The Role of the Renin-Angiotensin-Aldosterone System in Preeclampsia: a Review

Purpose of Review Preeclampsia (PE) is a complex human pregnancy-specific condition and is clinically characterized by new onset hypertension and proteinuria in the second half of pregnancy. The precise etiology of PE is unknown, but much of the pathophysiology has been elucidated, and it is accepted that the disorder is multifactorial in nature. Historically, because of the presence of proteinuria, the role of the renin-angiotensin-aldosterone system (RAAS) has been considered in the etiology of PE. However, the results of studies (including maternal circulatory angiotensin II, urinary angiotensinogen, plasma renin and prorenin, AT1 receptor antibodies, and gene polymorphisms) on the role of the RAAS in the etiology of PE have proved controversial. The purpose of this narrative review was to evaluate the contemporary literature on the RAAS and its role in the pathophysiology of pregnancy. Recent Findings The current review shows that although the RAAS has a role in the development of normal pregnancy, it does not have a significant role in the pathophysiology of PE except for the AT1-AA components. Despite many researchers having measured increases in s[P}RR and [P]RR, this may be independent of the RAAS. Our view is in keeping with contemporary thinking that the placenta rather than the RAAS plays a central role in elaborating pro-inflammatory factors (antiangiogenic and angiogenic) into the maternal circulation resulting in widespread endothelial dysfunction in all organ systems including the renal system.