الفهرس | Only 14 pages are availabe for public view |
Abstract Currently, non-alcoholic fatty liver disease (NAFLD) is the most predominant chronic liver disorder. NAFLD is a pathological condition which occurs as a result of the accumulation of fat (steatosis), either with or without necro-inflammation or fibrosis, if alcohol consumption isn’t excessive and other known causes of liver disorder e.g. viral or autoimmune hepatitis. The clinical spectrum of NAFLD ranges from hepatic steatosis (HS) to non-alcoholic steato-hepatitis (NASH), hepatocellular carcinoma, and cirrhosis. Several factors affect the development to fibrosis for instance inflammation, insulin resistance (IR), lipotoxicity, and oxidative stress, genetic factors. Chronic kidney disease (CKD) is a global health issue. Nowadays, it is well recognized that cardiovascular diseases (CVD) are the primary cause of mortality and morbidity in CKD. NAFLD occurrence and severity has been connected to the CKD incidence and stage independently of traditional CKD risk factors. Furthermore, the CKD occurrence elevates the overall mortality in NAFLD patients in comparison with the general population. There is accumulative evidence that both the synthesis and releasing of various pro-inflammatory cytokines is raised in people with NAFLD/NASH. Hence, the systemic production of different inflammatory promoters, such as the enhanced reactive oxygen species, TNF-, TGF-, plasminogen activator inhibitor-1, C-reactive protein (CRP), and IL-6, could be mediators for the linking of NAFLD and CKD. |