In this context, it is important to emphasize that renal dysfunction is associated with increasing molecule adhesion, a factor associated with platelet hyperactivity; furthermore, platelet activation in diabetic, obese, and hypertensive patients is imputed to endothelial dysfunction, oxidative stress, subclinical inflammation, and altered renin–angiotensin aldosterone system (RAAS) (2, 30). This evidence concerns the gene REN and Abnormal renal physiology.