Fetal High-Risk APOL1 Genotype Increases Risk for Small for Gestational Age in Term Infants Affected by Preeclampsia

Timur Azhibekov1, Razaq Durodoye2, Anna K Miller3

  • 1Division of Neonatology, Department of Pediatrics, MetroHealth Medical Center, Cleveland, Ohio, USA.

Neonatology
|April 16, 2023
PubMed

Insights

High-risk apolipoprotein L1 (APOL1) gene variants are linked to preeclampsia and fetal growth issues in Black women. This suggests APOL1 impacts pregnancy complications through placental insufficiency.

Area of Science:

  • Obstetrics and Gynecology
  • Genetics
  • Perinatal Medicine

Background:

  • Hypertensive disorders of pregnancy, including preeclampsia, significantly increase risks for fetal growth restriction and maternal complications, particularly in women of African ancestry.
  • Recent research has identified a potential association between preeclampsia risk and specific polymorphisms in the apolipoprotein L1 (APOL1) gene among women of African ancestry.

Purpose of the Study:

  • To investigate the effects of apolipoprotein L1 (APOL1) gene variations on pregnancy outcomes in both preeclamptic and non-preeclamptic pregnancies.
  • To determine if APOL1 genotype influences fetal growth and the risk of preeclampsia in different gestational contexts (term vs. preterm).

Main Methods:

  • An unmatched case-control study was conducted involving 1,358 mother-infant pairs.
  • Participants were drawn from two independent cohorts comprising Black women.

Main Results:

  • Among term pregnancies, high-risk APOL1 genotypes were significantly associated with infants being small for gestational age (OR 2.8 compared to low-risk cases, OR 5.5 compared to high-risk controls).
  • In preterm pregnancies, the fetal APOL1 genotype showed a notable association with the occurrence of preeclampsia.

Conclusions:

  • Fetal APOL1 genotype is implicated in preeclampsia risk for preterm infants and altered fetal growth in term infants.
  • These findings suggest that APOL1 genotype may contribute to a range of pregnancy complications, potentially through a shared mechanism of placental insufficiency.
Abstract

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