Fibroblast growth factor 23 is independently associated with renal magnesium handling in patients with chronic kidney disease.


Journal

Frontiers in endocrinology
ISSN: 1664-2392
Titre abrégé: Front Endocrinol (Lausanne)
Pays: Switzerland
ID NLM: 101555782

Informations de publication

Date de publication:
2022
Historique:
received: 16 09 2022
accepted: 28 11 2022
entrez: 26 1 2023
pubmed: 27 1 2023
medline: 28 1 2023
Statut: epublish

Résumé

Disturbances in magnesium homeostasis are common in patients with chronic kidney disease (CKD) and are associated with increased mortality. The kidney is a key organ in maintaining normal serum magnesium concentrations. To this end, fractional excretion of magnesium (FEMg) increases as renal function declines. Despite recent progress, the hormonal regulation of renal magnesium handling is incompletely understood. Fibroblast Growth Factor 23 (FGF23) is a phosphaturic hormone that has been linked to renal magnesium handling. However, it has not yet been reported whether FGF23 is associated with renal magnesium handling in CKD patients. The associations between plasma FGF23 levels, plasma and urine magnesium concentrations and FEMg was investigated in a cross-sectional cohort of 198 non-dialysis CKD patients undergoing renal biopsy. FGF23 was significantly correlated with FEMg (Pearson's correlation coefficient = 0.37, p<0.001) and urinary magnesium (-0.14, p=0.04), but not with plasma magnesium. The association between FGF23 and FEMg remained significant after adjusting for potential confounders, including estimated glomerular filtration rate (eGFR), parathyroid hormone and 25-hydroxyvitamin D. We report that plasma FGF23 is independently associated with measures of renal magnesium handling in a cohort of non-dialysis CKD patients. A potential causal relationship should be investigated in future studies.

Sections du résumé

Background
Disturbances in magnesium homeostasis are common in patients with chronic kidney disease (CKD) and are associated with increased mortality. The kidney is a key organ in maintaining normal serum magnesium concentrations. To this end, fractional excretion of magnesium (FEMg) increases as renal function declines. Despite recent progress, the hormonal regulation of renal magnesium handling is incompletely understood. Fibroblast Growth Factor 23 (FGF23) is a phosphaturic hormone that has been linked to renal magnesium handling. However, it has not yet been reported whether FGF23 is associated with renal magnesium handling in CKD patients.
Methods
The associations between plasma FGF23 levels, plasma and urine magnesium concentrations and FEMg was investigated in a cross-sectional cohort of 198 non-dialysis CKD patients undergoing renal biopsy.
Results
FGF23 was significantly correlated with FEMg (Pearson's correlation coefficient = 0.37, p<0.001) and urinary magnesium (-0.14, p=0.04), but not with plasma magnesium. The association between FGF23 and FEMg remained significant after adjusting for potential confounders, including estimated glomerular filtration rate (eGFR), parathyroid hormone and 25-hydroxyvitamin D.
Conclusions
We report that plasma FGF23 is independently associated with measures of renal magnesium handling in a cohort of non-dialysis CKD patients. A potential causal relationship should be investigated in future studies.

Identifiants

pubmed: 36699036
doi: 10.3389/fendo.2022.1046392
pmc: PMC9869122
doi:

Substances chimiques

Magnesium I38ZP9992A
Fibroblast Growth Factor-23 7Q7P4S7RRE
Fibroblast Growth Factors 62031-54-3

Types de publication

Journal Article Research Support, Non-U.S. Gov't

Langues

eng

Sous-ensembles de citation

IM

Pagination

1046392

Informations de copyright

Copyright © 2023 Grigore, Zuidscherwoude, Witasp, Barany, Wernerson, Bruchfeld, Xu, Olauson and Hoenderop.

Déclaration de conflit d'intérêts

The authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest.

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Auteurs

Teodora V Grigore (TV)

Radboud Institute for Molecular Life Sciences, Department of Physiology, Radboudumc, Nijmegen, Netherlands.

Malou Zuidscherwoude (M)

Radboud Institute for Molecular Life Sciences, Department of Physiology, Radboudumc, Nijmegen, Netherlands.

Anna Witasp (A)

Karolinska Institutet, Division of Renal Medicine, Department of Clinical Science, Intervention and Technology, Stockholm, Sweden.

Peter Barany (P)

Karolinska Institutet, Division of Renal Medicine, Department of Clinical Science, Intervention and Technology, Stockholm, Sweden.

Annika Wernerson (A)

Karolinska Institutet, Division of Renal Medicine, Department of Clinical Science, Intervention and Technology, Stockholm, Sweden.

Annette Bruchfeld (A)

Karolinska Institutet, Division of Renal Medicine, Department of Clinical Science, Intervention and Technology, Stockholm, Sweden.
Linköpings universitet Hälsouniversitetet, Department of Health, Medicine and Caring Sciences, Linköping, Sweden.

Hong Xu (H)

Karolinska Institutet, Division of Clinical Geriatrics, Department of Neurobiology, Department of Care Sciences and Society, Stockholm, Sweden.

Hannes Olauson (H)

Karolinska Institutet, Division of Renal Medicine, Department of Clinical Science, Intervention and Technology, Stockholm, Sweden.

Joost Hoenderop (J)

Radboud Institute for Molecular Life Sciences, Department of Physiology, Radboudumc, Nijmegen, Netherlands.

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