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New aspects in the pathophysiology of preeclampsia Davison JM; Homuth V; Jeyabalan A; Conrad KP; Karumanchi SA; Quaggin S; Dechend R; Luft FCJ Am Soc Nephrol 2004[Sep]; 15 (9): 2440-8Preeclampsia, the de novo occurrence of hypertension and proteinuria after the 20th week of gestation, continues to exert an inordinate toll on mothers and children alike. Recent clinical trials, new physiologic insights, and novel observations on pathogenesis have altered the thinking about preeclampsia. The mechanisms surrounding relaxin and its effects on the circulation and on matrix metalloproteinases have been elucidated. The growth factor's receptor, fms-like tyrosine kinase 1, has been shown to exist in a soluble form that is able to inactivate vascular endothelial-derived growth factor and human placental growth factor. Compelling evidence has been brought forth suggesting that fms-like tyrosine kinase 1 is a circulating factor that can cause preeclampsia. Preeclamptic women have high circulating levels of asymmetric dimethyl arginine that could account for the generalized endothelial dysfunction observed in preeclampsia. Preeclamptic women also produce novel autoantibodies that may serve to activate angiotensin receptors. These new observations raise the possibility that the treatment of preeclamptic women will soon be improved.|Angiogenic Proteins/antagonists & inhibitors/blood[MESH]|Autoantibodies/blood[MESH]|Cardiovascular Diseases/etiology[MESH]|Endothelium-Dependent Relaxing Factors/antagonists & inhibitors/physiology[MESH]|Female[MESH]|Humans[MESH]|Ischemia/etiology[MESH]|Placenta Diseases/etiology[MESH]|Placenta/blood supply[MESH]|Pre-Eclampsia/blood/complications/*physiopathology[MESH]|Pregnancy[MESH]|Relaxin/physiology[MESH]|Risk Factors[MESH] |
