Preeclampsia happens because the placenta doesn’t develop a proper blood supply early in pregnancy, which triggers a chain reaction of damage to the mother’s blood vessels and organs. The root cause starts weeks before any symptoms appear, when the placenta fails to remodel the arteries that feed it. This leads to a stressed, oxygen-deprived placenta that releases harmful proteins into the mother’s bloodstream, raising blood pressure and potentially damaging the kidneys, liver, and brain.
The Problem Starts With the Placenta
In a healthy pregnancy, the placenta essentially hijacks the mother’s uterine arteries to secure a massive blood supply for the growing fetus. Specialized cells from the placenta invade the walls of small uterine arteries called spiral arteries, stripping away their muscle layer. This transforms them from narrow, reactive tubes into wide, floppy channels that pour blood freely into the placenta. The result is a dramatic drop in resistance to blood flow, allowing the placenta to receive the enormous volume it needs.
In preeclampsia, this remodeling process fails. The spiral arteries keep their muscular walls, stay narrow, and continue to constrict and relax like normal arteries. The placenta receives less blood and less oxygen than it needs. This oxygen-starved, underperfused placenta becomes stressed, and it begins releasing signals into the mother’s circulation that cause widespread problems. Poor spiral artery remodeling is most strongly linked to early-onset preeclampsia (developing before 34 weeks) and fetal growth restriction, where the baby also suffers from the reduced blood supply.
How a Stressed Placenta Damages Blood Vessels
The oxygen-deprived placenta floods the mother’s bloodstream with proteins that attack the lining of her blood vessels. Two key proteins are involved. One blocks a growth factor that blood vessel cells depend on to stay healthy, and the other interferes with a signaling molecule that helps vessels relax and repair. Together, these proteins shut down the blood vessels’ ability to produce the chemicals that normally keep them dilated and prevent clotting.
The consequences are systemic. Blood vessels throughout the body become inflamed, constricted, and leaky. This is what drives the hallmark symptoms: blood pressure rises because vessels can no longer relax properly, and protein spills into the urine because the kidney’s delicate filtering blood vessels become damaged. Organs with especially fine, porous blood vessels, like the kidneys and liver, are hit hardest, which explains why preeclampsia so often causes kidney dysfunction, liver inflammation, and in severe cases, seizures when the brain’s blood supply is affected.
Early-Onset vs. Late-Onset Preeclampsia
Not all preeclampsia follows the same pathway. The condition is classified into two subtypes based on when it appears, and they have different underlying drivers.
Early-onset preeclampsia develops before 34 weeks and is primarily a placental disease. It stems from the failed artery remodeling described above and tends to be more severe, often requiring early delivery. Late-onset preeclampsia develops at 34 weeks or later and is more closely tied to the mother’s own cardiovascular and metabolic health. In these cases, the placenta may have developed relatively normally, but the mother’s body struggles to handle the cardiovascular stress of late pregnancy. Her blood vessels, already vulnerable due to factors like obesity or chronic high blood pressure, reach a tipping point.
This distinction matters because early-onset and late-onset preeclampsia can look different clinically. Early-onset cases more often involve fetal growth problems, while late-onset cases are more common overall and more closely tied to the mother’s pre-existing health profile.
Who Is Most at Risk
Several factors significantly raise the likelihood of developing preeclampsia. A higher body mass index is one of the strongest predictors: women with a BMI of 25 or above are roughly six times more likely to develop the condition than those with a lower BMI. A history of chronic high blood pressure or diabetes also increases risk substantially.
Other significant risk factors include a family history of preeclampsia, low physical activity during pregnancy, and dietary patterns with low protein intake and high calorie consumption. Genetics play a role too, though the picture is complicated. The tendency to develop preeclampsia can be influenced by genetic variations carried by either parent, and even genes carried by the fetus may contribute. Researchers have identified variations in genes related to blood vessel function, fluid balance, and placental development, but no single gene drives the condition. Many women who develop preeclampsia have no family history at all.
How Preeclampsia Is Identified
Preeclampsia is diagnosed when new high blood pressure develops after 20 weeks of pregnancy alongside signs of organ stress. The blood pressure threshold is a systolic reading of 140 or higher, or a diastolic reading of 90 or higher, measured on at least two occasions more than four hours apart. When this is paired with protein in the urine (300 mg or more over 24 hours), the diagnosis is preeclampsia without severe features.
Severe preeclampsia involves blood pressures reaching 160/110 or higher, or signs that organs are taking damage: low platelet counts, elevated liver enzymes, kidney function decline, fluid in the lungs, persistent severe headaches that don’t respond to pain relief, or visual disturbances like seeing spots. These warning signs indicate the condition is progressing and typically move the timeline for delivery forward significantly.
Blood tests measuring the ratio of two placental proteins can also help predict who will develop preeclampsia. A ratio below 38 can reliably rule out the condition within the next week, with a negative predictive value above 96%. Very high ratios are closely associated with the need to deliver within 48 hours.
Prevention With Low-Dose Aspirin
For women at elevated risk, daily low-dose aspirin (81 mg) is the primary preventive measure. The American College of Obstetricians and Gynecologists recommends starting it between 12 and 28 weeks of gestation, ideally before 16 weeks, and continuing daily until delivery. Starting early is important because aspirin works by improving blood flow to the developing placenta during the critical window when spiral artery remodeling is taking place. Once the placenta is fully established and the damage is done, aspirin’s preventive benefit diminishes.
Aspirin doesn’t eliminate the risk entirely, but it reduces it meaningfully, particularly for early-onset preeclampsia. Your provider will assess whether your combination of risk factors warrants aspirin based on your medical history, BMI, blood pressure, and family history.