Abstract
1 min readThe occurrence of seizures (eclampsia, from the Greek "eklampsis," sudden flashing) has been a long-known and feared complication of pregnancy, often killing both mother and child.Preeclampsia, or the condition preceding full-blown eclampsia, affects up to 5% of pregnant women and is diagnosed by the onset of hypertension and proteinuria in the second trimester (1).Preeclampsia may eventually progress to glomerular malfunction, thrombocytopenia, liver and brain edema, and associated life-threatening seizures (2) (Figure 1).Preeclampsia has been sometimes termed the "disease of theories," as several models for its pathogenesis have been proposed.But, as of today, no satisfactory unifying hypothesis has emerged (1).The restricted occurrence of preeclampsia to humans and primates and the lack of a suitable animal model have hampered the understanding of its pathogenesis (3).In this issue of the JCI, S.E.Maynard et al. ( 4) report the novel insight that circulating levels of two angiogenic growth factors, VEGF and placental growth factor (PlGF), may play a more important role than previously believed.In particular, the authors propose that, in pregnant women with preeclampsia, the placenta produces elevated levels of the soluble fms-like tyrosine kinase 1 (sFlt1) receptor, which captures free VEGF and PlGF.As a result, the normal vasculature in the kidney, brain, lungs, and other organs is deprived of essential survival and maintenance signals and […]
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