NAFLD and Chronic Kidney Disease

Abstract

Non-alcoholic fatty liver disease (NAFLD) is the most common cause of chronic liver disease in developed countries and it is now considered a risk factor for cardiovascular disease. Evidence linking NAFLD to the development and progression of chronic kidney disease (CKD) is emerging as a popular area of scientific interest. The rise in simultaneous liver-kidney transplantation as well as the significant cost associated with the presence of chronic kidney disease in the NAFLD population make this entity a worthwhile target for screening and therapeutic intervention. While several cross-sectional and case control studies have been published to substantiate these theories, very little data exists on the underlying cause of NAFLD and CKD. In this review, we will discuss the most recent publications on the diagnosis of NAFLD as well new evidence regarding the pathophysiology of NAFLD and CKD as an inflammatory disorder. These mechanisms include the role of obesity, the renin-angiotensin system, and dysregulation of fructose metabolism and lipogenesis in the development of both disorders. Further investigation of these pathways may lead to novel therapies that aim to target the NAFLD and CKD. However, more prospective studies that include information on both renal and liver histology will be necessary in order to understand the relationship between these diseases.

Keywords: chronic kidney disease; inflammation; non-alcoholic fatty liver disease; non-alcoholic steatohepatitis; review.

Figure 1

This figure demonstrates the various mechanisms associated with non-alcoholic fatty liver disease (NAFLD) and chronic kidney disease (CKD). The liver-kidney crosstalk in NAFLD includes altered renin-angiotensin system (RAS) and activated protein kinase (AMPK) activation, impaired antioxidant defense, and excessive dietary fructose intake, which affects renal injury through altered lipogenesis and inflammatory response. In turn, 8 the kidney reacts promoting further RAS activation, increased angiotensin II (ANGII) and uric acid production in a vicious cycle leading to fibrosis [20].