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8. Aspects of Fibroblast Growth Factor 23 in Mild to Moderate Renal Dysfunction

Author

Westerberg, Per-Anton

Subjects
stomatognathic diseases, FGF23, urologic and male genital diseases, elderly, mortality, phosphate, mineral metabolism
Abstract

Disturbances in mineral metabolism contribute to vascular calcification and mortality risk in chronic kidney disease (CKD). Serum levels of fibroblast growth factor (FGF)23, a bone derived, phosphaturic peptide, are associated with cardiovascular mortality in CKD. Membrane bound klotho(KL) is an obligate co receptor for FGF23 signaling in the kidney. To study aspects of FGF23 in mild to moderate impairment of renal function we have analyzed FGF23, estimated glomerular filtration rate (eGFR), parathyroid hormone(PTH), 1,25 (OH)2 vitamin D (1,25D), calcium and phosphate in one patient with a FGF23 producing tumor, before and after tumor removal (study 1), in 72 CKD patients with varying degree of renal dysfunction (study 2), in 9 healthy kidney donors, before and after nephrectomy (study 3). We also analyzed FGF23 (study 4), and performed genotyping of 27 single nucleotide polymorphisms (SNP) of the KL gene (study 5) in 2838 elderly Swedish men (MrOs study) and examined the association with mortality. FGF23 normalizes in 30-45 minutes after removal of a FGF23 producing tumor (study 1). 1,25D increases in hours and remains elevated months, even when the other parameters have normalized. FGF23 increase early in CKD, initially slowly, in correlation with PTH, but exponentially when hyperphosphatemia ensues (study 2). After unilateral nephrectomy (study 3) mineral homeostasis remain stable, initially due to a rise in PTH and later to an increase in FGF23. FGF23 levels are not correlated with mortality in elderly men after adjustment for eGFR, but with mortality due to cardiovascular disease, even in persons with normal eGFR (study 4). Polymorphism of the KL gene do not correlate with increased mortality risk in elderly men (study 5), but there is a modulating effect on FGF23 levels. FGF23 is of importance in maintaining phosphate homeostasis as renal function declines. It is co regulated with PTH until advanced renal dysfunction, and adjust the 1,25D to the actual GFR. FGF23 is associated with cardiovascular mortality. Further studies are needed to determine the mechanism, and if reduction of FGF23 by reducing phosphate intake may be beneficial even in persons with mild to moderate renal function.

Published
2013

9. High doses of cholecalciferol alleviate the progression of hyperparathyroidism in patients with CKD Stages 3-4: results of a 12-week double-blind, randomized, controlled study.

Author

Westerberg, Per-Anton, Sterner, Gunnar, Ljunggren, Östen, Isaksson, Elin, Elvarson, Fjölnir, Dezfoolian, Hamid, and Linde, Torbjörn

Subjects
*CHOLECALCIFEROL, *HYPERPARATHYROIDISM, *CHRONIC kidney failure, *RANDOMIZED controlled trials, *DISEASE progression, *GRIP strength
Abstract

Background. Calcidiol insufficiency may accelerate the development of secondary hyperparathyroidism (SHPT). We tested the effect of a substantial increase in calcidiol on mineral metabolism in patients with chronic kidney disease (CKD). Methods. Ninety-five patients with CKD Stages 3-4, parathyroid hormone (PTH) above 6.8pmol/L and calcidiol below 75nmol/L were randomized to receive either cholecalciferol 8000 IU/day or placebo for 12 weeks. The primary endpoint was difference in the mean change in iPTH after 12 weeks. The proportion of participants having a 30% reduction in PTH and the effect on hand grip strength, fatigue and different biochemical variables were also investigated. Results. Baseline calcidiol was 57.5622 and 56.8622 nmol/L in the cholecalciferol and placebo groups, respectively. The corresponding concentrations of PTH were 10.965 and 13.169 pmol/L. Calcidiol increased to 162 649 nmol/L in patients receiving cholecalciferol, and PTH levels remained constant at 10.565 pmol/L. In the placebo group, calcidiol remained stable and PTH increased to 15.2611 pmol/L. The mean change in PTH differed significantly between the two groups (P<0.01). The proportion of subjects reaching a 30% decrease in PTH did not differ. No effect on grip strength, fatigue, phosphate or fibroblast growth factor 23 was observed. Cholecalciferol treatment resulted in stable calcium concentrations and a substantial increase in calcitriol. Conclusion. Treatment with high daily doses of cholecalciferol in patients with CKD Stages 3-4 halts the progression of SHPT and does not cause hypercalcaemia or other side effects. [ABSTRACT FROM AUTHOR]

Published
2018
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11. Oncogenic osteomalacia illustrating the effect of fibroblast growth factor 23 on phosphate homeostasis.

