ABSTRACT
Hypertension is the leading driver of cardiovascular diseases and premature death worldwide. Obesity/overweight accounts for 65%–78% of the risk for primary (essential) hypertension and >70% of end-stage kidney disease via hypertension and diabetes mellitus. Because of the rising prevalence of obesity, the health care and economic burdens of hypertension, diabetes mellitus, and chronic kidney disease are also increasing in most countries. Increased renal sodium reabsorption plays an important role in initiating obesity–hypertension. The mediators of abnormal kidney function during development of obesity–hypertension include renal compression by fat in and around the kidneys, activation of the renin–angiotensin–aldosterone system, and increased sympathetic nervous system activity. Additional factors such as hyperglycemia, dyslipidemia, immune cell activation, and inflammation interact with hypertension to cause target organ damage and to exacerbate hypertension. Lifestyle interventions represent the cornerstone for treating obesity. However, high rates of recidivism, prolonged obesity, and progressive target organ damage often lead to treatment-resistant hypertension, requiring multiple antihypertensive drugs and medications for other risk factors including dyslipidemia, insulin resistance, diabetes, and inflammation. Although adequate control of this constellation of disorders is challenging, progress is being made in developing more effective therapies for obesity and accompanying cardiorenal and metabolic disorders.
