Activation of the SNS and RAAS is considered crucial in HF and renal dysfunction.1 Persistent activation of RAAS may be at the core of the pathophysiology of cardiorenal interactions, exerting detrimental effects on both the heart and the kidneys through a series of reactions mediated by increased Angiotensin II and aldosterone [1, 24]. This evidence concerns the gene AGT and hydrops fetalis.