scholarly journals Fibroblast Growth Factor and Mineral Metabolism Parameters among Prevalent Kidney Transplant Patients

2012 ◽  
Vol 2012 ◽  
pp. 1-6 ◽  
Author(s):  
Madhumathi Rao ◽  
Priyanka Jain ◽  
Temitope Ojo ◽  
Gautam Surya ◽  
Vaidyanathapuram Balakrishnan
Keyword(s):  
Growth Factor ◽  
Fibroblast Growth Factor ◽  
Kidney Transplant ◽  
Mineral Metabolism ◽  
Serum Phosphate ◽  
Fibroblast Growth ◽  
Post Transplant ◽  
Transplant Patients ◽  
Kidney Transplant Patients ◽  
Fgf 23

Background. Chronic kidney disease (CKD) related mineral bone disorders persist after kidney transplantation, but little is known about the relationship between fibroblast growth factor-23 (FGF-23) and mineral metabolism in prevalent post-transplant patients.Objectives. To examine mineral metabolism parameters and their relationship to FGF-23 and parathyroid hormone (PTH) in prevalent kidney transplant patients.Methods. Cross-sectional study of 106 kidney transplant patients enrolled November 2005–October 2009 at Tufts Medical Center (TMC), Boston.Results. The prevalence of hypophosphatemia was 34%, hypercalcemia 3%, and elevated PTH levels 66%, at a median (25th–75th percentile) duration of 12.8 (7.5–30.9) months post-transplant. Males had significantly higher levels of PTH (P=0.04) and lower levels of serum phosphate (P=0.002). Serum PTH levels did not relate to eGFR, corrected calcium levels or serum phosphate. FGF-23 levels were above the reference limits in 7% of patients; higher levels were associated with higher serum phosphate and PTH levels after adjustment for transplant kidney function.Conclusion. FGF-23 is an important driver of mineral metabolism in prevalent transplant patients. Its modulatory role in mineral metabolism homeostasis may be heightened as feedback suppression of PTH is disturbed. Its role in long term cardiovascular and graft outcomes needs further study.

scholarly journals Soluble Klotho and intact fibroblast growth factor 23 in long-term kidney transplant patients

2015 ◽  
Vol 172 (4) ◽  
pp. 343-350 ◽  
Author(s):  
Inger H Bleskestad ◽  
Inga Strand Thorsen ◽  
Grete Jonsson ◽  
Øyvind Skadberg ◽  
Harald Bergrem ◽  
...  
Keyword(s):  
Growth Factor ◽  
Fibroblast Growth Factor ◽  
Kidney Transplant ◽  
Fibroblast Growth Factor 23 ◽  
Fibroblast Growth ◽  
Kidney Transplants ◽  
Transplant Patients ◽  
Kidney Transplant Patients ◽  
Functioning Kidney

BackgroundControversies exist whether disturbances in mineral and bone disorder (MBD) normalise or persist after kidney transplantation. We assessed markers of MBD in patients with well-functioning kidney transplants to minimise confounding by reduced transplant function.MethodsIn this cross-sectional study, 40 patients aged ≥18 years who received a first kidney transplant more than 10 years ago were included. A well-functioning transplant was defined as an estimated glomerular filtration rate (eGFR) ≥45 ml/min per 1.73 m2.ResultsMedian time since transplantation was 18.3 years (inter quartile range (IQR) 12.2–26.2). Albumin-corrected serum calcium levels were above upper limit of normal in 15% of the transplanted patients, and serum phosphate levels below lower limit of normal in 31%. The median levels of intact parathyroid hormone (iPTH) and intact fibroblast growth factor 23 (iFGF23) were significantly higher than that in a group of healthy volunteers (11.3 pmol/l (IQR: 8.7–16.2) vs 4.4 pmol/l (IQR: 3.8–5.9), P<0.001 and 75.0 pg/ml (IQR: 53.3–108.0) vs 51.3 pg/ml (IQR: 36.3–67.6), P=0.004 respectively). There was a non-significant reduction in soluble Klotho (sKlotho) levels (605 pg/ml (IQR: 506–784) vs 692 pg/ml (IQR: 618–866)). When compared with a control group matched for eGFR, levels of iPTH were significantly higher (P<0.001), iFGF23 had a non-significant trend towards higher levels and sKlotho towards lower levels.ConclusionsIn long-term kidney transplant patients with well-functioning kidney transplants, we found inappropriately high levels of iPTH and iFGF23 consistent with a state of persistent hyperparathyroidism. We speculate that the primary defect, FGF23 resistance, has evolved in the parathyroid gland before transplantation, and persists due to long half-life of the parathyroid cells.

scholarly journals Relationship between Fibroblast Growth Factor-23 and Mineral Metabolism in Chronic Kidney Disease

2010 ◽  
Vol 2010 ◽  
pp. 1-7 ◽  
Author(s):  
Kosaku Nitta
Keyword(s):  
Chronic Kidney Disease ◽  
Growth Factor ◽  
Kidney Disease ◽  
Fibroblast Growth Factor ◽  
Fibroblast Growth Factor 23 ◽  
Left Ventricular ◽  
Serum Phosphate ◽  
Maintenance Hemodialysis ◽  
Fibroblast Growth ◽  
Fgf 23

