scholarly journals Perioperative changes of FGF23 in patients undergoing surgery for primary hyperparathyroidism

2021 ◽  
Author(s):  
Magdalena Fortova ◽  
Lenka Hanouskova ◽  
Martin Valkus ◽  
Jana Cepova ◽  
Richard Prusa ◽  
...  
Keyword(s):  
Primary Hyperparathyroidism ◽  
Cystatin C ◽  
Inorganic Phosphate ◽  
Fibroblast Growth Factor 23 ◽  
Reference Interval ◽  
Significant Negative Correlation ◽  
The Other ◽  
Fibroblast Growth ◽  
Postoperative Changes ◽  
Upper Level

Background: Fibroblast growth factor-23 (FGF23) is a key regulator of urine phosphate excretion. The aim of the study was to investigate the perioperative (intraoperative and postoperative) changes of plasma intact and C-terminal FGF23 (iFGF23, cFGF23) concentrations in patients with primary hyperparathyroidism (pHPT) submitted to surgery. Materials and methods: Study involved 38 adult patients with pHPT caused by adenoma. PTH levels were investigated intraoperatively (just before the incision and 10 minutes after adenoma excision). cFGF23, iFGF23, phosphate, eGFR and P1NP were measured intraoperatively and postoperatively (next day after the surgery). Results: PTH levels decreased intraoperatively (13.10 vs. 4.17 pmol/L, P<0.0001). FGF23 levels measured intraoperatively were at the upper level of reference interval. cFGF23 decreased postoperatively compared with values measured just before the incision (cFGF23: 89.17 vs. 22.23 RU/mL, P<0.0001). iFGF23 decreased as well, but postoperative values were low. Postoperative inorganic phosphate values increased (1.03 mmol/L vs. 0.8 mmol/L, P=0.0025). We proved significant negative correlation of perioperative FGF23 with inorganic phosphate (cFGF23: Spearman r=-0.253,P=0.0065; iFGF23: Spearman r =-0.245, P=0.0085). We also found FGF23 values just before incision correlated with eGFR (cystatin C) (cFGF23: Spearman r=-0.499, P=0.0014; iFGF23: Spearman r=-0.413, P=0.01). Conclusion: Intraoperative iFGF23 and cFGF23 did not change despite PTH decreased significantly. cFGF23 and iFGF23 significantly decreased one day after parathyroidectomy and are associated with increase of inorganic phosphate in pHPT patients. cFGF23 and iFGF23 just before incision correlated with eGFR (cystatin C). The similar results found in both iFGF23 and cFGF23 suggest each could substitute the other.

scholarly journals The effect of GH treatment on serum FGF23 and Klotho in GH-deficient children

2016 ◽  
Vol 174 (4) ◽  
pp. 473-479 ◽  
Author(s):  
Alexandra Efthymiadou ◽  
Dimitra Kritikou ◽  
Stefanos Mantagos ◽  
Dionisios Chrysis
Keyword(s):  
Biochemical Parameters ◽  
Linear Growth ◽  
Fibroblast Growth Factor 23 ◽  
Serum Phosphate ◽  
The Other ◽  
Phosphate Metabolism ◽  
Fibroblast Growth ◽  
Phosphate Homeostasis ◽  
Gh Treatment ◽  
Opposing Effects

