Measurement of the Renin-Angiotensin System

Abstract

Renovascular disease irrespective of the cause activates multiple pressor systems, most specifi cally the renin-angiotensin-aldosterone system (RAAS). This complex hormone system exerts several renal and vascular effects, and seminal studies have outlined the sentinel importance of this system in the context of renovascular disease. Experiments using Goldblatt's classic 2 kidneys-1-clip model generate the prototype of angiotensin-dependent hypertension (Laragh, Am J Hypertens 4: 541S-545S, 1991; Pickering, Semin Nucl Med 19:79-88, 1989). In humans, numerous methods to assess the levels of these hormones in the plasma have been proposed to characterize the hemodynamic signifi cance of renovascular disease and to provide guidance on who will benefi t of revascularization. However, in recent years, many of these diagnostic methods have been abandoned due to complex work-up, relatively low sensitivity and specifi city, and the advent of more reliable non-invasive imaging techniques (Covic and Gusbeth-Tatomir, Prog Cardiovasc Dis 52:204-208, 2009). Although one could argue that the pressure in identifying the pressors roles has decreased, since preservation of function has become the most predominant argument, still, characterization of the RAAS system is important since it may provide useful additional information, including those for important therapeutic decisions.Several screening laboratory tests have been proposed over the years to identify patients with renovascular hypertension. Some of these studies remain based on the identifi cation of the activation of the RAAS system and some may depend on the comparison of the kidneys side-by-side assuming that one kidney is not affected. However, even under the best conditions, these studies are rarely more than 80 % sensitive or specifi c. As a result, their value as predictors depends greatly on the pretest probability

From anatomy to function: diagnosis of atherosclerotic renal artery stenosis

“…However, serum values showed poor sensitivity and specificity and studies were prone to reporting bias. [55] A recent study explored potential novel biomarkers sampled peripherally and from renal veins in matched groups with ARAS and essential hypertension. [56,57] Higher systemic and stenotic renal vein levels of neutrophil gelatinase-associated lipocalin, plasminogen activator inhibitor-1 and soluble urokinase-type plasminogen activator receptor were noted in ARAS.…”