Preeclampsia is a pregnancy complication characterized by new-onset high blood pressure and signs of damage to other organ systems, most often the liver and kidneys. This condition appears after 20 weeks of pregnancy. While the exact causes are not fully understood, preeclampsia involves complex interactions that can affect both the mother and the developing fetus.
The Placental Origin
Preeclampsia originates in the placenta, the organ connecting mother and fetus. In a typical pregnancy, specialized cells called trophoblasts deeply invade the mother’s uterine wall. These cells remodel maternal blood vessels, specifically the spiral arteries, transforming them into wide, low-resistance vessels. This remodeling ensures a substantial and continuous blood supply to the growing fetus.
In preeclampsia, this process goes awry. Trophoblasts fail to adequately invade the spiral arteries, preventing necessary remodeling. These vessels remain narrow and resistant, limiting blood flow to the placenta. Insufficient blood flow leads to placental ischemia, meaning the placenta receives inadequate oxygen and nutrients.
The stressed, underperfused placenta experiences oxidative stress and hypoxia. This placental stress is the foundational step in preeclampsia’s pathophysiology. The abnormal conditions within the placenta trigger the release of various substances into the mother’s bloodstream, setting the stage for the widespread maternal syndrome.
Systemic Cascade: Endothelial Dysfunction and Inflammation
The stressed placenta releases harmful substances into the mother’s circulation. These include anti-angiogenic factors, such as soluble fms-like tyrosine kinase-1 (sFlt-1) and soluble endoglin (sEng), along with inflammatory cytokines and products of oxidative stress. Normally, angiogenic factors promote new blood vessel growth. In preeclampsia, increased anti-angiogenic factors disrupt this balance.
Elevated sFlt-1 binds to and neutralizes pro-angiogenic proteins like vascular endothelial growth factor (VEGF) and placental growth factor (PlGF), essential for healthy blood vessels. This imbalance damages the endothelium, the inner lining of blood vessels. Endothelial dysfunction is a central feature of preeclampsia, contributing to its clinical manifestations.
This dysfunction causes blood vessels to become leaky, allowing fluid and proteins to escape into surrounding tissues. It also increases vascular resistance, causing blood vessels to constrict more readily and contributing to high blood pressure. Systemic inflammation and oxidative stress activate the coagulation system, increasing blood clot risk in small vessels. These placental factors and resulting endothelial damage create a systemic cascade impacting various maternal organ systems.
Impact on Key Organ Systems
Endothelial dysfunction and systemic inflammation, initiated by the compromised placenta, affect various maternal organ systems. Kidneys are significantly affected; reduced blood flow and damage to filtration units lead to proteins, particularly albumin, leaking into the urine (proteinuria).
The liver can experience impaired blood flow and cellular damage from endothelial dysfunction. This can lead to elevated liver enzymes, indicating liver cell injury, and may cause pain in the upper abdomen. In severe cases, this can progress to serious liver complications.
The brain and central nervous system are vulnerable to blood vessel dysfunction. Vasoconstriction and fluid shifts can lead to symptoms like persistent headaches and visual disturbances, such as blurred vision or seeing flashing lights. In its most severe form, uncontrolled preeclampsia can lead to seizures, a condition termed eclampsia.
Within the blood, coagulation activation and endothelial damage can result in platelet dysfunction and decreased platelet count. This can impair the blood’s ability to clot properly and is a marker of disease severity. Widespread vasoconstriction and fluid retention ultimately contribute to the characteristic high blood pressure in preeclampsia.