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Research article
gholamhossein Ranjbar omrani
shiraz endocrinology and metabolism research center
Corresponding Author
ORCiD: https://orcid.org/0000-0003-2224-7250
License:
This work is licensed under a CC BY 4.0 License. Read Full License
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.
Keywords
FGF-23, FE PO4, Hypoparathyroidism, PO4
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CURRENT STATUS: Published
View the published article at BMC Nephrology.
Version 2
Posted 18 Dec, 2019
No community comments so far
Editorial decision: Accept
On 22 Apr, 2020
Review #2 received
Received 15 Apr, 2020
Review #1 received
Received 12 Apr, 2020
Reviewer #1 agreed
On 25 Mar, 2020
Reviewer #2 agreed
On 25 Mar, 2020
Reviewers invited
Invitations sent on 25 Mar, 2020
Editor assigned
On 16 Dec, 2019
Submission checks complete
On 15 Dec, 2019
Editor invited
On 15 Dec, 2019
No comments provided
Editorial decision: Major revision
On 11 Nov, 2019
Review #2 received
Received 05 Nov, 2019
Reviewer #2 agreed
On 23 Oct, 2019
Review #1 received
Received 30 Sep, 2019
Reviewer #1 agreed
On 12 Sep, 2019
Reviewers invited
Invitations sent on 11 Sep, 2019
Editor assigned
On 20 Aug, 2019
Submission checks complete
On 26 Jul, 2019
Editor invited
On 26 Jul, 2019
First submitted
On 07 Jul, 2019
Metrics
Comments: 0
PDF Downloads: ...
HTML Views: ...
Subject Areas
Urology & Nephrology
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A new preprint design is coming!
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See the published version of this preprint at BMC Nephrology.
This is a preprint, a preliminary version of a manuscript that has not completed peer review at a journal. Research Square does not conduct peer review prior to posting preprints. The posting of a preprint on this server should not be interpreted as an endorsement of its validity or suitability for dissemination as established information or for guiding clinical practice.
Learn more about In Review
Research article
gholamhossein Ranjbar omrani
shiraz endocrinology and metabolism research center
Corresponding Author
ORCiD: https://orcid.org/0000-0003-2224-7250
Badges
Prescreen
This manuscript passed our Prescreen assessment
Complete author information
Appropriate declaration statements
Potential risks to human health
Prescreen
Peer Review Timeline
CURRENT STATUS: Published
View the published article at BMC Nephrology.
Version 2
Posted 18 Dec, 2019
No community comments so far
Editorial decision: Accept
On 22 Apr, 2020
Review #2 received
Received 15 Apr, 2020
Review #1 received
Received 12 Apr, 2020
Reviewer #1 agreed
On 25 Mar, 2020
Reviewer #2 agreed
On 25 Mar, 2020
Reviewers invited
Invitations sent on 25 Mar, 2020
Editor assigned
On 16 Dec, 2019
Submission checks complete
On 15 Dec, 2019
Editor invited
On 15 Dec, 2019
No comments provided
Editorial decision: Major revision
On 11 Nov, 2019
Review #2 received
Received 05 Nov, 2019
Reviewer #2 agreed
On 23 Oct, 2019
Review #1 received
Received 30 Sep, 2019
Reviewer #1 agreed
On 12 Sep, 2019
Reviewers invited
Invitations sent on 11 Sep, 2019
Editor assigned
On 20 Aug, 2019
Submission checks complete
On 26 Jul, 2019
Editor invited
On 26 Jul, 2019
First submitted
On 07 Jul, 2019
Metrics
Comments: 0
PDF Downloads: ...
HTML Views: ...
Subject Areas
Urology & Nephrology
License:
This work is licensed under a CC BY 4.0 License. Read Full License
View the published article at BMC Nephrology.
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.
Figure 1
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