Fibroblast growth factor 23, calcium and phosphate serum levels in experimental preeclampsia: impact of vitamin D(3) status

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