AGT and hydrops fetalis: The early stages of heart failure are characterized by reduced ability to increase natriuresis in response to salt load, thus leading to sodium retention [22, 23] via overactivation of the sodium reabsorption in the proximal tubule level is a key mechanisms of the sodium retention in HF, due to an imbalance of angiotensin II (AT II) and nitrite oxide (NO) and it is reversed by converting enzyme inhibitors (CEIs) reducing levels of AT II and increasing levels of NO [24, 25], which has vasorelaxant characteristics and is a physiological antagonist of AT II in the kidney [26].