This may result from the imbalance of glucose and lipid metabolism regulated by the kidney, which involves in MetS pathogenesis through hemodynamic changes, sympathetic nerve excitation, increased reactive oxygen species (ROS) production, renin-angiotensin-aldosterone system (RAAS) activation, and adipokine abnormalities due to insulin resistance (IR), obesity, hypertension, and hyperlipidemia [30, 31]. This evidence concerns the gene REN and hyperlipidemia.