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FGF-21 levels in polyuria-polydipsia syndrome.

Julie Refardt1,2, Clara Odilia Sailer1,2, Bettina Winzeler1,2

  • 1Departments of Endocrinology, Diabetology and Metabolism, University Hospital Basel, Basel, Switzerland.

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|December 29, 2018
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Summary

Fibroblast growth factor 21 (FGF-21) is not elevated in primary polydipsia patients. This study found no link between FGF-21 and excessive fluid intake in primary polydipsia, challenging previous animal data.

Keywords:
FGF21copeptindiabetes insipidusosmotic stimulationprimary polydipsia

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Area of Science:

  • Endocrinology
  • Metabolic Research

Background:

  • Primary polydipsia's underlying mechanisms remain unclear.
  • Animal studies suggest fibroblast growth factor 21 (FGF-21) influences fluid intake independently of arginine-vasopressin (AVP) and osmotic regulation.

Purpose of the Study:

  • To investigate circulating FGF-21 levels in patients with primary polydipsia compared to those with central diabetes insipidus and healthy controls.
  • To determine if FGF-21 plays a role in the pathophysiology of primary polydipsia.

Main Methods:

  • Prospective cohort study involving 20 primary polydipsia patients, 20 central diabetes insipidus patients, and 20 healthy volunteers.
  • Measurement of FGF-21 levels before and after hypertonic saline infusion to induce osmotic stimulation (target plasma sodium ≥150 mmol/L).
  • Statistical analysis including multivariate linear regression to adjust for confounding factors.

Main Results:

  • No significant difference in baseline FGF-21 levels was observed between primary polydipsia patients and healthy volunteers.
  • While baseline FGF-21 was higher in central diabetes insipidus patients, this finding was not supported by multivariate analysis.
  • Osmotic stimulation did not alter FGF-21 levels in any of the groups.

Conclusions:

  • Circulating FGF-21 levels are not elevated in patients with primary polydipsia.
  • FGF-21 does not appear to be a causal factor in the excessive fluid intake associated with primary polydipsia.
  • These findings do not support the role of FGF-21 in the pathomechanism of primary polydipsia.