Significant changes in fetal
iron status potentially occur in pregnancies in which reduced fetal nutrient delivery is severe enough to result in
intrauterine growth retardation (IUGR), particularly if chronic
fetal hypoxia is also present and increases fetal
iron demand for
hemoglobin synthesis. Neonates rarely die following IUGR secondary to maternal
preeclampsia, but
bilateral renal agenesis, which is also characterized by reduced maternal-fetal blood flow, late gestation placental failure, and IUGR, is uniformly fatal. We measured neonatal liver
iron concentration, as an assessment of fetal storage
iron status, and heart and brain
iron concentrations, as assessments of nonheme tissue
iron status, in 11 infants who died in the neonatal period of
bilateral renal agenesis, and compared them with values for gestational age-matched control infants whose gestation was not complicated by
fetal growth retardation or
hypoxia. Stainable nonheme
iron in the hepatocytes was significantly reduced in all and completely absent in 8 of the 11 cases of
renal agenesis (P < .001 compared with control). The mean +/- SEM liver
iron concentration of the
bilateral renal agenesis group (999 +/- 218 micrograms/g dry tissue weight) was 26% of the control value (3894 +/- 548 micrograms/g dry tissue weight; P < .001). Brain
iron concentration was also lower in the group with
bilateral renal agenesis (109 +/- 17 vs. 161 +/- 19; P = .015) and was correlated with liver
iron concentration (
r = .47; P = .03). Heart
iron concentrations were similar in the two groups. Nine of the subjects with
bilateral renal agenesis had placental weights below the fifth percentile for gestational age. The
bilateral renal agenesis group had a lower mean
birth weight (P < .001) and had a higher prevalence of
fetal growth retardation (55% vs. 0%; P < .001). We conclude that infants with
bilateral renal agenesis are at risk for severe
iron deficiency of storage and nonstorage tissues. Liveborn infants with nonfatal fetal conditions characterized by significant restriction of maternal-fetal blood flow may also be at significant risk for postnatal
iron deficiency.