In patients with type 2 CRS, hemodynamic changes induced by CHF cause the activation of renin-angiotensin-aldosterone system and release neurotransmitters including nitric oxide (NO), BNP and AngII, which can subsequently lead to renal vasoconstriction, hypoxia, cytokine release, inflammation, and renal fibrosis (Jois and Mebazaa, 2012). Here, AGT is linked to renal fibrosis.