Correction: Creatinine-to-cystatin C ratio and all-cause and ardiovascular mortality in U.S. adults with nonalcoholic fatty liver disease: a nationwide cohort study

Yuanyuan Chen¹Bing Yang²Huihui Chen³Jun Chen¹Jinmin Cao⁴Huijie Wang⁵Chuantie Chen^2*

• ¹Department of Liver Diseases, Shenzhen Third People's Hospital, Shenzhen, China
• ²Department of Gastroenterology, Longgang Central Hospital of Shenzhen, Shenzhen, China
• ³Master's degree in progress, Guangzhou University of Chinese Medicine, Guangzhou, China
• ⁴Department of Dermatology, Hunan Aerospace Hospital, Changsha, China
• ⁵Department of Endoscopy, Shijiazhuang Traditional Chinese Medicine Hospital, Shijiazhuang, China

1IntroductionNonalcoholic fatty liver disease (NAFLD) is the prevalent chronic liver condition globally, impacting around 24% of the world's population (1). NAFLD includes a range of liver damage, from simple hepatic steatosis to nonalcoholic steatohepatitis, potentially advancing to cirrhosis, liver failure and hepatocellular carcinoma (2,3). It is also associated with extrahepatic metabolic disorders, including cardiovascular events and type 2 diabetes mellitus (4). Notably, patients with hepatic steatosis accompanied by advanced liver fibrosis exhibit a significantly elevated risk of both all-cause mortality (5,6) and cardiovascular disease mortality (7,8). The increased cardiovascular risk in these patients is thought to be driven by involving interrelated pathways of insulin resistance, oxidative stress, chronic inflammation, endothelial dysfunction, gut microbiota alterations, and dysregulated lipid metabolism (9–12) . The newly proposed metabolic dysfunction-associated fatty liver disease (MAFLD) (13) and metabolic dysfunction-associated steatotic liver disease (MASLD) (14) concepts place greater emphasis on the metabolic nature of this disease. However, given their substantial population overlap with NAFLD, this study maintains the traditional NAFLD diagnostic criteria.Low muscle mass has been established as a significant risk factor for the progression of NAFLD (15). Creatinine, primarily derived from muscle tissue, particularly skeletal muscle (16) , is a byproduct of muscle metabolism and is almost entirely excreted by the kidneys. However, creatinine production is not solely dependent on muscle mass but is also influenced by various factors such as age, sex, ethnicity, and dietary habits (e.g., meat intake), especially in elderly individuals or patients with impaired renal function (17). CysC is a small, non-ionic protein synthesized by all nucleated cells. It is filtered by the glomeruli and then fully reabsorbed and metabolized by proximal tubular cells, making it less affected by muscle mass (18). CCR was calculated as serum creatinine to cystatin C ratio. It is considered a marker for muscle mass and a surrogate indicator of sarcopenia (19–21).