History of fetal growth restriction is more strongly associated with severe rather than milder pregnancy-induced hypertension.

We assessed whether fetal growth restriction without pregnancy-induced hypertension (PIH) is associated with the different clinical subgroups of PIH in the subsequent pregnancy. We also assessed the maternal and paternal contributions to this effect. Pairs of first and second, second and third, third and fourth, and fourth and fifth births were identified among all of the births in Norway: 137 375 pairs with same mother and father, 18 376 pairs with same mother and different fathers, and 18 916 pairs with same father and different mothers. Second births in each pair were restricted to those that occurred in 1998-2005. Odds ratios to predict early onset, severe, and mild preeclampsia and transient hypertension in the second birth from birth weight <1500 g in the first compared with 3500 to 3999 g were 13.8, 7.1, 3.5, and 2.2, respectively. Odds ratios to predict early onset, severe, and mild preeclampsia and transient hypertension from birth weight below the 2.5th percentile compared with percentiles 10.0 to 89.9 were 4.2, 2.5, 2.1, and 1.7, respectively. Men who fathered a child with low birth weight in 1 woman were not more likely to later father a PIH pregnancy in another woman. The results indicate that placental dysfunction and PIH share a genetic factor that can be expressed as fetal growth restriction in 1 pregnancy and PIH in a subsequent pregnancy. Future genetic study is needed to confirm whether the association is caused by delayed genetic expression of endothelial dysfunction and whether the clinical subgroups of PIH have different genetic backgrounds.