Eclampsia often follows preeclampsia, which is characterized by high blood pressure occurring in pregnancy and, rarely, postpartum. Other findings may also be present such as protein in the urine. If your preeclampsia worsens and affects your brain, causing seizures, you have developed eclampsia. They can explain how the symptoms of preeclampsia may lead to eclampsia. High blood pressure Preeclampsia is when your blood pressure, or the force of blood against the walls of your arteries, becomes high enough to damage your arteries and other blood vessels.
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See other articles in PMC that cite the published article. Abstract Pre-eclampsia is a pregnancy-specific hypertensive disorder that may lead to serious maternal and fetal complications. It is a multisystem disease that is commonly, but not always, accompanied by proteinuria. Its cause s remain unknown, and delivery remains the only definitive treatment. It is increasingly recognized that many pathophysiological processes contribute to this syndrome, with different signaling pathways converging at the point of systemic endothelial dysfunction, hypertension, and proteinuria.
Different animal models of pre-eclampsia have proven utility for specific aspects of pre-eclampsia research, and offer insights into pathophysiology and treatment possibilities. Therapeutic interventions that specifically target these pathways may optimize pre-eclampsia management and may improve fetal and maternal outcomes.
In addition, recent findings regarding placental, endothelial, and podocyte pathophysiology in pre-eclampsia provide unique and exciting possibilities for improved diagnostic accuracy. Emerging evidence suggests that testing for urinary podocytes or their markers may facilitate the prediction and diagnosis of pre-eclampsia. In this review, we explore recent research regarding placental, endothelial, and podocyte pathophysiology. We further discuss new signaling and genetic pathways that may contribute to pre-eclampsia pathophysiology, emerging screening and diagnostic strategies, and potential targeted interventions.
Pre-eclampsia is commonly viewed as one of the hypertensive pregnancy disorders, which cover a spectrum of clinical presentations from chronic hypertension i. The rationale to treat these disorders as a continuum comes from clinical evidence demonstrating that either chronic or gestational hypertension may progress to pre-eclampsia commonly evidenced by new-onset or worsening of proteinuria , while pre-eclampsia may progress to more severe forms, such as eclampsia or HELLP syndrome.
An alternative approach views pre-eclampsia as a separate disease entity. Either way, it is recognized that pre-eclampsia is a heterogeneous disease. Different clinical subtypes may reflect distinct underlying pathological mechanisms. Recent evidence suggests that women with early severe pre-eclampsia, who are at particularly high risk for adverse pregnancy outcomes, may have a more pronounced anti-angiogenic imbalance than those with late pre-eclampsia and more favorable outcomes.
Our recent data suggest that podocyturia i. These findings set the stage for future studies of podocyturia in women who meet all of the clinical criteria, for the diagnosis of pre-eclampsia, except proteinuria. The main objective of this review is to discuss emerging theories regarding pre-eclampsia pathophysiology, focusing on the different causal pathways that translate into different subtypes clinical phenotypes of pre-eclampsia; highlight animal models that may advance the understanding of the roles of specific mechanisms in pre-eclampsia; examine emerging evidence indicating that different signaling pathways may converge at the point of podocyte damage, which may be at the core of renal injury and ultimately lead to proteinuria; and discuss their possible implications for pre-eclampsia diagnosis and management.
These causal pathways are believed to converge at the point of systemic endothelial dysfunction, which leads to hypertension and proteinuria Figure 1. Placental hypoxia is frequently viewed as an early event that may cause placental production of soluble factors leading to endothelial dysfunction.
This soluble receptor, commonly referred to as soluble fms-like tyrosine kinase receptor-1 sFlt-1 , may bind and neutralize VEGF, and thus limit the availability of free VEGF for fetal and placental angiogenesis. Several rodent models simulate pre-eclampsia by exogenous sFlt-1 administration. In the most direct model, intraperitoneal sFlt-1 injections produce short-term elevations of sFlt Administration of an adenoviral vector encoding sFlt-1 leads to longer-term sFlt-1 exposure in rats.
However, these factors are likely a consequence, rather than the cause, of placental ischemia in pre-eclampsia.
Advances in the pathophysiology of pre-eclampsia and related podocyte injury
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