BackgroundNormal phosphate homeostasis is essential for normal linear growth. The phosphaturic fibroblast growth factor 23 (FGF23)/Klotho axis is a major regulator of phosphate homeostasis; therefore, an intact FGF23/Klotho axis is important for normal linear growth. On the other hand, GH/IGF1 axis has opposing effects on phosphate homeostasis, but the underline mechanisms remain unclear.AimThe main objective of this study was to investigate the possible interactions of FGF23 and its co-receptor Klotho, with growth hormone (GH)/IGF1 axis in the regulation of phosphate metabolism in GH-deficient children under GH treatment.MethodsWe studied 23 GH-deficient children, before and 3 months after the onset of GH treatment. Anthropometry and assessment of biochemical parameters were performed, as well as measurement of FGF23 (intact FGF23/iFGF23 and C-terminal FGF23/cFGF23) and soluble α-Klotho (sKlotho) levels.ResultsAfter 3 months on GH treatment, the elevation of serum phosphate and TmPO4/GFR (P<0.0001 and P<0.01 respectively) was accompanied by a significant increase in cFGF23 (P<0.01), iFGF23 (P<0.0001), sKlotho (P<0.0001) and IGF1 (P<0.0001). Serum phosphate and TmPO4/GFR were positively associated with iFGF23 (P<0.01 and P<0.05) and IGF1 (P<0.05 and P<0.05). iFGF23 levels were positively correlated with sKlotho (P<0.001), IGF1 (P<0.0001) and height SDS (P<0.0001), whereas sKlotho was positively associated with IGF1 (P<0.0001) and height SDS (P<0.001).ConclusionThe increase in serum phosphate, which we found in GH-deficient children under GH treatment, is not associated with suppression but rather than with upregulation of the phosphaturic FGF23/Klotho axis.

scholarly journals Increased circulating levels of FGF23: an adaptive response in primary hyperparathyroidism?

2012 ◽  
Vol 166 (1) ◽  
pp. 55-60 ◽  
Author(s):  
Janneke E Witteveen ◽  
Antoon H van Lierop ◽  
Socrates E Papapoulos ◽  
Neveen A T Hamdy
Keyword(s):  
Primary Hyperparathyroidism ◽  
Fibroblast Growth Factor 23 ◽  
Negative Relationship ◽  
Significant Negative Correlation ◽  
Fgf23 Concentration ◽  
Biochemical Evaluation ◽  
Turnover Markers ◽  
The Relationship ◽  
Circulating Levels

IntroductionFibroblast growth factor 23 (FGF23) and parathyroid hormone (PTH) are major players in the bone–parathyroid–kidney axis controlling phosphate homeostasis. In patients with primary hyperparathyroidism (PHPT), data on the relationship between PTH and FGF23 are scarce and not always concordant.ObjectiveThe aim of our study was to evaluate the relationship between PTH and FGF23 in patients with PHPT and in euparathyroid patients cured after successful parathyroidectomy (PTx).Patients and methodsTwenty-one patients with PHPT and 24 patients in long-term cure after successful PTx (EuPTH) were studied. All patients underwent biochemical evaluation of renal function, parathyroid status, vitamin D status, bone turnover markers, and serum intact FGF23 levels.ResultsMean serum FGF23 concentration was significantly higher in PHPT than in EuPTH patients (50.8±6.1 vs 33.1±2.6 pg/ml,P=0.01). FGF23 levels significantly correlated with PTH levels (r=0.361,P=0.02), also after correction for 1,25(OH)2D levels (r=0.419,P=0.01). FGF23 levels showed a significant negative correlation with 1,25(OH)2D, which was more pronounced in PHPT than in EuPTH patients (r=−0.674,P=0.001, vsr=−0.509,P=0.01).ConclusionOur findings suggest that in PHPT, FGF23 levels are increased independent of 1,25(OH)2D levels. The more pronounced negative relationship between FGF23 and 1,25(OH)2D in the presence of high circulating PTH levels suggests that the increase in FGF23 levels may be an adaptive mechanism to counteract the PTH-induced increase in 1,25(OH)2D levels, although not completely overriding it.

scholarly journals Phosphate Transporter Regulator That Prevents Abnormal Hyperphosphatemia.

