At least in part, they might be induced by systemic activation of the renin–angiotensin–aldosterone system (RAAS), which occurs in response to reduced cardiac output and renal perfusion.50 Elevated levels of angiotensin II and aldosterone promote vasoconstriction, inflammation, and fibroblast activation, thereby contributing to interstitial fibrosis in the kidney after MI.50 Such mechanisms may amplify the adverse feedback loop between cardiac injury and renal dysfunction. This evidence concerns the gene AGT and myocardial infarction.