Even in patients without CKD, small decrements in renal function (measured by cystatin C), are associated with higher risk of incident HF.[4] Dysfunctional pathways contributing to this high risk of HF putatively include sympathetic over-activity leading to renin-angiotensin activation[16], and in turn, volume overload;[17] inflammation and volume overload leading to cardiac remodeling;[18] and inflammation,[19] oxidative stress and higher levels of asymmetric dimethylarginine[20] leading to endothelial dysfunction.[21] Unfortunately, we have few therapeutic targets within these pathways. This evidence concerns the gene CST3 and hydrops fetalis.