RAAS in CKD

Presentation Description / Summary: The renin-angiotensin-aldosterone system (RAAS) is a major regulator of systemic arterial blood pressure, extracellular fluid volume, and electrolyte balance. While the RAAS plays a critical role in the homeostatic control of blood pressure in health, overactivity of this system is well known to contribute to the pathogenesis of chronic kidney disease (CKD). The deleterious effects of RAAS activation in kidney diseases are mediated by its hemodynamic effects, which promote systemic and intraglomerular hypertension and an increase in glomerular filtration of plasma proteins, and the non-hemodynamic effect of angiotensin II and aldosterone, which promote renal and cardiovascular injury. The complexity of the RAAS is evidenced by the existence of a classic and an alternative counterbalancing pathway of the circulating system and the presence of local, tissular systems, including the intra-renal renin-angiotensin system.
The importance of the RAAS in the progression of CKD is, perhaps, best shown by the positive outcomes achieved by the administration of its antagonists to people and companion animals affected by CKD, particularly those with renal proteinuria. However, while these medications are administered to slow the progression of kidney disease, their effects on renal hemodynamics and glomerular filtration rate complicate their use in individuals with advanced CKD.

Learner Outcomes:

• Detail the net effects of activation of the renin-angiotensin-aldosterone system (RAAS) in health and disease, and explain how the hemodynamic and nonhemodynamic effects of the RAAS promote ongoing renal damage;


• Describe the different components of the RAAS, including those of the classic and alternative pathways of the circulating system, and the intra-renal renin-angiotensin system;


• List the evidence that supports the use of RAAS antagonists in animals with CKD, particularly those with renal proteinuria and systemic arterial hypertension.