Fibroblast growth factor- (FGF-)23 is a recently discovered regulator of calcium-phosphate metabolism. FGF-23 appears to decrease in synthesis and accelerated degradation of 1,25(OH)2D. Together with its cofactor Klotho, FGF-23 maintains serum phosphate levels within the normal range by increasing renal phosphate excretion. In chronic kidney disease (CKD), FGF-23 levels rise in parallel with the decline in renal function long before a significant increase in serum phosphate concentration occurs. Both Klotho and FGF-23, linked by a receptor mechanism, affect vitamin D synthesis and parathyroid hormone (PTH) secretion. Previous studies have shown a close association between reduced FGF-23 or Klotho activities and vascular calcification. The possible association of FGF-23 and left ventricular hypertrophy or vascular dysfunction has been proposed. Finally, prospective studies have shown that high serum FGF-23 concentrations predict more rapid disease progression in CKD patients who were not on dialysis and increased mortality in patients on maintenance hemodialysis. FGF-23 may therefore prove to be an important therapeutic target for the management of CKD.

Effect of acute changes of serum phosphate on fibroblast growth factor (FGF)23 levels in humans

2007 ◽  
Vol 25 (6) ◽  
pp. 419-422 ◽  
Author(s):  
Nobuaki Ito ◽  
Seiji Fukumoto ◽  
Yasuhiro Takeuchi ◽  
Shu Takeda ◽  
Hisanori Suzuki ◽  
...  
Keyword(s):  
Growth Factor ◽  
Fibroblast Growth Factor ◽  
Serum Phosphate ◽  
Fibroblast Growth ◽  
Acute Changes ◽  
Fgf 23

Role of fibroblast growth factor 23 in the development of cardiovascular diseases in patients with end-stage renal failure on programmed hemodialysis

2016 ◽  
Vol 88 (12) ◽  
pp. 51-56
Author(s):  
F U Dzgoeva ◽  
M Yu Sopoev ◽  
T L Bestaeva ◽  
O V Khamitsaeva ◽  
F A Ktsoeva ◽  
...  
Keyword(s):  
Renal Failure ◽  
Growth Factor ◽  
Fibroblast Growth Factor ◽  
Troponin I ◽  
Mineral Metabolism ◽  
Fibroblast Growth Factor 23 ◽  
Left Ventricular ◽  
Fibroblast Growth ◽  
End Stage ◽  
Fgf 23

Aim. To determine the nature of changes in fibroblast growth factor 23 (FGF-23) and other bone mineral metabolism parameters detectable in the blood of patients with end-stage chronic renal failure (CRF) and to analyze their links to the development of cardiovascular events in uremic intoxication. Subjects and methods. A total of 75 patients (45 men and 30 women) aged 23 to 66 years (mean age, 53±2.1 years) with Stage VD CKF were examined. The levels of parathyroid hormone (PTH), calcium, phosphorus, the morphogenetic protein FGF-23, and the cardiospecific protein troponin I were investigated. Doppler echocardiography was performed on an Aloka 4000 machine. Left ventricular (LV) mass index (LVMI), LV systolic and diastolic function, and peak systolic blood flow velocity in the aortic arch (Vps) were estimated. Results. As LVMI became higher, there were increases in the level of PTH and that of FGF-23 that plays a significant role in the processes of bone remodeling and vascular calcification. Analysis of correlations between a change in FGF-23 concentrations depending on the morphological and functional parameters of the cardiovascular system (CVS) revealed a strong direct correlation between FGF-23 levels and LVMI (r=0.746; p

Fibroblast Growth Factor 23 (FGF23) and the kidney

2009 ◽  
Vol 32 (4) ◽  
pp. 232-239 ◽  
Author(s):  
George Tsagalis ◽  
Erasmia Psimenou ◽  
Efstathios Manios ◽  
Antonios Laggouranis
Keyword(s):  
Growth Factor ◽  
Fibroblast Growth Factor ◽  
Fibroblast Growth Factor 23 ◽  
Serum Phosphate ◽  
Phosphate Concentration ◽  
Hypophosphatemic Rickets ◽  
Fibroblast Growth ◽  
Autosomal Dominant Hypophosphatemic Rickets ◽  
Fgf 23

Phosphate homeostasis in humans is a complex phenomenon involving the interplay of several different organs and circulating hormones. Among the latter, parathyroid hormone (PTH), and vitamin D3 (Vit D3) were thought to be the main regulators of serum phosphate concentration since they mediated the intestinal, renal and bone responses that follow fluctuations in serum phosphate levels. The study of three rare disorders – tumor-induced osteomalacia (TIO), autosomal dominant hypophosphatemic rickets (ADHR) and X-linked hypophosphatemic rickets (XLH) – has offered a completely new insight into phosphate metabolism by unraveling the role of a group of peptides that can directly affect serum phosphate concentration by increasing urinary phosphate excretion. Fibroblast growth factor-23 (FGF-23) is the most extensively studied “phosphatonin”. The production, mechanism of action, effects in various target tissues, and its role in common clinical disorders are the focus of this review.

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.

Sign in / Sign up

Export Citation Format

Share Document