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Preeclampsia afflicts one in 20 expectant mothers. A predecessor of eclampsia, which brings on fatal seizures, the condition is difficult to predict and hard to treat--often the only course of action is an early delivery. Doctors still don't understand exactly what causes preeclampsia, but two studies published today in the Journal of Clinical Investigation provide new insight into how the disease arises and could point to novel therapies.
Sharon E. Maynard of Harvard Medical School and her colleagues determined that women suffering from preeclampsia display elevated levels of a protein known as sFlt1, which is produced by the placenta. This protein binds to two growth factors--vascular endothelial growth factor (VEGF) and placental growth factor (PlGF)--that promote the development of new blood vessels and the maintenance of the vascular system. According to the report, high levels of sFlt1 could result in a compromised vascular system by reducing the available amount of these growth factors in the blood supply. In rats, high levels of sFlt1 led to symptoms reminiscent of preeclampsia in humans, regardless of whether or not the animals were pregnant. Taking that into consideration, the authors suggest that excess circulating sFlt1 contributes to the condition.
In related work, Susan Quaggin of Mount Sinai Hospital in Toronto and her co-workers investigated the link between one type of VEGF and kidney disease. They found that reducing the level of VEGF-A in mouse kidney cells caused kidney failure very similar to that seen in women suffering from preeclampsia. Together the two studies indicate a plausible new scenario for what causes the disorder. In an accompanying commentary, Aernout Luttun and Peter Carmeliet of Katholieke University in Belgium note that "at the very least, these studies raise new hopes that novel strategies may be designed to combat preeclampsia and thereby improve the chances of the mother and child for a healthy future."
