scholarly journals Fibroblast growth factor 23 (FGF-23) and chronic kidney disease in children

2021 ◽  
Vol 11-12 (221-222) ◽  
pp. 43-48
Author(s):  
Altynay Balmukhanova ◽  
◽  
Kairat Kabulbayev ◽  
Assiya Kanatbayeva ◽  
◽  
...  

Chronic kidney disease (CKD) in children is a complex medical and social problem in healthcare. One of the serious complications is mineral bone disorder (MBD), the pathogenesis of which is related to a new biomarker of bone origin - fibroblast growth factor 23 (FGF-23). The aim. To study the features of fibroblast growth factor 23 (FGF-23) in children with chronic kidney disease. Material and methods. A cross-sectional study was carried out on 73 children with CKD and 14 healthy children. Inclusion criteria: chronic kidney disease stage 1-5, written informed consent of the participants. The exclusion criteria: tubulopathy, infectious and inflammatory processes, oncological diseases, kidney transplant, condition after surgery, taking glucocorticosteroids, calcium and vitamin D drugs. We took fasting blood samples of participants and carried out an enzyme-linked immunosorbent assay in order determine the level of FGF-23 (Biomedica Medizinprodukte GmbH, Austria). The obtained data were analyzed using IBM SPSS, version 22 (New York, USA). Results and discussion. In healthy children, the median (Q1-Q3) level of FGF-23 in serum was 0.65 (0.22-0.98) pmol/l, in patients with stage 1 CKD it was 0.65 (0.22-1.08) pmol/l. At stage 2, the level of FGF-23 significantly increased in comparison with healthy individuals and with patients of stage 1, p≤0.05. Further, there is a gradual increase by stages, p≤0.05. Thus, in stage 3 patients, the median FGF-23 value was 1.9 (1.15-3.5) pmol/l, at stage 4 - 3.55 (2.48-6.35) pmol/l, at 5 stages - 14 (7.5-18.75) pmol/l. As a percentage, there were 7.1% of patients at the stage 1 with increased levels of phosphatonin, at stage 2 - 53.3%, at stage 3 - 69.2%, respectively. At stages 4 and 5, absolutely 100% of patients had high levels of FGF-23. At the same time, FGF-23 did not depend on gender, age, birth weight and type of renal replacement therapy at stage 5, p>0.05. Conclusions. Thus, in our study, we determined the features of changes FGF-23 in serum in children at various stages of CKD. The obtained results allow us to consider FGF-23 as a predictor of the clinical course of CKD. Keywords: fibroblast growth factor 23, phosphatonin, pediatric nephrology, chronic kidney disease, mineral-bone disorder.

2019 ◽  
Author(s):  
Eleni Manou ◽  
Elias Thodis ◽  
George Arsos ◽  
Ploumis Pasadakis ◽  
Stylianos Panagoutsos ◽  
...  

Abstract Background: Fibroblast Growth Factor 23 (FGF-23) and α-Klotho contribute to the patho-genesis of chronic kidney disease - mineral and bone disorders (CKD-MBD). The aim of our study was to evaluate the association of FGF-23 and α-Klotho levels with CKD-MBD parameters, as well as with renal prognosis and mortality, in CKD patients stage 1-5, not in renal replacement therapy (RRT). Methods: 128 patients were included. At enrollment GFR was measured (mGFR) and plasma levels of carboxyl terminal FGF-23 (cFGF-23) and soluble α-Klotho (sKlotho) were determined by ELISA. Abdominal aorta calcification (AAC) score was assessed in lateral abdominal X ray. The composite end point (event) was initiation of RRT or death. Follow-up was five years (median 36, range 2-60 months). Results: mGFR significantly correlated with cFGF-23 and sKlotho negatively and posi-tievely respectively (p<0.0001 for both). Multiple regression analysis showed an inde-pendent correlation of cFGF-23 with mGFR, 25-OH vitamin D, presence of diabetes melli-tus and AAC score, of sKlotho with mGFR and phosphate and of AAC score with sKlotho and cFGF-23. Multivariate regression tree analysis, led to the formation of three regression groups (A, B, C) based on two “cut off” values: mGFR levels of 60.85 ml/min/1.73m2 and serum phosphate levels of 3.7 mg/dl. These groups significantly correlated with the five CKD stages and additionally cFGF-23 and sKlotho plasma levels (p<0.0001 for both). During follow-up, 40 out of the 128 patients, (31.2%) either initiated RRT or died (31 and 9 respectively). Kaplan Meier survival analysis showed that groups of patients with cFGF-23 levels less than median and those with sKlotho more than median value showing a more favorable course, regarding outcome (p=0.0003 for cFGF-23, p=0.004 for s-Klotho). In Cox regression analysis the association of cFGF-23 (p=0.04), sKlotho (p=0.008) and AAC score (p=0.01) with the presence of “event” remained significant after adjustment for traditional and CKD- related covariates. Conclusions: In CKD patients stage 1-5, cFGF-23 and sKlotho levels are associated with adverse clinical outcomes. mGFR and serum phosphate, in association with sKlotho lev-els, may provide a “new classification” of CKD patients, which appears to be predictive of outcome.


