Molecular and cellular regulation of renal phosphate transporters in X-linked hypophosphatemia

Miyamoto, Ken‐ichi; Taketani, Yutaka; Morita, Kyoko; Segawa, Hiroko; Nii, Tomoko; Fujioka, Ai; Kido, Shinsuke; Arai, Hidekazu; Tani, Yuji; Katai, Kanako; Tatsumi, Sawako; Takeda, Eiji

doi:10.1007/bf02480555

Cited by 3 publications

(3 citation statements)

References 14 publications

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“…Moreover, PTH increases FGF-23 gene expression [35]. [41][42][43][44],autosomal dominant hypophosphatemic rickets [45,46], Autosomal recessive hypophosphatemic rickets (ARHR) [47,48] or Fibrous dysplasia (FD)/McCune-Albright syndrome [49].…”

Section: Resultsmentioning

confidence: 99%

Interaction between serum FGF-23 and PTH in renal phosphate excretion, a case-control study in hypoparathyroid patients

Saki

Kassaee

Salehifar

et al. 2019

Preprint

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Background phosphate homeostasis is mediated through complex counter regulatory feed-back balance between parathyroid hormone, FGF-23 and 1,25(OH)2D. Both parathyroid hormone and FGF-23 regulate proximal tubular phosphate excretion through signaling on sodium- phosphate cotransporters IIa and IIc. However, the interaction between these hormones on phosphate excretion is not clearly understood. We performed the present study to evaluate whether the existence of sufficient parathyroid hormone is necessary for full phosphaturic function of FGF-23 or not. Methods In this case-control study, 19 patients with hypoparathyroidism and their age- and gender-matched normal population were enrolled. Serum calcium, phosphate, alkaline phosphatase,parathyroid hormone, FGF-23, 25(OH)D, 1,25(OH)2D and Fractional excretion of phosphorous were assessed and compared between the two groups, using SPSS software. Results The mean serum calcium and parathyroid hormone level was significantly lower in hypoparathyroid patients in comparison with the control group(P<0.001 and P<0.001, respectively). We found high serum level of phosphate and FGF-23 in hypoparathyroid patients compared to the control group (P<0.001 and P<0.001,respectively). However, there was no significant difference in Fractional excretion of phosphorous or 1,25OH2D level between the two groups. There was a positive correlation between serum FGF-23 and Fractional excretion of phosphorous just in the normal control population(P <0.001, r = 0.79). Conclusions Although the FGF-23 is a main regulator of urinary phosphate excretion but the existence of sufficient parathyroid hormone is necessary for the full phosphaturic effect of FGF-23.

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Section: Resultsmentioning

confidence: 99%

Interaction between serum FGF-23 and PTH in renal phosphate excretion, a case-control study in hypoparathyroid patients

Saki

Kassaee

Salehifar

et al. 2019

Preprint

View full text Add to dashboard Cite

show abstract

“…In the presence of normal parathyroid and kidney function inappropriate high serum FGF-23 could result in urinary PO 4 loss and hypophosphatemia such as Xlinked dominant hypophosphatemic rickets (XLH), [41][42][43][44], autosomal dominant hypophosphatemic rickets [45,46], Autosomal recessive hypophosphatemic rickets (ARHR) [47,48] or Fibrous dysplasia (FD)/ McCune-Albright syndrome [49]. As well as some acquired disorders such as Tumor-induced osteomalacia (TIO) [50][51][52].…”

Section: Discussionmentioning

confidence: 99%

Interaction between serum FGF-23 and PTH in renal phosphate excretion, a case-control study in hypoparathyroid patients

