Australian researchers discover a novel cause of preeclampsia

Preeclampsia is a life-threatening, pregnancy-induced disorder unique to humans. It is diagnosed by the sudden onset of maternal hypertension after 20 weeks of pregnancy plus one other symptom including elevated urinary protein, other organ damage or fetal growth restriction. If left unmanaged, preeclampsia can lead to maternal seizures (eclampsia) and death. Preeclampsia affects between 3-4% of all pregnancies in Australia, with 10,000 women diagnosed in Australia each year.

This dangerous condition is caused by a damaged placenta which releases toxins into the maternal blood stream, causing the clinical symptoms. It is widely accepted that preeclampsia arises due to abnormal placental development during the early stages of pregnancy however studying human placental development is very difficult and the mechanisms leading to poor placental development remain unclear.

New research published in Hypertension by Dr Ellen Menkhorst and Professor Eva Dimitriadis from the University of Melbourne and the Royal Women’s Hospital, has identified that a protein called galectin-7 is abnormally elevated in the early pregnancy placenta of women who subsequently develop preterm preeclampsia. The researchers were able to show that elevations of this protein in mice caused classic symptoms of preeclampsia, including hypertension and elevated urinary protein. Galectin-7 was also shown to regulate key components of the renin-angiotensin system, a central hormone system controlling blood pressure.

Overall this new research suggests that elevated placental production of galectin-7 during early pregnancy contributes to abnormal placental development and altered renin-angiotensin system function which may ultimately lead to the development of preeclampsia. 

The researchers hope this discovery will lead to the identification of new treatment options to improve placental development during early pregnancy and prevent preeclampsia.

Written by Drs Ellen Menkhorst and Liza O’Donnell