Current theories of CRS type II etiology in chronic heart failure (CHF) suggest that low cardiac output, sustained increases in sympathetic nerve activity, and activation of the renin-angiotensin-aldosterone system (RAAS) combine to produce venous congestion and increased abdominal pressure, and that all of these together contribute to renal hypoperfusion, hypoxia, and tissue injury (Zannad and Rossignol, 2018; Costanzo, 2022; Patel et al., 2022). Here, REN is linked to congestive heart failure.