2020

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Background: phosphate homeostasis is mediated through complex counter regulatory feedback balance between parathyroid hormone, FGF-23 and 1,25(OH)2D. Both parathyroid hormone and FGF-23 regulate proximal tubular phosphate excretion through signaling on sodium-phosphate cotransporters II a and II c. However, the interaction between these hormones on phosphate excretion is not clearly understood. We performed the present study to evaluate whether the existence of sufficient parathyroid hormone is necessary for full phosphaturic function of FGF-23 or not. Methods: In this case-control study, 19 patients with hypoparathyroidism and their age-and gender-matched normal population were enrolled. Serum calcium, phosphate, alkaline phosphatase,parathyroid hormone, FGF-23, 25(OH)D, 1,25(OH)2D and Fractional excretion of phosphorous were assessed and compared between the two groups, using SPSS software. Results: The mean serum calcium and parathyroid hormone level was significantly lower in hypoparathyroid patients in comparison with the control group (P < 0.001 and P < 0.001, respectively). We found high serum level of phosphate and FGF-23 in hypoparathyroid patients compared to the control group (P < 0.001 and P < 0.001, respectively). However, there was no significant difference in Fractional excretion of phosphorous or 1,25OH2D level between the two groups. There was a positive correlation between serum FGF-23 and Fractional excretion of phosphorous just in the normal individuals (P < 0.001, r = 0.79). Conclusions: Although the FGF-23 is a main regulator of urinary phosphate excretion but the existence of sufficient parathyroid hormone is necessary for the full phosphaturic effect of FGF-23.

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“…In the presence of normal parathyroid and kidney function inappropriate high serum FGF-23 could result in urinary PO 4 loss and hypophosphatemia such as X-linked dominant hypophosphatemic rickets (XLH), [41][42][43][44],autosomal dominant hypophosphatemic rickets [45,46], Autosomal recessive hypophosphatemic rickets (ARHR) [47,48] or Fibrous dysplasia (FD)/McCune-Albright syndrome [49].…”

Section: Pth Also Increases Renal Po 4 Excretion At Proximal Tubule Omentioning

confidence: 99%

Interaction between serum FGF-23 and PTH in renal phosphate excretion, a case-control study in hypoparathyroid patients

Saki

Kassaee

Salehifar

et al. 2019

Preprint

View full text Add to dashboard Cite

Background:phosphate homeostasis is mediated through complex counter regulatory feed-back balance between parathyroid hormone, FGF-23 and 1,25(OH)2D. Both parathyroid hormone and FGF-23 regulate proximal tubular phosphate excretion through signaling on sodium- phosphate cotransporters II a and II c . However, the interaction between these hormones on phosphate excretion is not clearly understood. We performed the present study to evaluate whether the existence of sufficient parathyroid hormone is necessary for full phosphaturic function of FGF-23 or not. Methods:In this case-control study, 19 patients with hypoparathyroidism and their age- and gender-matched normal population were enrolled. Serum calcium, phosphate, alkaline phosphatase,parathyroid hormone, FGF-23, 25(OH)D, 1,25(OH)2D and Fractional excretion of phosphorous were assessed and compared between the two groups, using SPSS software. Results:The mean serum calcium and parathyroid hormone level was significantly lower in hypoparathyroid patients in comparison with the control group(P<0.001 and P<0.001, respectively). We found high serum level of phosphate and FGF-23 in hypoparathyroid patients compared to the control group (P<0.001 and P<0.001,respectively). However, there was no significant difference in Fractional excretion of phosphorous or 1,25OH2D level between the two groups. There was a positive correlation between serum FGF-23 and Fractional excretion of phosphorous just in the normal individuals (P <0.001, r = 0.79). Conclusions:Although the FGF-23 is a main regulator of urinary phosphate excretion but the existence of sufficient parathyroid hormone is necessary for the full phosphaturic effect of FGF-23.

show abstract

Molecular and cellular regulation of renal phosphate transporters in X-linked hypophosphatemia

Cited by 3 publications

References 14 publications

Interaction between serum FGF-23 and PTH in renal phosphate excretion, a case-control study in hypoparathyroid patients

Interaction between serum FGF-23 and PTH in renal phosphate excretion, a case-control study in hypoparathyroid patients

Interaction between serum FGF-23 and PTH in renal phosphate excretion, a case-control study in hypoparathyroid patients

Interaction between serum FGF-23 and PTH in renal phosphate excretion, a case-control study in hypoparathyroid patients

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