Acceleration of bone formation during fracture healing by poly(pro-hyp-gly)10and basic fibroblast growth factor containing polycystic kidney disease and collagen-binding domains fromClostridium histolyticumcollagenase

2016 ◽  
Vol 104 (6) ◽  
pp. 1372-1378 ◽  
Author(s):  
Hiroyuki Sekiguchi ◽  
Kentaro Uchida ◽  
Gen Inoue ◽  
Osamu Matsushita ◽  
Wataru Saito ◽  
...  
Keyword(s):  
Growth Factor ◽  
Kidney Disease ◽  
Bone Formation ◽  
Fracture Healing ◽  
Fibroblast Growth Factor ◽  
Polycystic Kidney Disease ◽  
Fibroblast Growth ◽  
Polycystic Kidney ◽  
Collagen Binding ◽  
Binding Domains

scholarly journals Relationship between fibroblast growth factor and arrhythmogenesis in normotensive patients with polycystic kidney disease

2015 ◽  
Vol 1 (3) ◽  
pp. 106
Author(s):  
Kemal Karaagac ◽  
Abdulmecit Yildiz ◽  
Osman Can Yontar ◽  
Erhan Tenekecioglu ◽  
Fahriye Vatansever ◽  
...  
Keyword(s):  
Growth Factor ◽  
Kidney Disease ◽  
Fibroblast Growth Factor ◽  
Polycystic Kidney Disease ◽  
Fibroblast Growth ◽  
Polycystic Kidney

scholarly journals Hepatic Production of Fibroblast Growth Factor 23 in Autosomal Dominant Polycystic Kidney Disease

2018 ◽  
Vol 103 (6) ◽  
pp. 2319-2328 ◽  
Author(s):  
Frank Bienaimé ◽  
Ariane Ambolet ◽  
Béatrice Aussilhou ◽  
François Brazier ◽  
Marie Fouchard ◽  
...  
Keyword(s):  
Growth Factor ◽  
Kidney Disease ◽  
Fibroblast Growth Factor ◽  
Polycystic Kidney Disease ◽  
Plasma Levels ◽  
Autosomal Dominant ◽  
Fibroblast Growth ◽  
Polycystic Kidney ◽  
Autosomal Dominant Polycystic Kidney ◽  
Cystic Liver

Abstract Context The bone-derived hormone fibroblast growth factor (FGF) 23 controls phosphate homeostasis and urinary phosphate excretion. FGF23 plasma levels increase in the early stage of renal insufficiency to prevent hyperphosphatemia. Recent evidence suggests that this increase has effects on cardiac and immune cells that compromise patients’ health. Patients with autosomal dominant polycystic kidney disease (ADPKD) have been reported to have higher FGF23 concentrations than other patients with similar renal function. The significance of this finding has remained unknown. Methods and Results Analyzing the FGF23 plasma levels in 434 patients with ADPKD and 355 control subjects with a measured glomerular filtration rate (mGFR) between 60 and 120 mL/min per 1.73 m2, we confirmed that patients with ADPKD had higher FGF23 plasma concentrations than controls. Remarkably, this difference did not translate into renal phosphate leakage. Using different assays for FGF23, we found that this discrepancy was explained by a predominant increase in the cleaved C-terminal fragment of FGF23, which lacks phosphaturic activity. We found that FGF23 plasma concentration independently correlated with the severity of cystic liver disease in ADPKD. We observed that, in contrast to control liver tissues, the cystic liver from patients with ADPKD markedly expressed FGF23 messenger RNA and protein. In line with this finding, the surgical reduction of polycystic liver mass was associated with a decrease in FGF23 plasma levels independently of any modification in mGFR, phosphate, or iron status. Conclusion Our findings demonstrate that severely polycystic livers produce FGF23 and increase levels of circulating FGF23 in patients with ADPKD.

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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