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FGF23 in kidney transplant: the strange case of Doctor Jekyll and Mister Hyde

View Article: PubMed Central - PubMed

ABSTRACT

During the last decade, a new view into the molecular mechanisms of chronic kidney disease-mineral bone disorder (CKD-MBD) has been proposed, with fibroblast growth factor 23 (FGF23) as a novel player in the field. Enhanced serum FGF23 levels cause a reduction in serum phosphate, together with calcitriol suppression and consequent hyperparathyroidism (HPT). In contrast, reduced serum FGF23 levels are associated with hyperphosphatemia, higher calcitriol levels and parathyroid hormone (PTH) suppression. In addition, serum FGF23 levels are greatly increased and positively correlated with serum phosphate levels in CKD patients. In this population, high serum FGF23 concentration seems to predict the occurrence of refractory secondary HPT and to be associated with higher mortality risk in incident haemodialysis patients. In living-donor kidney transplant recipients, a faster normalization of FGF23 and phosphate levels with a lower prevalence of HPT, may be considered a major pathway to investigate.

No MeSH data available.


Trends of PTH, FGF23 and phosphate (P) levels at 1 year after renal transplantation in a well-functioning graft. Deceased kidney donors are shown with a solid line while living kidney donors are shown with a dashed line.
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SFW072F1: Trends of PTH, FGF23 and phosphate (P) levels at 1 year after renal transplantation in a well-functioning graft. Deceased kidney donors are shown with a solid line while living kidney donors are shown with a dashed line.

Mentions: Hypophosphataemia is present in up to 90% of transplant recipients [14], with the majority (70%) of the cases being mild to moderate (serum phosphate level >1.5 to <2.3 mg/dL); phosphate levels remain low for longer than in patients with CKD matched for the GFR [15]. Acute or chronic post-transplant hypophosphataemia may cause detrimental effects. In the early post-transplant period, when serum phosphate levels are lower, muscle weakness may occur [16], whereas effects of chronic hypophosphataemia are less clear. There are few studies on the parallel changes in PTH, FGF23 and phosphate levels and mostly detailed in deceased-donor kidney transplantation with a follow-up of <1 year. Based on the data available, it is estimated that the effect of these phosphaturic hormones on hypophosphataemia changes over time after transplantation. FGF23 has emerged as an important mediator of early hypophosphataemia, and its phosphaturic effect is enforced by persistent hyperparathyroidism and 1,25-dihydroxyvitamin D deficiency. In the long term, hypophosphataemia and renal phosphate loss are mainly related to persistent hyperparathyroidism [17, 18] (Figure 1).Fig. 1.


FGF23 in kidney transplant: the strange case of Doctor Jekyll and Mister Hyde
Trends of PTH, FGF23 and phosphate (P) levels at 1 year after renal transplantation in a well-functioning graft. Deceased kidney donors are shown with a solid line while living kidney donors are shown with a dashed line.
© Copyright Policy - creative-commons
Related In: Results  -  Collection

License
Show All Figures
getmorefigures.php?uid=PMC5036904&req=5

SFW072F1: Trends of PTH, FGF23 and phosphate (P) levels at 1 year after renal transplantation in a well-functioning graft. Deceased kidney donors are shown with a solid line while living kidney donors are shown with a dashed line.
Mentions: Hypophosphataemia is present in up to 90% of transplant recipients [14], with the majority (70%) of the cases being mild to moderate (serum phosphate level >1.5 to <2.3 mg/dL); phosphate levels remain low for longer than in patients with CKD matched for the GFR [15]. Acute or chronic post-transplant hypophosphataemia may cause detrimental effects. In the early post-transplant period, when serum phosphate levels are lower, muscle weakness may occur [16], whereas effects of chronic hypophosphataemia are less clear. There are few studies on the parallel changes in PTH, FGF23 and phosphate levels and mostly detailed in deceased-donor kidney transplantation with a follow-up of <1 year. Based on the data available, it is estimated that the effect of these phosphaturic hormones on hypophosphataemia changes over time after transplantation. FGF23 has emerged as an important mediator of early hypophosphataemia, and its phosphaturic effect is enforced by persistent hyperparathyroidism and 1,25-dihydroxyvitamin D deficiency. In the long term, hypophosphataemia and renal phosphate loss are mainly related to persistent hyperparathyroidism [17, 18] (Figure 1).Fig. 1.

View Article: PubMed Central - PubMed

ABSTRACT

During the last decade, a new view into the molecular mechanisms of chronic kidney disease-mineral bone disorder (CKD-MBD) has been proposed, with fibroblast growth factor 23 (FGF23) as a novel player in the field. Enhanced serum FGF23 levels cause a reduction in serum phosphate, together with calcitriol suppression and consequent hyperparathyroidism (HPT). In contrast, reduced serum FGF23 levels are associated with hyperphosphatemia, higher calcitriol levels and parathyroid hormone (PTH) suppression. In addition, serum FGF23 levels are greatly increased and positively correlated with serum phosphate levels in CKD patients. In this population, high serum FGF23 concentration seems to predict the occurrence of refractory secondary HPT and to be associated with higher mortality risk in incident haemodialysis patients. In living-donor kidney transplant recipients, a faster normalization of FGF23 and phosphate levels with a lower prevalence of HPT, may be considered a major pathway to investigate.

No MeSH data available.