Both experimental and clinical studies have shown that CKD-specific risk factors, such as uremic toxins and renal anemia, as well as the overactivation of the renin–angiotensin–aldosterone system and the sympathetic nervous system, with increased nitro-oxidative stress and lower nitric oxide levels, can provoke the development of a uremic cardiomyopathy and increase the risk of further cardiovascular complications such as arrhythmias and acute myocardial infarction, regardless of pressure and volume overload [10,11]. This evidence concerns the gene REN and chronic kidney disease.