Preeclampsia is a multisystem disorder affecting 2%–8% of pregnancies (1). It is a rapidly progressive condition clinically defined by elevated blood pressure and proteinuria occurring after 20 weeks of gestation and intrauterine growth restriction (IUGR) in the fetus. In one study, it was suggested that 60% of preeclampsia-related deaths were preventable, making early diagnosis essential (2). Blood pressure is a traditional screening test, but it is only useful when preeclampsia has already started to develop, so it only modestly predicts later preeclampsia. Clinical guidelines such as the National Institute for Health and Care Excellence (NICE) and American College of Obstetricians and Gynecologists (ACOG) guidelines applied in early pregnancy has very limited predictive ability (3). Diagnosis of preeclampsia remains elusive often due to mild symptoms that are not identified prior to disease progression. While all the contributions for preeclampsia are not well understood, dysregulation of the pro- and anti-angiogenic factors within the developing placenta play a major role in the development of preeclampsia later in pregnancy. Two such factors include the pro-angiogenic factor, placental growth factor (PlGF) and the anti-angiogenic factor soluble fms-like tyrosine kinase 1 (sFlt-1). PlGF and sFlt-1 must be balanced appropriately in order to produce a functional placenta that provides oxygen and nutrients to the developing fetus. In pregnancies affected with preeclampsia, the anti-angiogenic factor, sFlt-1, predominates resulting in reduced arterial flow from mother to fetus.