Obesity and kidney disease: differential effects of obesity on adipose tissue and kidney inflammation and fibrosis

Purpose of review To provide a perspective by investigating the potential cross-talk between the adipose tissue and the kidney during obesity. Recent findings It is well established that excessive caloric intake contributes to organ injury. The associated increased adiposity initiates a cascade of cellular events that leads to progressive obesity-associated diseases such as kidney disease. Recent evidence has indicated that adipose tissue produces bioactive substances that contribute to obesity-related kidney disease, altering the renal function and structure. In parallel, proinflammatory processes within the adipose tissue can also lead to pathophysiological changes in the kidney during the obese state. Summary Despite considerable efforts to better characterize the pathophysiology of obesity-related metabolic disease, there are still a lack of efficient therapeutic strategies. New strategies focused on regulating adipose function with respect to AMP-activated protein kinase activation, NADPH oxidase function, and TGF-beta may contribute to reducing adipose inflammation that may also provide renoprotection.