidney Disease ◽  
Fibroblast Growth Factor ◽  
Fibroblast Growth Factor 23 ◽  
Reference Ranges ◽  
Fibroblast Growth ◽  
Advanced Chronic Kidney Disease ◽  
Fgf 23

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. Methods: Prospective pan-Canadian cohort of 1,812 patients with mean estimated GFR (eGFR) 28.9 mL/min/1.73 m2 followed for a median of 52 months. Repeated log-rank tests were used to identify optimal cutoffs for PTH1–84 and FGF-23 within eGFR strata (<20, 20–29 and ≥30 mL/min/1.73 m2) that maximally differentiated high- and low-risk populations for (1) cardiovascular (CV) events (fatal or nonfatal myocardial infarction, coronary revascularization, stroke, heart failure) and (2) renal events (initiation of chronic renal replacement therapy). In multivariable models, we examined the association between ­GFR-specific cutoffs and outcomes and compared their added prognostic value to existing uniform thresholds. Results: Risk-based cutoffs for PTH1–84 and FGF-23 increased in a graded fashion with decreasing eGFR. Among patients with eGFR <20 mL/min/1.73 m2, CV risk-based cutoffs for PTH1–84 and FGF-23 were 3.4 and 5.5 times the upper limit of normal, respectively, and reclassified 31.9 and 35.1% of patients when added to a multivariable base model for CV events. In contrast, the addition of PTH1–84 and FGF-23 to the base model using uniform cutoffs failed to reclassify such patients. Similar findings were demonstrated for renal outcomes. Conclusion: GFR-specific risk-based cutoffs for PTH1–84 and FGF-23 may facilitate more meaningful risk stratification in advanced CKD than current GFR-agnostic reference ranges derived from healthy adults. This may be most applicable in those with severely reduced GFR.

scholarly journals Lipocalin 2 stimulates bone fibroblast growth factor 23 production in chronic kidney disease

Bone Research ◽  
2021 ◽  
Vol 9 (1) ◽  
Author(s):  
Guillaume Courbon ◽  
Connor Francis ◽  
Claire Gerber ◽  
Samantha Neuburg ◽  
Xueyan Wang ◽  
...  
Keyword(s):  
Chronic Kidney Disease ◽  
Growth Factor ◽  
Kidney Disease ◽  
Iron Deficiency ◽  
Fibroblast Growth Factor ◽  
Kidney Function ◽  
Fibroblast Growth Factor 23 ◽  
Left Ventricular ◽  
Fibroblast Growth ◽  
Lipocalin 2

AbstractBone-produced fibroblast growth factor 23 (FGF23) increases in response to inflammation and iron deficiency and contributes to cardiovascular mortality in chronic kidney disease (CKD). Neutrophil gelatinase-associated lipocalin (NGAL or lipocalin 2; LCN2 the murine homolog) is a pro-inflammatory and iron-shuttling molecule that is secreted in response to kidney injury and may promote CKD progression. We investigated bone FGF23 regulation by circulating LCN2. At 23 weeks, Col4a3KO mice showed impaired kidney function, increased levels of kidney and serum LCN2, increased bone and serum FGF23, anemia, and left ventricular hypertrophy (LVH). Deletion of Lcn2 in CKD mice did not improve kidney function or anemia but prevented the development of LVH and improved survival in association with marked reductions in serum FGF23. Lcn2 deletion specifically prevented FGF23 elevations in response to inflammation, but not iron deficiency or phosphate, and administration of LCN2 increased serum FGF23 in healthy and CKD mice by stimulating Fgf23 transcription via activation of cAMP-mediated signaling in bone cells. These results show that kidney-produced LCN2 is an important mediator of increased FGF23 production by bone in response to inflammation and in CKD. LCN2 inhibition might represent a potential therapeutic approach to lower FGF23 and improve outcomes in CKD.

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