Fibroblast growth factor-23 (FGF-23) is independently correlated to aortic calcification in haemodialysis patients

Nasrallah, M. M.; El-Shehaby, Amal; Salem, Mona M; Osman, Noha A.; Sheikh, Esam El; Din, Usama A.A. Sharaf El

doi:10.1093/ndt/gfq089

Cited by 188 publications

(142 citation statements)

References 32 publications

Supporting

Mentioning

113

Contrasting

Unclassified

Order By: Relevance

“…Nasrallah et al [13], found that Fibroblast growth factor-23 (FGF-23) is independently correlated to aortic calcification in haemodialysis patients. A reasonable explanation for this phenomenon is that FGF-23 may cause thickening and fibrosis of the carotid intima by binding to its receptor [14].…”

Section: Discussionmentioning

confidence: 99%

Plasma Fibroblast Growth Factor-23 Level and its Relation to Carotid Artery Atherosclerosis in Hemodialysis Patients

Ghonemy¹

2017

UNOAJ

View full text Add to dashboard Cite

Background: Abnormalities in bone metabolism are a prevalent condition in CKD patients. FGF23 has been suggested to play a role in vascular calcification in patients on regular hemodialysis (HD).Objective: This work was carried out to evaluate the prevalence of carotid artery atherosclerosis in patients with end stage renal disease (ESRD) on regular haemodialysis and the role of FGF-23 in this event.Subject and methods: A total number of 50 patients aged over 18 years and on regular haemodialysis for one or more years were included in this study. Intact FGF-23 and other laboratory parameters were measured by specific methods for all patients; Also Duplex scan of the carotid arteries was performed to assess carotid intima-media thickness (CIMT) by high-resolution real-time B mode ultrasonography.Results: Serum phosphorus, CIMT, LDL, There found to be significantly high with increasing FGF 23 levels (pis 0.005, 0.001, 0.02 and 0.001 respectively). While albumin level was significantly lower with increasing FGF-23 level (p is 0.013). Levels of phosphorus, Parathyroid hormone (PTH) and CRP got significantly higher with the increase in (CIMT) (p is 0.007, 0.001 and 0.004 respectively). FGF 23 levels were significantly correlated with each of CIMT, phosphorus and PTH levels. Correlation was significant between CIMT and age of patient, blood pressure, diabetes, smoking habits, more hemodialysis duration, CRP, higher phosphorus level, FGF23 level, low serum albumin, and higher PTH level. From multiple regression analysis, the most important risk factors correlated to carotid artery atherosclerosis are FGF23, higher phosphorus level, CRP and Diabetes in the order. Conclusion:FGF23 is a risk factor for the occurrence of vascular atherosclerosis in hemodialysis patients Monitoring of the FGF23 levels may be recommended to predict the possibility of vascular atherosclerosis in those types of patients.

show abstract

Section: Discussionmentioning

confidence: 99%

Plasma Fibroblast Growth Factor-23 Level and its Relation to Carotid Artery Atherosclerosis in Hemodialysis Patients

Ghonemy¹

2017

UNOAJ

View full text Add to dashboard Cite

show abstract

“…It is unknown whether elevated serum FGF-23 regulates urinary phosphate excretion in dialysis patients. On the contrary, recent data have established a relationship between high levels of FGF-23 and increased mortality and vascular calcifications in hemodialysis patients (9,10). However, the mechanism is unclear.…”

Section: Introductionmentioning

confidence: 98%

Association of Circulating Fibroblast Growth Factor-23 with Renal Phosphate Excretion among Hemodialysis Patients with Residual Renal Function

Wang

et al. 2013

Clinical Journal of the American Society of Nephrology

View full text Add to dashboard Cite

SummaryBackground and objectives High serum levels of fibroblast growth factor-23 (FGF-23) are associated with mortality in patients with ESRD, but whether it still acts as a phosphaturic factor is unknown. This study aimed to explore the role of circulating FGF-23 on urinary phosphate excretion and phosphate balance in maintenance hemodialysis (MHD) patients with residual renal function (RRF).Design, setting, participants, & measurements There were 134 MHD patients enrolled in this cross-sectional study from June to July 2010. Demographics, laboratory data, and excretion capacity of phosphate were recorded. Multivariable linear regression was used to analyze the relationship of serum phosphate and the tubular reabsorption rate of phosphate with other factors.Results The median age of the patients was 61.0 years and 47.8% were male. Thirty percent of the patients had high urinary output (.200 ml/d) accompanied by lower serum levels of phosphate, calcium, intact parathyroid hormone, and FGF-23 compared with those with low urine output (#200 ml/d). The independent predictors of serum phosphate were normalized protein nitrogen appearance, intact parathyroid hormone, and FGF-23 in the low urine output group and female sex and GFR in the high urine output group. The tubular reabsorption rate of phosphate decreased to 50% of the normal level in patients with RRF. Elevated circulating FGF-23 was significantly associated with lower tubular phosphate reabsorption after adjusting for GFR.Conclusions RRF is associated with significant capacity to excrete phosphate in MHD patients and high levels of serum FGF-23 may promote phosphate excretion by remnant nephrons.