Author

Westerberg, Per-Anton, Linde, Torbjörn, Vanderschueren, Dirk, Billen, Jaak, Jans, Ivo, and Ljunggren, Östen

Subjects
*OSTEOMALACIA, *FIBROBLAST growth factors, *CARCINOGENESIS, *PHOSPHATES, *HOMEOSTASIS, *CALCITRIOL, *MINERAL metabolism
Abstract

In oncogenic osteomalacia (OOM), fibroblast growth factor 23 (FGF23) induces renal phosphate wasting and inhibits the appropriate increase of calcitriol. A patient suffering from OOM is described. Serum calcium, phosphate, biointact parathyroid hormone and intact FGF23 as well as the calcitriol and 24,25-vitamin D levels were measured before and after tumour removal. The clinical approach to a patient with hypophosphataemia is discussed and the changes in mineral metabolism after removal of a FGF23-producing tumour are described. [ABSTRACT FROM PUBLISHER]

Published
2012

13. The roles of cytochrome P450 3A4 and lA2 in the 3-hydroxylation of quinine in vivo*

Author

Mirghani, Rajaa A., Hellgren, Urban, Westerberg, Per Anton, Ericsson, Orjan, Bertilsson, Leif, and Gustafsson, Lars L.

Abstract

Objective: To investigate the roles of CYP3A4 and CYP1A2 in the 3-hydroxylation of quinine in vivo.Methods: In a randomized, three-way crossover study, nine healthy Swedish volunteers received single oral doses of quinine hydrochloride (500 mg), quinine hydrochloride (500 mg) plus ketoconazole (100 mg twice daily for 3 days), and quinine hydrochloride (500 mg) plus fluvoxamine (25 mg twice daily for 2 days) on three different occasions. Blood and urine samples were collected before quinine intake and up to 96 hours thereafter. Plasma and urine samples were analyzed for both quinine and its main metabolite 3-hydroxyquinine with HPLC methods.Results: Coadministration with ketoconazole (which inhibits CYP3A4) decreased the mean apparent oral clearance of quinine significantly (P < .001) by 31%(from 8.7 to 6.0 L/h), whereas coadministration with fluvoxamine (which inhibits CYP1A2 and to some extent CYP2C19) had no significant effect (P > .05) on the mean apparent oral clearance of quinine. Coadministration with ketoconazole also decreased the mean area under the plasma concentration versus time curve (AUC) of 3-hydroxyquinine (from 28.4 to 19.7 μmol · h · L−1; P < .001), whereas coadministration with fluvoxamine increased 3-hydroxyquinine AUC significantly (from 28.4 to 30.2 μmol · h · L−1; P < .05).Conclusion: Cytochrome P450 3A4 is important for the 3-hydroxylation of quinine in vivo. On the other hand, CYP1A2 had no significant effect on this metabolic pathway.

Published
1999
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14. [Osteomalacia due to phosphate deficiency caused by a tumor. Focus on FGF23 in physiology and clinic].

Author

Westerberg PA, Linde T, and Ljunggren O

Subjects
Aged, Female, Fibroblast Growth Factor-23, Fibroblast Growth Factors genetics, Fluorodeoxyglucose F18, Humans, Neoplasms, Connective Tissue diagnosis, Paraneoplastic Syndromes diagnosis, Phosphates physiology, Positron-Emission Tomography, Radiopharmaceuticals, Fibroblast Growth Factors physiology, Hypophosphatemia complications, Hypophosphatemia etiology, Neoplasms, Connective Tissue complications, Osteomalacia etiology, Paraneoplastic Syndromes complications
Published
2012

15. Oncogenic osteomalacia illustrating the effect of fibroblast growth factor 23 on phosphate homeostasis.

Author

Westerberg PA, Linde T, Vanderschueren D, Billen J, Jans I, and Ljunggren Ö

Abstract

In oncogenic osteomalacia (OOM), fibroblast growth factor 23 (FGF23) induces renal phosphate wasting and inhibits the appropriate increase of calcitriol. A patient suffering from OOM is described. Serum calcium, phosphate, biointact parathyroid hormone and intact FGF23 as well as the calcitriol and 24,25-vitamin D levels were measured before and after tumour removal. The clinical approach to a patient with hypophosphataemia is discussed and the changes in mineral metabolism after removal of a FGF23-producing tumour are described.

Published
2012
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