Differential Diagnosis of Preeclampsia

Abstract

Preeclampsia is a pregnancy-associated condition, clinically characterized by hypertension, proteinuria, and progressive edema, affecting 3% to 5% of all pregnancies.1 Preeclampsia can occur in previously healthy women and in women with underlying conditions, such as hypertension, lupus nephritis, or the antiphospholipid syndrome (APS).1,2 Conversely, pregnancy can be a trigger to activate underlying diseases. A well-known example is lupus nephritis, which can flare during pregnancy, especially when the disease is still active in the months preceding pregnancy or during conception.3 In the United States there are yearly ≈4500 pregnancies with systemic lupus erythematosus (SLE), and of these pregnancies, 13% to 35% are complicated by preeclampsia and 14% to 65% by a lupus flare.2 The clinical features of a lupus nephritis flare closely mimic those of preeclampsia. Differentiation between these 2 conditions on clinical grounds can therefore be a challenge, particularly because lupus nephritis itself predisposes to preeclampsia.2,3 However, such differentiation is critical to optimal management: a lupus flare requires initiation or intensification of immunosuppressive therapy, whereas delivery of the child and the placenta is the only treatment currently available for severe preeclampsia. In recent years, an imbalance between proangiogenic and antiangiogenic proteins derived from the placenta has been suggested to play a role in the pathophysiology of preeclampsia, and measurement of these proteins in the maternal circulation is coming of age as a tool to diagnose or to provide prognostic information of this condition.4,5 Compared with normal pregnancies, the serum concentration of the antiangiogenic soluble Fms-like tyrosine kinase 1 (sFlt-1) is markedly increased, whereas that of placental growth factor (PlGF) is decreased in preeclampsia.4,6–10 Because of the reciprocal changes of these markers, the ratio of sFlt-1/PlGF appears to be a superior marker of (early …