Could carbonic anhydrase IX predict fetal growth restriction in early onset preeclampsia?

Placental insufficiency, which plays a crucial role in both preeclampsia and fetal growth restriction, can cause oxidative stress and high reactive oxygen species production that could lead to hypoxia. Carbonic anhydrase IX is induced by hypoxia-inducible factor-1α, an important transcriptional regulator of genes involved in response to hypoxia. Considering this, we aimed to determine carbonic anhydrase IX levels in early preeclampsia with and without fetal growth restriction, and also to evaluate the predictive role of carbonic anhydrase IX for the development of fetal growth restriction in early onset preeclampsia.

This prospective study included a total of 180 participants, who were divided into two groups-early onset preeclampsia (n=90) and control (n=90). Then, preeclamptic patients were followed and subgrouped as preeclampsia with fetal growth restriction (n=35) and without fetal growth restriction (n=55). Sociodemographic and obstetric characteristics and laboratory features including carbonic anhydrase IX were compared between groups.

Median carbonic anhydrase IX was higher in preeclampsia than controls [2.07 (0.78-5.48) vs. 1.32 (0.63-2.12), p<0.001]. Moreover, median carbonic anhydrase IX was higher in the preeclampsia with fetal growth restriction group as compared to the preeclampsia without fetal growth restriction group [2.76 (0.78-5.48) vs. 1.77 (0.89-5.14), p=0.018]. The carbonic anhydrase IX >1.83 pg/mL predicted fetal growth restriction with 77.14% sensitivity and 52.73% specificity (p=0.015, AUC=0.649) in the early onset preeclampsia.

Carbonic anhydrase IX could reflect the insufficiency of the placenta in early onset preeclampsia and fetal growth restriction, and it could be used in early onset preeclampsia patients for the prediction of fetal growth restriction.