SUN-359 Antenatal Oral Iron Supplementation, FGF23 and Bone Metabolism in Kenyan Women and Their Offspring: A Randomised Controlled Trial

Abstract Objectives: FGF23 decreases reabsorption and increases phosphate excretion in the kidney and regulates vitamin D metabolism. Maternal iron deficiency may be implicated in the pathogenesis of hypophosphataemia-driven rickets in offspring through perturbed FGF23 expression. We aimed to determine the effect of antenatal oral iron supplementation on maternal and neonatal markers of bone mineral regulation. Methods: 470 rural Kenyan women with singleton pregnancies and haemoglobin concentrations ≥90g/L were randomly allocated to daily, supervised supplementation iron (60mg as ferrous fumarate) or placebo from 13–23 weeks gestational age until 1 month postpartum. We analysed maternal and neonatal plasma samples collected at birth, with primary outcomes being concentrations of FGF23 in its intact form (I-FGF23, the phosphate- and vitamin D-regulating hormone) and its C-terminal fragment (C-FGF23). Results: In mothers and neonates, antenatal iron supplementation reduced C-FGF23 concentration by 62.6% (95%CI: -70.3% to -53.0%) and 15.2% (-28.4% to 0.3%), respectively; increased neonatal I-FGF23 concentration by 21.6% (1.2% to 46.1%); increased maternal hepcidin concentration by 136%, (86% to 200%); and decreased maternal 25-hydroxyvitamin D concentrations by 6.1nmol/L (1.2 to 11.0nmol/L). We found no effect on markers of bone turnover in either mothers or neonates. The magnitude of the effect of antenatal iron supplementation on concentrations of C-FGF23, I-FGF23 and phosphate, and on estimated glomerular filtration rate (a measure of kidney glomerular function) depended on maternal iron status at baseline Conclusions: Antenatal iron supplementation may provide health benefits to pregnant women and their offspring beyond increasing iron status. Whether iron supplementation reduces present and future infant risk of rickets remains unclear.