Table of Contents Author Guidelines Submit a Manuscript
Gastroenterology Research and Practice
Volume 2014 (2014), Article ID 847539, 6 pages
Review Article

Chronic Kidney Disease and Nonalcoholic Fatty Liver Disease—Is There a Link?

1Division of Internal Medicine, Department of Nephrology and Dialysis, University Hospital Center Rijeka, 51000 Rijeka, Croatia
2Division of Internal Medicine, Department of Gastroenterology, University Hospital Center Rijeka, 51000 Rijeka, Croatia

Received 19 December 2013; Accepted 4 February 2014; Published 6 March 2014

Academic Editor: Gyorgy Baffy

Copyright © 2014 L. Orlić et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.


Research in recent years has led to the recognition of the importance of nonalcoholic fatty liver disease (NAFLD) and its relationship to the metabolic syndrome (MS). This has led to a growing interest in the potential prognostic value of NAFLD for adverse cardiovascular disease (CVD) outcome. On the other hand, searching for new risk factors for chronic kidney disease (CKD) development and progression is very important. Growing evidence suggests that the MS is an important factor in the pathogenesis of CKD. The best confirmation of this pathogenic link is hypertensive and diabetic nephropathy as the main causes of CKD. Furthermore, the possible link between NAFLD and CKD has also attracted research interest and recent data suggest an association between these two conditions. These findings have fuelled concerns that NAFLD may be a new and added risk factor for the development and progression of CKD. NAFLD and CKD share some important cardiometabolic risk factors and possible common pathophysiological mechanisms, and both are linked to an increased risk of incident CVD events. Therefore, common factors underlying the pathogenesis of NAFLD and CKD may be insulin resistance, oxidative stress, activation of rennin-angiotensin system, and inappropriate secretion of inflammatory cytokines by steatotic and inflamed liver.