Abstract:

Obesity is a risk factor for chronic kidney disease and nonalcoholic fatty liver disease. Recent studies identify mechanisms common to both disease linked through an interorgan communication orchestrated by Fetuin-A, Adiponectin and 5’-AMP activated protein kinase (AMPK). In liver and kidney, the energy sensor AMPK is pivotal to directing podocytes and hepatocytes to compensatory and potentially deleterious pathways, leading to inflammatory and profibrotic cascades culminating in end-organ damage. Regulation of these early upstream pathways may provide new therapeutic targets for these common sequelae of obesity.

Key words: obesity-related glomerulopathy, honalcoholic fatty liver disease,fetuin-A, adiponectin AMPK