I. V. Poladych¹*, I. O. Shymanskyi², A. V. Khomenko²,
M. M. Veliky², D. O. Govsieiev¹

¹Department of Obstetrics and Gynecology No. 1, Bogomolets National Medical University, Kyiv, Ukraine;
²Department of Biochemistry of Vitamins and Coenzymes, Palladin Institute of Biochemistry,
National Academy of Sciences of Ukraine, Kyiv;
*e-mail: iren.poladich@gmail.com

Received: 25 August 2025; Revised: 02 October2025;
Accepted: 30 January 2026; Available on-line: February 2026

Preeclampsia (PE) is a major cause of maternal and perinatal morbidity, with its pathogenesis involving, in particular, impaired mineral homeostasis. Recent evidence suggest that fibroblast growth factor 23 (FGF23), a key regulator of phosphate balance and vitamin D₃ metabolism, may contribute to pregnancy complications, however, its role in PE remains poorly understood. This study aimed to evaluate serum FGF23 level and its relationship with vitamin D₃ and calcium–phosphate balance at preeclampsia development in animal experimental model. Thirty-five Wistar female rats were divided into three groups: controls on a standard­ diet; vitamin D₃-deficient rats; vitamin D₃-deficient rats supplemented with cholecalciferol. Within each group, PE was induced by Nω-nitro-L-arginine methyl ester administration. Serum concentrations of 25(OH)D₃, FGF23, parathyroid hormone (PTH), total calcium, inorganic phosphate, and alkaline phosphatase (ALP) activity were determined by ELISA and biochemical assays. It was shown that vitamin D₃ deficiency was accompanied by hypocalcemia, hypophosphatemia, elevated FGF23 and increased ALP activity in the serum. Supplementation with vitamin D₃ increased 25(OH)D₃, markedly reduced FGF23 levels and normalized mine­ral parameters. Induction of PE caused significant disturbances in calcium–phosphate status, hypertension, and 100% mortality of vitamin D₃-deficient animals. In the presence of preeclampsia vitamin D₃ efficacy was limited. In PE group, despite of vitamin D₃ supplementation, serum FGF23 was markedly elevated, indicating impaired vitamin D₃ metabolism. Our findings demonstrate that vitamin D₃ deficiency amplifies PE severity through disruption of mineral homeostasis and FGF23 dependent signaling.

Keywords: 25OHD3, calcium–phosphate metabolism, L-NAME, preeclampsia, vitamin D3 deficiency