show abstract

“…These facts suggest that FGF23 may have a protective effect on vascular calcification by hyperphosphatemia suppression. In contrast, several hemodialysis studies reported that elevated FGF23 levels were associated with aortic calcification (6) and mortality (7,8) independent of serum phosphorus levels. Elevated serum FGF23 levels, even within the normal range, are reportedly associated with increased left ventricular mass index and increased risk for the presence of left ventricular hypertrophy in elderly subjects (9).…”

mentioning

confidence: 93%

Oral Phosphorus Supplementation Secondarily Increases Circulating Fibroblast Growth Factor 23 Levels at Least Partially via Stimulation of Parathyroid Hormone Secretion

Takasugi

Akutsu

Nagata

2014

J Nutr Sci Vitaminol

View full text Add to dashboard Cite

Phosphorus is an essential nutrient for many biological functions, including cellular signal transduction, mineral metabolism, and energy exchange. On the other hand, a relatively high serum phosphorus level is reportedly a risk factor for cardiovascular disease (1, 2) because inorganic phosphates have been shown to stimulate differentiation of vascular smooth muscle cells into calcifying vascular cells (3). Therefore, serum phosphorus regulation may help to prevent cardiovascular diseases.Fibroblast growth factor 23 (FGF23) is a bone-derived hormone that plays a regulatory role in phosphorus homeostasis. FGF23 has been shown to reduce serum phosphorus levels by inhibition of proximal tubular phosphorus reabsorption through decreased expression of types 2a and 2c sodium-phosphate cotransporters and by decreasing intestinal phosphorus absorption through inhibiting calcitriol synthesis in the kidney (4). Moreover, FGF23-null mice were shown to exhibit severe vascular calcification with concomitant hyperphosphatemia (5). These facts suggest that FGF23 may have a protective effect on vascular calcification by hyperphosphatemia suppression. In contrast, several hemodialysis studies reported that elevated FGF23 levels were associated with aortic calcification (6) and mortality (7, 8) independent of serum phosphorus levels. Elevated serum FGF23 levels, even within the normal range, are reportedly associated with increased left ventricular mass index and increased risk for the presence of left ventricular hypertrophy in elderly subjects (9). Furthermore, a recent study suggested that elevated FGF23 levels contributed directly to high rates of left ventricular hypertrophy and mortality in individuals with chronic kidney diseases (10). Thus, FGF23 regulation may also play a clinically significant role in the prevention of cardiovascular diseases.Oral phosphorus supplementation is known to stimulate FGF23 secretion, although the underlying mechanism has not been clarified. In our preliminary study, we found that plasma FGF23 levels in rats increased after oral phosphorus administration at a physiological dose; however, this increase slowly began around the time that plasma phosphorus levels had decreased (unpublished data). Based on these findings, we reasoned that oral phosphorus supplementation may secondarily increase FGF23 secretion. Parathyroid hormone (PTH) is also secreted in response to phosphorus administration (11) and subsequently increases urinary phosphorus excre- Note Oral Phosphorus Supplementation Secondarily Increases Circulating Fibroblast Growth Factor 23 Levels at Least Partially via Stimulation of Parathyroid Hormone SecretionSatoshi Takasugi, Miho Akutsu and Masashi Nagata Food Science Research Laboratories, Division of Research and Development, Meiji Co., Ltd., 540 Naruda, Odawara, Kanagawa 250-0862, Japan (Received August 20, 2013) Summary Oral phosphorus supplementation stimulates fibroblast growth factor 23 (FGF23) secretion; however, the underlying mechanism remains unclear. The aim of this ...

show abstract

Fibroblast growth factor-23 (FGF-23) is independently correlated to aortic calcification in haemodialysis patients

Abstract: In haemodialysis patients, FGF-23 and ACI were significantly increased, and FGF-23 was independently associated with aortic calcification.

Cited by 188 publications

References 32 publications

Plasma Fibroblast Growth Factor-23 Level and its Relation to Carotid Artery Atherosclerosis in Hemodialysis Patients

Plasma Fibroblast Growth Factor-23 Level and its Relation to Carotid Artery Atherosclerosis in Hemodialysis Patients

Association of Circulating Fibroblast Growth Factor-23 with Renal Phosphate Excretion among Hemodialysis Patients with Residual Renal Function

Oral Phosphorus Supplementation Secondarily Increases Circulating Fibroblast Growth Factor 23 Levels at Least Partially via Stimulation of Parathyroid Hormone Secretion

Contact Info

Product

Resources

About