Introduction: Fetal growth restriction increases adverse pregnancy outcomes including preterm birth and intrauterine death. Apelin is a secreted peptide expressed in placental syncytiotrophoblast and downregulated in fetal growth restriction. We tested the hypothesis that adverse pregnancy outcome is associated with low maternal plasma apelin at diagnosis of early-onset fetal growth restriction. Methods: Plasma samples and fetomaternal blood flow Doppler velocimetry measurements were obtained from pregnant women (n=59) at diagnosis of early-onset fetal growth restriction in the second trimester. Plasma apelin was determined by ELISA and pregnancy outcome recorded. Placental gene expression was analysed after birth by qRT-PCR, compared to term placentas from women with late-onset fetal growth restriction or appropriate-for-gestational age infants. Results: Maternal plasma apelin concentration at diagnosis of early-onset fetal growth restriction did not differ between women who subsequently had an intrauterine fetal death or delivered extremely preterm (<28 weeks gestation) and women who had a livebirth ≥28 weeks. There was no correlation between plasma apelin and estimated fetal weight, placental thickness or indices of uteroplacental perfusion in the second trimester. Placental gene expression of apelin, but not the apelin receptor or its alternative ligand elabela, correlated with gestational age at delivery and was lower in women with early-onset fetal growth restriction delivering preterm than in appropriate-for-gestational-age, term controls. Discussion: Maternal circulating apelin during the second trimester is not associated with uteroplacental perfusion or subsequent adverse pregnancy outcome in severe, early-onset fetal growth restriction. However, placental apelin deficiency may contribute to the pathogenesis of early-onset fetal growth restriction.