SGLT-2i may slow edema development and HF progression by blocking the activity of sodium–hydrogen exchangers (NHE) expressed in the myocardium (NHE-1 isoform) and in the proximal convoluted tubule of kidneys (NHE-3 isoform) [90], as well as the activity of the late component of the cardiac sodium channel current in cardiomyocytes [91]. Here, SLC9A1 is linked to hydrops fetalis.