With or without the kidney: the role of FGF23 in CKD.

@article{Fukagawa2005WithOW,
  title={With or without the kidney: the role of FGF23 in CKD.},
  author={Masafumi Fukagawa and Junichiro J Kazama},
  journal={Nephrology, dialysis, transplantation : official publication of the European Dialysis and Transplant Association - European Renal Association},
  year={2005},
  volume={20 7},
  pages={
          1295-8
        }
}
  • M. Fukagawa, J. Kazama
  • Published 1 July 2005
  • Biology, Medicine
  • Nephrology, dialysis, transplantation : official publication of the European Dialysis and Transplant Association - European Renal Association
The systemic balance of phosphate is maintained mainly by three organs, i.e. the intestine, kidney and bone. Several factors including parathyroid hormone (PTH) and vitamin D play a critical role in this system. Fibroblast growth factor 23 (FGF23) is a recently identified phosphatonin which also is implicated [1,2]. It has been demonstrated in several diseases that excessive activity of FGF23 resulted in hypophosphataemia, low plasma 1,25-dihydroxyvitamin D (1,25D) levels and osteomalacia [3–5… 
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FGF23: a key player in mineral and bone disorder in CKD.
  • H. Komaba, M. Fukagawa
  • Medicine, Biology
    Nefrologia : publicacion oficial de la Sociedad Espanola Nefrologia
  • 2009
TLDR
In patients with chronic kidney disease (CKD), circulating FGF23 levels are progressively elevated to compensate for persistent phosphate retention and thereby stimulate secretion of parathyroid hormone, suggesting its critical role in the pathogenesis of altered mineral homeostasis in CKD.
The role of FGF23 in CKD—with or without Klotho
TLDR
In patients with end-stage renal disease, markedly increased levels of FGF23 fail to exert Klotho-dependent effects owing to the absence of a functioning kidney and downregulation of the parathyroid complex of KlothO and FGF receptor 1.
The kidney and bone metabolism: Nephrologists' point of view
TLDR
It is quite important to identify severe cases of hyperparathyroidism refractory to medical therapy, and the size of the parathyroid glands, serum levels of fibroblast growth factor (FGF)23, and, possibly, the overproduction of a novel form ofParathyroid hormone (PTH), serve as useful markers for this purpose.
Fibroblast growth factor 23 production in bone is directly regulated by 1{alpha},25-dihydroxyvitamin D, but not PTH.
TLDR
The results suggest that FGF23 synthesis in bone is regulated by 1,25(OH)(2)D(3) directly, not by PTH, and that increased VDR mRNA expression induced the relatively swift and strong response in the uremic group.
FGF23-parathyroid interaction: implications in chronic kidney disease.
TLDR
Recent insights into the role of FGF23 in mineral homeostasis are summarized and the involvement of its direct and indirect interaction with the parathyroid gland is discussed, particularly focusing on the pathophysiology of secondary hyperparathyroidism in chronic kidney disease.
Regulation of Fibroblast Growth Factor 23 Production in Bone in Uremic Rats
TLDR
Elevated plasma F GF23 levels in uremic rats reflect the increased expression of FGF23 in bone, which may be regulated by a PTH-1,25(OH)2D3 axis-dependent pathway and another PTH/PTH-dependent and 1,25-dihydroxyvitamin D/D3-independent pathway in u Remic rats.
Study Of Fibroblast Growth Factor 23 ( Fgf23 ) And Anemia In Hemodialysis Patients And Ckd Patients Stage s 3 & 4
TLDR
PTH and phosphate are not the only factors affecting FGF23 in CKD and HD patients, b ut also Iron and Iron parameters have a great impact on F GF23 serum level.
Osteo-renal cross-talk and phosphate metabolism by the FGF23-Klotho system.
TLDR
How the FGF23/klotho system might influence systemic phosphate metabolism, and consequences of its abnormal regulation will be briefly described are summarized.
PHOSPHORUS METABOLISM AND MANAGEMENT IN CHRONIC KIDNEY DISEASE: Role of Fibroblast Growth Factor 23 in Phosphate Homeostasis and Pathogenesis of Disordered Mineral Metabolism in Chronic Kidney Disease
The discovery of fibroblast growth factor 23 (FGF23), a novel bone‐derived hormone that inhibits phosphate reabsorption and calcitriol production by the kidney, has uncovered primary regulatory…
CKD-MBD as a systemic disorder.
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References

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Circulating FGF-23 Is Regulated by 1α,25-Dihydroxyvitamin D3 and Phosphorus in Vivo*
TLDR
There was a feedback loop existing among serum phosphorus, 1α,25(OH)2D3, and FGF-23, in which the novel phosphate-regulating bone-kidney axis integrated with the parathyroid hormone-vitamin D3 axis in regulating phosphate homeostasis.
The phosphatonin pathway: new insights in phosphate homeostasis.
TLDR
A new class of phosphate-regulating factors, collectively known as the phosphatonins, have been shown to be associated with the hypophosphatemic diseases, tumor-induced osteomalacia (TIO), X-linked hypoph phosphate-linked rickets (XLH), and autosomal-dominant hypoph phosphatemic rickets and their role under normal or pathologic conditions is not yet clear.
Circulating concentration of FGF-23 increases as renal function declines in patients with chronic kidney disease, but does not change in response to variation in phosphate intake in healthy volunteers.
TLDR
Circulating FGF-23 was significantly elevated in patients with CKD and its concentration correlated with renal creatinine clearance, and in healthy volunteers, F GF-23 levels did not change after phosphate deprivation or phosphate loading.
Targeted ablation of Fgf23 demonstrates an essential physiological role of FGF23 in phosphate and vitamin D metabolism.
TLDR
Evidence is presented that FGF23 is a physiological regulator of serum phosphate and 1,25-dihydroxyvitamin D (1,25[OH]2D) by generating FGF 23-null mice, indicating that F GF23 is essential for normal phosphate and vitamin D metabolism.
Fibroblast growth factor-23 relationship to dietary phosphate and renal phosphate handling in healthy young men.
TLDR
F GF-23 was inversely related to renal Pi transport and serum calcitriol levels in healthy young men, suggesting that FGF-23 may be implicated in the physiological regulation of Pi homeostasis in response to dietary phosphate changes, independent of PTH.
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TLDR
Serum phosphate, calcium, and intact PTH could be regulators of FGF-23 levels in uremic patients on maintenance hemodialysis and may provide new insights into the pathophysiologic effects of F GF-23 on calcium-phosphate homeostasis.
Intravenous Calcitriol Therapy Increases Serum Concentrations of Fibroblast Growth Factor-23 in Dialysis Patients with Secondary Hyperparathyroidism
TLDR
Intravenous calcitriol decreased serum intact PTH level and increased serum FGF-23 levels significantly and may be attributed, at least in part, to the cumulative dose of vitamin D in patients with refractory secondary hyperparathyroidism.
Total parathyroidectomy reduces elevated circulating fibroblast growth factor 23 in advanced secondary hyperparathyroidism.
TLDR
It is suggested that hyperplastic parathyroid glands, together with hyperphosphatemia, affect abnormal FGF-23 metabolism in patients with stage 5 CKD with advanced secondary hyperparathyroidism.
Possible involvement of circulating fibroblast growth factor 23 in the development of secondary hyperparathyroidism associated with renal insufficiency.
TLDR
FGF-23 becomes a potential uremic toxin to decrease 1,25D levels when it loses its hypophosphatemic action because of a decreased number of viable nephrons in patients with advanced renal failure and may be an important determinant in the regulation of mineral metabolism with renal insufficiency.
Bone as a source of FGF23: regulation by phosphate?
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