3rd Place: Kidney Disease in Pregnancy: Initial Blood Pressure as a Risk Factor for Preeclampsia

2018 Research Scholar Winner: 3rd Place Mentor: Sharon Maynard, M

Hypertension in Pregnancy

Hypertensive disorders complicate up to 10 % of pregnancies, and are a major cause of maternal and neonatal morbidity and mortality. Hypertensive disorders of pregnancy include four categories: chronic hypertension, gestational hypertension, preeclampsia, and superimposed preeclampsia. The diagnosis and management of hypertension in pregnancy requires a special approach with attention toward the maternal and fetal effects of both the disease and the treatment. This chapter reviews the pathogenesis, epidemiology, diagnosis, management, and prognosis of hypertensive disorders of pregnancy

Acute kidney injury in pregnancy: the thrombotic microangiopathies.

Acute kidney injury (AKI) is a rare but serious complication of pregnancy. Although prerenal and ischemic causes of AKI are most common, renal insufficiency can complicate several other pregnancy-specific conditions. In particular, severe preeclampsia/HELLP syndrome, acute fatty liver of pregnancy (AFLP) and thrombotic thrombocytopenic purpura (TTP) are all frequently complicated by AKI, and share several clinical features which pose diagnostic challenges to the clinician. In this article, we discuss the clinical and laboratory features, pathophysiology and treatment of these 3 conditions, with particular attention to renal manifestations. It is imperative to distinguish these conditions to make appropriate therapeutic decisions which can be lifesaving for the mother and fetus. Typically AFLP and HELLP improve after delivery of the fetus, whereas plasma exchange is the first-line treatment for TTP

Angiogenic Factors and Preeclampsia

Preeclampsia, a hypertensive disorder peculiar to pregnancy, is a systemic syndrome that appears to originate in the placenta and is characterized by widespread maternal endothelial dysfunction. Until recently, the molecular pathogenesis of phenotypic preeclampsia was largely unknown, but recent observations support the hypothesis that altered expression of placental anti-angiogenic factors are responsible for the clinical manifestation of the disease. Soluble Flt1 and soluble endoglin, secreted by the placenta, are increased in the maternal circulation weeks before the onset of preeclampsia. These anti-angiogenic factors produce systemic endothelial dysfunction, resulting in hypertension, proteinuria, and the other systemic manifestations of preeclampsia. The molecular basis for placental dysregulation of these pathogenic factors remains unknown, and as of 2010 the role of angiogenic proteins in early placental vascular development was starting to be explored. The data linking angiogenic factors to preeclampsia have exciting clinical implications, and likely will transform the detection and treatment of preeclampsia