The Role of Overweight and Obesity in the Cardiorenal Syndrome

Abstract

The presence of a group of interactive maladaptive factors including hypertension, insulin resistance, metabolic dyslipidemia, obesity, microalbuminuria, and/or reduced renal function constitute the cardiorenal metabolic syndrome (CRS). Overweight, obesity, and chronic kidney disease (CKD) have grown to pandemic proportions in industrialized countries during the past decade. The fact that these interactive factors promote heart and renal disease has been documented in large population-based studies. Obesity seems to be the driving force behind the development of heart disease and CKD and therefore the CRS. The relationship between overweight/obesity and kidney disease begins in early childhood and appears to be related to overconsumption of high-fructose corn syrup and insufficient physical activity. Today, 13 million children are obese, and over 70% of these children are likely to become obese adults. Indeed, approximately 30% of male and 34% of female adults in the United States are obese. This lifestyle-related epidemic will be a major societal medical and economic problem that will accentuate the current epidemic of CKD in the United States and other industrialized and emerging industrialized countries. In this article, we will review the potential mechanisms by which obesity and other metabolic abnormalities interact to promote heart and progressive kidney disease.

Keywords: Adiposity; Cardiorenal metabolic syndrome; Chronic kidney disease; Heart failure; Metabolic dyslipidemia; Obesity.

Fig. 1

The interrelationship between adiposity and maladaptive changes in the heart and kidney in CRS. GFR = Glomerular filtration rate; IL = interleukin; PAI = plasminogen activator inhibitor; RAAS = renin-angiotensin-aldosterone system; ROS = reactive oxygen species; TNF = tumor necrosis factor; TPA = tissue plasminogen activator.