2021 ◽  
Author(s):  
Sumire Sasaki ◽  
Yuji Shiozaki ◽  
Ai Hanazaki ◽  
Megumi Koike ◽  
Kazuya Tanifuji ◽  
...  
Keyword(s):  
Parathyroid Hormone ◽  
Inorganic Phosphate ◽  
Fibroblast Growth Factor 23 ◽  
Kidney Injury ◽  
Proximal Tubules ◽  
Type Ii ◽  
Fibroblast Growth ◽  
Sodium Dependent ◽  
Fgf23 Concentration

Abstract Renal type II sodium-dependent inorganic phosphate (Pi) transporters NaPi2a and NaPi2c cooperate with other organs to strictly regulate the plasma Pi concentration. A high Pi load induces the phosphaturic hormones parathyroid hormone (PTH) and fibroblast growth factor 23 (FGF23), enhances urinary Pi excretion and prevents the onset of hyperphosphatemia. How FGF23 is induced from the bones by a high Pi load and the setpoint of the plasma Pi concentration, however, are unclear. Here, we investigated the role of transporter-associated protein (TRAP), found in gene co-expression networks in NaPi2a and NaPi2c function. TRAP is localized in the renal proximal tubules and interacts with NaPi2a. In TRAP-knockout (KO) mice, the serum FGF23 concentration was markedly increased but increased Pi excretion and hypophosphatemia were not observed. In addition, TRAP-KO mice exhibit reduced NaPi2a responsiveness to FGF23 and PTH administration. Furthermore, a dietary Pi load causes marked hyperphosphatemia and abnormal NaPi2a regulation in TRAP-KO mice. Thus, TRAP is thought to be associated with FGF23 induction in bones and the regulation of NaPi2a to prevent an increase in the plasma Pi concentration due to a high Pi load and kidney injury.

scholarly journals Parathyroid Hormone Regulates Fibroblast Growth Factor-23 in a Mouse Model of Primary Hyperparathyroidism

2007 ◽  
Vol 18 (10) ◽  
pp. 2683-2688 ◽  
Author(s):  
Takehisa Kawata ◽  
Yasuo Imanishi ◽  
Keisuke Kobayashi ◽  
Takami Miki ◽  
Andrew Arnold ◽  
...  
Keyword(s):  
Parathyroid Hormone ◽  
Growth Factor ◽  
Mouse Model ◽  
Primary Hyperparathyroidism ◽  
Fibroblast Growth Factor ◽  
Fibroblast Growth Factor 23 ◽  
Fibroblast Growth

scholarly journals Circulating Fibroblast Growth Factor-23 Level and Paraoxonase-1 Lactonase Activity in Chronic Hemodialysis Patients: Their Impact on the Incidence of Native AV Fistula Thrombosis

2016 ◽  
Vol 39 (5) ◽  
pp. 173
Author(s):  
Samir F. Zohny ◽  
Mahmoud Abd El-Fattah ◽  
Jalaluddin A. Khan
Keyword(s):  
Growth Factor ◽  
Fibroblast Growth Factor ◽  
Fibroblast Growth Factor 23 ◽  
Significant Negative Correlation ◽  
Chronic Hemodialysis ◽  
Paraoxonase 1 ◽  
Fibroblast Growth ◽  
Av Fistula ◽  
Av Fistulas ◽  
Fgf 23

Purpose: Thrombosis of native arteriovenous (AV) fistula is an important cause of complications in hemodialysis (HD) patients. The purpose of this study was to investigate the usefulness of measuring circulating fibroblast growth factor-23 (FGF-23) level and paraoxonase-1 (PON1) lactonase activity as potential predictors of native AV fistula thrombosis in chronic HD patients. Methods: This study included 83 HD patients (48 with thrombosed and 35 with non-thrombosed native AV fistulas) and 38 healthy volunteers. Serum FGF-23 level was measured using the ELISA technique, while serum PON1 lactonase activity was measured spectrophotometrically using gamma-thiobutyrolactone as a substrate. Results: FGF-23 was significantly increased while PON1 lactonase was markedly decreased in both thrombosed and non-thrombosed HD patients compared with controls (P < 0.001). FGF-23 was elevated whereas PON1 lactonase was decreased in HD patients with thrombosed native AV fistulas compared with HD patients with non-thrombosed native AV fistulas (P = 0.001 and 0.002, respectively). A significant negative correlation was found between FGF-23 and PON1 lactonase in HD patients with thrombosed native AV fistulas (r = −0.342, P = 0.017). Conclusions: This study shows a potential value of FGF-23 and PON1 lactonase as predictors of native AV fistula thrombosis in HD patients.

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