The rationale for expanding the analysis to consider hyponatremia with sST2 was based on the fact that HF patients with low sodium have more severe upregulation of the renin-angiotensin-aldosterone system (RAAS) [29,30], and angiotensin II (AngII) produced during RAAS activation has recently been studied for its role in mediating cardiac fibrosis. This evidence concerns the gene AGT and hydrops fetalis.