MetS causes renal damage through mechanisms like oxidative stress, chronic inflammation, perirenal adipose tissue (PRAT) compression, and the overactivation of the renin-angiotensin-aldosterone system (RAAS), mineralocorticoid receptors (MR), and sympathetic nervous system (SNS), leading to renal hemodynamic changes, systemic insulin resistance, and lipotoxicity, which ultimately result in kidney damage and cardiovascular diseases (5). This evidence concerns the gene NR3C2 and metabolic syndrome.