Gene/Protein Disease Symptom Drug Enzyme Compound
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The essential EPH-gestosis seems to have multiple aetiological factors and the disease develops already a long time before the appearance of the classical symptoms. The disturbed renal function is the main point among secondary pathological effects as the damaged placenta, the disseminated coagulation, the glomerular endotheliosis, the increased retention of water and sodium with increased arterial responsiveness. It may be that this reduced reversible renal function is of extra-renal origin. As predisposing factors were discussed the reduced uteroplacental circulation with the release of still unknown pressor substances or decreased inactivation of pressor amines, the uterorenal reflex mechanism, the disturbed homeostasis of the body fluids and the vegetativ-hypothalamic crisis etc. But other factors may also be participate on this disease as immunological and hormonal aspects, especially the renin-angiotensin-aldosteron-system and prostaglandins. To find out the aetiological factors we should examine the disease at the beginning in comparison with normal pregnancy. These factors must explain why the true EPH-gestosis appears mainly during the first pregnancy and frequently in twins and so on.
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PMID:[A critical review of hypothetical causes of EPH-gestosis]. 98 86

Preeclampsia is a disorder of hypertension and proteinuria that affects 6 - 8% of normal pregnancies. Recent research has revealed many molecular mechanisms that may contribute to systemic endothelial dysfunction, glomerular capillary endotheliosis, dysregulation of the glomerular filtration apparatus, and podocyte loss. An ischemic placenta elaborates soluble FMS-like tyrosine kinase 1 (sFlt-1), a soluble receptor for vascular endothelial growth factor (VEGF). A variety of mediators, including nitric oxide, Angiotensin II receptor autoantibodies (AT1AA), and endothelin-1 may serve to maintain placental ischemia and systemic endothelial dysfunction. Endothelin-1 and decreased vascular endothelial growth factor may adversely affect overall expression and distribution of podocyte foot process proteins, leading to proteinuria. Podocyte derangements may lead to podocyte apoptosis and loss, as evidenced by the detection of live podocytes and podocyte products in the urine of preeclamptic women. In this review, we explore recent research elucidating the interactions of placenta, endothelium, and podocyte leading to the clinical syndrome of preeclampsia.
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PMID:From placenta to podocyte: vascular and podocyte pathophysiology in preeclampsia. 2287 14