Both pre-clinical and clinical studies showed that CKD-specific risk factors such as uremic toxins, renal anemia, the over-activation of the renin–angiotensin–aldosterone system and sympathetic nervous system with increased oxidative/nitrative/nitrosative stress and decreased nitric oxide levels could provoke the development of uremic cardiomyopathy and increase the burden of AMI regardless of pressure- and volume overload [10]. This evidence concerns the gene REN and chronic kidney disease.