scholarly journals FP044COMPARISON OF TWO ASSAYS OF FIBROBLAST GROWTH FACTOR 23 IN RELATION TO RANGES OF ESTIMATED GLOMERULAR FILTRATION RATE (eGFR) IN ELDERLY POPULATION

2015 ◽  
Vol 30 (suppl_3) ◽  
pp. iii79-iii79
Author(s):  
Jerzy Chudek ◽  
Maria Bozentowicz-Wikarek ◽  
Aleksander Owczarek ◽  
Piotr Kocelak ◽  
Magdalena Olszanecka-Glinianowicz ◽  
...  
Keyword(s):  
Glomerular Filtration Rate ◽  
Growth Factor ◽  
Glomerular Filtration ◽  
Fibroblast Growth Factor ◽  
Filtration Rate ◽  
Elderly Population ◽  
Estimated Glomerular Filtration Rate ◽  
Fibroblast Growth Factor 23 ◽  
Fibroblast Growth

scholarly journals C-Terminal to Intact Fibroblast Growth Factor 23 Ratio in Relation to Estimated Glomerular Filtration Rate in Elderly Population

2016 ◽  
Vol 41 (5) ◽  
pp. 519-526 ◽  
Author(s):  
Maria Bożentowicz-Wikarek ◽  
Aleksander Owczarek ◽  
Piotr Kocełak ◽  
Magdalena Olszanecka-Glinianowicz ◽  
Andrzej Więcek ◽  
...  
Keyword(s):  
Glomerular Filtration Rate ◽  
Growth Factor ◽  
Glomerular Filtration ◽  
Fibroblast Growth Factor ◽  
Filtration Rate ◽  
Elderly Population ◽  
Estimated Glomerular Filtration Rate ◽  
Fibroblast Growth Factor 23 ◽  
Fibroblast Growth

Pathophysiological impact of serum fibroblast growth factor 23 in patients with nonischemic cardiac disease and early chronic kidney disease

2014 ◽  
Vol 307 (10) ◽  
pp. H1504-H1511 ◽  
Author(s):  
Miki Imazu ◽  
Hiroyuki Takahama ◽  
Hiroshi Asanuma ◽  
Akira Funada ◽  
Yasuo Sugano ◽  
...  
Keyword(s):  
Chronic Kidney Disease ◽  
Glomerular Filtration Rate ◽  
Growth Factor ◽  
Kidney Disease ◽  
Glomerular Filtration ◽  
Fibroblast Growth Factor ◽  
Cardiac Disease ◽  
Filtration Rate ◽  
Estimated Glomerular Filtration Rate ◽  
Fibroblast Growth

Although the important role of fibroblast growth factor (FGF)23 on cardiac remodeling has been suggested in advanced chronic kidney disease (CKD), little is known about serum (s)FGF23 levels in patients with heart failure (HF) due to nonischemic cardiac disease (NICD) and early CKD. The present study aimed to investigate sFGF23 levels in NICD patients and identify the responsible factors for the elevation of sFGF23 levels. We prospectively measured sFGF23 levels in consecutive hospitalized NICD patients with early CKD (estimated glomerular filtration rate ≥ 40 ml·min−1·1.73 m−2) and analyzed the data of both echocardiography and right heart catheterization. Of the 156 NICD patients (estimated glomerular filtration rate range: 41–128 ml·min−1·1.73 m−2), the most severe HF symptom (New York Heart Association class III-IV, 53% vs. 33%, P = 0.015) was found in the above median sFGF23 (39.1 pg/ml) group compared with the below median sFGF23 group. sFGF23 levels were higher in patients with HF hospitalization history compared with those without HF [median: 46.8 (interquartile range: 38.8–62.7) vs. 34.7 (interquartile range: 29.6–42.4) pg/ml, P < 0.0001]. In the multivariate analysis, HF hospitalization was independently related to elevated sFGF23 levels ( P = 0.022). Both systolic dysfunction and high plasma aldosterone concentration were identified as predictors of high sFGF23 levels ( P < 0.05). Among the neurohormonal parameters, elevated sFGF23 levels were the only factor to predict a declining left ventricular ejection fraction ( P = 0.001). These findings suggest that the progression of HF per se contributes to the elevation of sFGF23 levels even in the early stages of CKD, which leads to further myocardial dysfunction, potentially creating a vicious cycle.

Plasma fibroblast growth factor 23 concentration and iron status. Does the relationship exist in the elderly population?

2015 ◽  
Vol 48 (6) ◽  
pp. 431-436 ◽  
Author(s):  
Maria Bożentowicz-Wikarek ◽  
Piotr Kocełak ◽  
Aleksander Owczarek ◽  
Magdalena Olszanecka-Glinianowicz ◽  
Małgorzata Mossakowska ◽  
...  
Keyword(s):  
Growth Factor ◽  
Fibroblast Growth Factor ◽  
Elderly Population ◽  
Iron Status ◽  
Fibroblast Growth Factor 23 ◽  
The Elderly ◽  
Fibroblast Growth ◽  
The Relationship

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.

High serum soluble α-Klotho levels in patients with autosomal dominant polycystic kidney disease

2016 ◽  
Vol 65 (2) ◽  
pp. 358-362 ◽  
Author(s):  
Funda Sari ◽  
Ayca Inci ◽  
Suleyman Dolu ◽  
Hamit Yasar Ellidag ◽  
Ramazan Cetinkaya ◽  
...  
Keyword(s):  
Growth Factor ◽  
Kidney Disease ◽  
Fibroblast Growth Factor ◽  
Polycystic Kidney Disease ◽  
Autosomal Dominant ◽  
Estimated Glomerular Filtration Rate ◽  
Fibroblast Growth Factor 23 ◽  
Fibroblast Growth ◽  
Polycystic Kidney ◽  
Autosomal Dominant Polycystic Kidney

This study aims to determine fibroblast growth factor-23 and soluble α-Klotho levels in patients with autosomal dominant polycystic kidney disease. A total of 76 patients with autosomal dominant polycystic kidney disease and 32 healthy volunteers were included in the study. Serum fibroblast growth factor-23 and soluble α-Klotho levels were measured with ELISA kits. Parathyroid hormone, phosphate, calcium, creatinine, 25-hydroxyvitamin D3 levels, urinary protein to creatinine ratio and estimated glomerular filtration rate were also measured or calculated. Patients with autosomal dominant polycystic kidney disease had significantly higher serum parathyroid hormone (p<0.001), fibroblast growth factor-23 (p<0.001), soluble α-Klotho levels (p=0.001) and lower serum 25-hydroxyvitamin D3 levels (p<0.001) as compared with healthy volunteers. Serum fibroblast growth factor-23, soluble α-Klotho and 25-hydroxyvitamin D3 levels were similar in all five chronic kidney disease stages of autosomal dominant polycystic kidney disease (p>0.05). Fibroblast growth factor-23 (r=−0.251, p=0.034) and soluble α-Klotho levels (r=−0.251, p=0.034) were found to be negatively correlated with estimated glomerular filtration rate. This study shows increased fibroblast growth factor-23 levels in patients with autosomal dominant polycystic kidney disease which is in harmony with the general trend in patients with chronic kidney disease of other aetiologies, but, unlike them, also a significant increase in serum soluble α-Klotho levels in patients with autosomal dominant polycystic kidney disease suggesting an aberrant production or a decreased clearance of α-Klotho molecule. Considering the unique increases in erythropoietin levels due to erythropoietin production in renal cysts, we assume, patients with autosomal dominant polycystic kidney disease may potentially have different soluble α-Klotho production/clearance characteristics than the patients with other parenchymal renal diseases.

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