Strong evidence found for a number of genetic variations near to the FLT1 gene being linked to increased risk of pre–eclampsia.
A major new international study has revealed for the first time that some features in a baby’s DNA can increase the risk of its mother developing pre–eclampsia – a potentially dangerous condition in pregnancy.

These results from the InterPregGen study erre published in the journal Nature Genetics.

The work was carried out by genetics experts from the UK, Nordic countries and Central Asia and is the first to show an effect of DNA from the fetus on the health of its mother.

Pre–eclampsia affects up to 5 per cent of pregnancies and is first suspected when a woman is found to have high blood pressure, usually in the second half of pregnancy. The condition can cause serious complications including fits, stroke, liver and blood problems and in some cases the death of mother and baby.

The five–year study involved teams from the UK, Iceland, Finland, Norway, Kazakhstan and Uzbekistan. They studied the genetic make–up of 4,380 babies born from pre–eclamptic pregnancies and compared their DNA with over 300,000 healthy individuals.

Dr Linda Morgan, from the University of Nottingham’s School of Life Sciences, coordinated the five–year study, which included DNA samples contributed from Iceland, Norway and Finland as well as from more than 20 universities and maternity units in the UK.

Laboratory and statistical analysis performed at the Wellcome Trust Sanger Institute (UK) and deCODE Genetics (Iceland) pinpointed the location in the baby’s DNA that increases risk of pre–eclampsia. This location was confirmed by other InterPregGen members to fit hand–in–glove with other medical information about pre–eclampsia.

The baby’s DNA comes from both its mother’s and its father’s genes – in keeping with the inherited risk of pre–eclampsia. The DNA changes associated with pre–eclampsia are common – more than 50 per cent of people carry this sequence in their DNA so the inherited changes are not sufficient in themselves to cause disease, but they do increase the risk of pre–eclampsia.

The research found DNA variations close to the FLT1 gene that makes a protein called sFlt–1 with significant differences between the babies born from pre–eclamptic pregnancies and the control group.

At high levels sFlt–1 released from the placenta into the mother’s bloodstream can cause damage to her blood vessels, leading to high blood pressure and damage to her kidneys, liver and brain – all features of pre–eclampsia. If a baby carried these genetic variants it increased the risk of that pregnancy developing pre–eclampsia.

DNA from a further 4,220 babies from pre–eclamptic pregnancies in Kazakhstan and Uzbekistan is currently being analysed in an extended study to see if the same variations occur near the gene encoding sFlt–1.