The renin-angiotensin aldosterone system (RAAS) plays a pivotal role in the regulation of salt and fluid balance.1 This elegant multienzymatic system exists to protect the organism from eventual circulatory collapse in states of profound solute deprivation and shock. However, dysregulation of the RAAS has been shown to contribute to pathophysiologic end-organ damage of the cardiovascular system in a variety of disease states. Thus, interruption of the RAAS with pharmacologic inhibition is a mainstay of therapy for patients with hypertension, heart failure, and diabetes mellitus.