2014 ◽  
Vol 20 (30) ◽  
pp. 36-41
Author(s):  
Дзгоева ◽  
Fatima Dzgoeva ◽  
Бестаева ◽  
Tamara Bestaeva ◽  
Сопоев ◽  
...  

The aim of our study was to investigate the association of fibroblast growth factor 23 (FGF-23) with сardiorenal outcomes in chronic kidney disease stages III-V. FGF-23 was measured using commercially kits in 83 CKD stages III-V patients (40 females and 43 males aged 37-68 years). The patients were examined clinically with estimation of the levels of parathormone, calcium, phosphorus. Echocardiography on Aloka-4000 unit was made. Left ventricular geometry was assessed by J.Gottdiener classification. Therapeutic policy aimed of correction of anemia, arterial hypertension and phosphorus-calcium metabolism. FGF-23 correlated with renal function and weight of left ventricular hypertrophy. We have shown that changes in bone mediator and phosphate metabolism induced by CKD are independently associated with сardiorenal dysfunction.


2010 ◽  
Vol 2010 ◽  
pp. 1-7 ◽  
Author(s):  
Kosaku Nitta

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.


2021 ◽  
pp. 104063872098556
Author(s):  
Jiabao Lin ◽  
Luqi Lin ◽  
Siyu Chen ◽  
Lifang Yu ◽  
Songjie Chen ◽  
...  

Fibroblast growth factor 23 (FGF-23) is an independent monitor of the progression of chronic kidney disease (CKD) in human medicine, and FGF-23 may have value as a biomarker in feline CKD. We evaluated the relationship between serum FGF-23 and CKD stages, and the effect of age on FGF-23 in normal cats. We measured FGF-23 and intact parathyroid hormone (iPTH) concentrations by ELISA, with intra- and inter-assay CVs ≤ 15%. The percentage recovery of FGF-23 and iPTH remained stable for up to 7 d in samples stored at −20°C and −80°C. We measured FGF-23 in 304 cats, among which 196 were diagnosed with CKD. The 108 clinically healthy cats were divided into 5 subgroups based on growth stage (0–2 y, 3–6 y, 7–10 y, 11–14 y, ≥ 15 y). No statistical difference was found in FGF-23 among age groups ( p = 0.15) or by sex in healthy subjects. Using the International Renal Interest Society guideline, 34 cats were defined as CKD stage 1, 74 stage 2, 51 stage 3, and 37 stage 4. FGF-23 was higher in cats in all CKD stages than in controls. Higher serum phosphorus was observed in stage 3 ( p = 0.04) and 4 ( p < 0.01) compared to controls. iPTH increased as CKD progressed. Pearson analysis indicated a positive linear relationship between FGF-23 and iPTH (control: r = 0.70, p < 0.01; CKD: r = 0.46, p = 0.02). FGF-23 may be a useful biomarker of feline CKD and may precede hyperphosphatemia in advanced feline CKD.


2021 ◽  
Vol 5 (2) ◽  
pp. 31-35
Author(s):  
Riri Andri Muzasti ◽  
Junita Tarigan

Introduction Chronic kidney disease (CKD) is a global problem with increasing prevalence, poor prognosis, and high costs. Most deaths of CKD patients with hemodialysis (HD) is cardiovascular disorders. One of  risk factors related to cardiovascular disorder is Fibroblast Growth Factor-23 (FGF-23). FGF-23 level is associated with increased mortality in CKD patients with HD. Aim & Objectives The aim of this study is to show the effect of Fibroblast Growth Factor-23 (FGF-23 on two year mortality rate in chronic kidney disease patients with hemodialysis. Materials and Method This retro-prospective mixcohort study with survival analysis obtained data from medical records of CKD patients undergoing HD at the Rasyidah Renal Hospital in the first week of January 2018. Patients were followed up next two years until 31st of December 2019. Kaplan Meier analysis was used to determine the effect of independent variables on dependent variable that was two years mortality, multivariate cox regression analysis to determine the dominant factor and magnitude of the association between independent variable and dependent variable. P-value <0.05 indicates a significant association. Result Kaplan Meier curve showed significant effect of FGF-23 level and Diabetes Mellitus on a two-year survival rate of patients (p = 0.01 and p = 0.04). Based on cox regression multivariate analysis, it was found patients with FGF-23 levels> 365ng/ml had a risk of 3.53 (CI95% 1,104-11,337) times more than group of patients with FGF-23 ≤ 365ng/ml while the presence of diabetes mellitus was  risk factor on mortality with HR 3.71 (CI 1,279-10,796). Conclusion Statistically, FGF-23 level> 365 ng/ml is dominant factor that significantly influences 2-year mortality rate of CKD patients with HD other than Diabetes Mellitus. Key Words: Fibroblast Growth Factor, Chronic kidney disease on Hemodialysis, Mortality  


2019 ◽  
Vol 50 (2) ◽  
pp. 105-114
Author(s):  
Mark Canney ◽  
Ognjenka Djurdjev ◽  
Mila Tang ◽  
Claudia Zierold ◽  
Frank Blocki ◽  
...  

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.


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