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Published ahead of print on February 11, 2010
J Am Soc Nephrol 21: 406-412, 2010
© 2010 American Society of Nephrology
doi: 10.1681/ASN.2009080820
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Brief Reviews

Mechanisms Linking Obesity, Chronic Kidney Disease, and Fatty Liver Disease: The Roles of Fetuin-A, Adiponectin, and AMPK

Joachim H. Ix*,{dagger} and Kumar Sharma*,{ddagger}

*Division of Nephrology and Hypertension, Department of Medicine, University of California–San Diego/Veterans Affairs San Diego Healthcare System;
{dagger}Division of Preventive Medicine, Department of Family and Preventive Medicine, University of California–San Diego; and
{ddagger}Center for Renal Translational Medicine, University of California–San Diego/Veterans Affairs San Diego Healthcare System, San Diego, California

Correspondence: Dr. Kumar Sharma, Director, Center for Renal Translational Medicine, University of California–San Diego/Veterans Affairs San Diego Healthcare System, La Jolla, CA 92093-0711. Phone: 858-822-0860; Fax: 858-822-7483; E-mail: kusharma{at}ucsd.edu

Obesity is a risk factor for chronic kidney disease (CKD) and nonalcoholic fatty liver disease (NAFLD). Recent studies identify mechanisms common to both diseases linked through an interorgan communication orchestrated by fetuin-A and adiponectin. In liver and kidney, the energy sensor 5'-AMP activated protein kinase (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 increasingly common sequelae of obesity.




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