• Int J Med Sci · Jan 2021

    Observational Study

    Circulating hepassocin level in patients with stable angina is associated with fatty liver and renal function.

    • I-Ting Tsai, Wei-Chin Hung, Yung-Chuan Lu, Cheng-Ching Wu, Thung-Lip Lee, Chin-Feng Hsuan, Teng-Hung Yu, Ching-Ting Wei, Fu-Mei Chung, Yau-Jiunn Lee, and Chao-Ping Wang.
    • Department of Emergency, E-Da Hospital, Kaohsiung 82445 Taiwan.
    • Int J Med Sci. 2021 Jan 1; 18 (1): 1-7.

    AbstractBackground: Chronic kidney disease (CKD) is a major risk factor for coronary artery disease and it is often associated with hepatic steatosis. Hepassocin (also known as hepatocyte-derived fibrinogen related protein or fibrinogen-like 1) is a novel hepatokine that causes hepatic steatosis and induces insulin resistance. However, the role of hepassocin in renal function status remains unclear. Our objective was to investigate the association of plasma hepassocin level with fatty liver and renal function status in patients with stable angina. Methods: Plasma hepassocin levels were determined by enzyme-linked immunosorbent assays in 395 consecutive patients with stable angina. Renal function was defined as an estimated glomerular filtration rate (eGFR). Fatty liver was defined by ultrasonography and fibrosis-4 (FIB-4) index. Results: With increasing hepassocin tertiles, patients had higher prevalence of fatty live, an increased waist-to-hip ratio, and neutrophil count, monocyte count, and FIB-4 index, higher levels of uric acid, blood urine nitrogen and higher sensitivity C-reactive protein. They also had incrementally lower eGFR, serum hemoglobin and albumin levels. In multiple linear stepwise regression analysis, only eGFR was significantly independent negatively associated with plasma hepassocin levels. Conclusion: Our results indicate that circulating hepassocin in patients with stable angina is associated with fatty liver and renal function, which suggests that increased plasma hepassocin may be involved in the pathogenesis of fatty liver and CKD.© The author(s).

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