中文｜English
ISSN 1001-5256 (Print)
ISSN 2097-3497 (Online)
CN 22-1108/R
Volume 38 Issue 2
Feb.  2022
Turn off MathJax
Article Contents
Article Navigation >  Journal of Clinical Hepatology  > 2022  >  38(2): 322-327

Value of urinary α1-microglobulin and N-acetyl-β-D-glucosaminidase/urinary creatinine in monitoring early renal injury in patients with chronic hepatitis B virus-related liver diseases

DOI: 10.3969/j.issn.1001-5256.2022.02.014

  • Department of Gastroenterology, The Second Affiliated Hospital of Kunming Medical University, Kunming 650000, China

Research funding:

Research funding: National Natural Science Foundation of China (81660102);

Research funding: National Natural Science Foundation of China (81360072);

Yunnan Provincial Health Science and Technology Program Project Fund Grant (2017NS280);

Natural Science Foundation of Yunnan Province (2018FE001[-051])

More Information
  • Corresponding author: TANG Yingmei, tangyingmei_med@kmmu.edu.cn
  • Received Date: 2021-07-02
  • Accepted Date: 2021-08-10
  • Published Date: 2022-02-20
    Abstract
  •   Objective  To investigate the value of urinary α1-microglobulin (α1-MG) and N-acetyl-β-D-glucosaminidase/urinary creatinine (NAG/UCr) in monitoring renal injury in patients with chronic hepatitis B virus (HBV)-related liver diseases.  Methods  A total of 85 patients with HBV-related liver diseases who attended The Second Affiliated Hospital of Kunming Medical University from August 2019 to August 2020 were enrolled, and according to the history of treatment with nucleos(t)ide analogues (NUC), they were divided into NUC treatment group with 57 patients and non-NUC treatment group with 28 patients; according to the type of NUC used, the NUC treatment group was further divided into entecavir (ETV) treatment group with 32 patients and tenofovir disoproxil fumarate (TDF) treatment group with 25 patients; according to the results of HBV serum antigen and antibody markers, the patients were divided into HBeAg-negative group with 57 patients and HBeAg-positive group with 28 patients; according to the results of serum HBV DNA quantification, the patients were divided into HBV DNA-negative group with 47 patients and HBV DNA-positive group with 38 patients; according to abdominal imaging findings, the patients were divided into non-liver cirrhosis group with 47 patients and liver cirrhosis group with 38 patients. The data on medical history and laboratory markers were collected for comparison between two groups. The t-test was used for comparison of normally distributed continuous data between two groups, and the Mann-Whitney U test was used for comparison of data with skewed distribution between two groups; the chi-square test was used for comparison of categorical data between two groups. The McNemar test was used to compare the diagnostic merit of each index; a Spearman correlation analysis was used to investigate the correlation of each factor with α1-MG, and NAG/UCr; the multiple linear regression analysis was used to analyze the independent influencing factors for α1-MG and NAG/UCr.  Results  The non-NUC treatment group, the HBeAg-positive group, and the HBV DNA-positive group had significantly higher levels of urinary α1-MG than the NUC treatment group (Z=-2.054, P=0.04), the HBeAg-negative group (Z=-2.293, P=0.022), and the HBV DNA-negative group (Z=-2.229, P=0.026), respectively. The HBV DNA-positive group and the liver cirrhosis group had significantly higher levels of NAG and NAG/UCr than the HBV DNA-negative group (Z=-2.908 and -2.824, both P < 0.05) and the non-liver cirrhosis group (Z=-3.204 and -3.412, both P < 0.05), respectively. There was a significant difference in the proportion of patients with abnormal α1-MG and that of patients with abnormal estimated glomerular filtration rate (eGFR) (31.8% vs 20.0%, χ2=7.178, P=0.007), and the proportion of patients with abnormal α1-MG and NAG/UCr was significantly higher than that of patients with abnormal eGFR (35.3% vs 20.0%, χ2=8.049, P=0.005). There was a significant difference in diagnostic merit between α1-MG+NAG/UCr and eGFR (P=0.015). Age (β=0.246, P < 0.05), positive HBeAg (β=0.284, P < 0.01), and liver cancer (β=0.291, P < 0.01) were independent risk factors for the increase in α1-MG, while the increase in FIB-4 value (β=0.352, P < 0.05), ascites (β=0.260, P < 0.05), esophagogastric varices(β=-0.248, P < 0.05), positive HBV DNA (β=0.197, P < 0.05), and high total bilirubin (β=0.257, P < 0.05) were independent risk factors for the increase in NAG/UCr.  Conclusion  In patients with chronic HBV-related liver diseases, renal injury may occur during the whole course of active viral replication, liver cirrhosis, and deterioration of liver function. Antiviral therapy with NUC can alleviate renal impairment caused by HBV and is safe and reliable within a certain course of treatment. Combined measurement of urinary α1-MG and NAG/UCr has more advantages over eGFR in the diagnosis of early renal injury, and it is an effective method for renal function monitoring in patients with chronic HBV-related liver diseases.

     

    • FullText(HTML)
  • loading
    • References(12)
  • [1]
    SCHWEITZER A, HORN J, MIKOLAJCZYK RT, et al. Estimations of worldwide prevalence of chronic hepatitis B virus infection: A systematic review of data published between 1965 and 2013[J]. Lancet, 2015, 386(10003): 1546-1555. DOI: 10.1016/S0140-6736(15)61412-X.
    [2]
    TERRAULT NA, LOK A, MCMAHON BJ, et al. Update on prevention, diagnosis, and treatment of chronic hepatitis B: AASLD 2018 hepatitis B guidance[J]. Hepatology, 2018, 67(4): 1560-1599. DOI: 10.1002/hep.29800.
    [3]
    YANG YT, WANG X, ZHANG YY, et al. The histone demethylase LSD1 promotes renal inflammation by mediating TLR4 signaling in hepatitis B virus-associated glomerulonephritis[J]. Cell Death Dis, 2019, 10(4): 278. DOI: 10.1038/s41419-019-1514-4.
    [4]
    YANG YT, WANG X, ZHANG YY, et al. Hepatitis B virus X protein and proinflammatory cytokines synergize to enhance TRAIL-induced apoptosis of renal tubular cells by upregulation of DR4[J]. Int J Biochem Cell Biol, 2018, 97: 62-72. DOI: 10.1016/j.biocel.2018.02.006.
    [5]
    CHEN J, LI D, LUO E. Telbivudine antagonizes TLR4 to inhibit the epithelial-to-mesenchymal transition in human proximal tubular epithelial cells in vitro[J]. Int Immunopharmacol, 2019, 74: 105683. DOI: 10.1016/j.intimp.2019.105683.
    [6]
    WANG X, ZHOU Y, ZHU N, et al. The deposition of Notch1 in hepatitis B virus-associated nephropathy and its role in hepatitis B virus X protein-induced epithelial-mesenchymal transdifferentiation and immunity disorder in renal tubular epithelial cells[J]. J Viral Hepat, 2014, 21(10): 734-743. DOI: 10.1111/jvh.12244.
    [7]
    KAYAASLAN B, GUNER R. Adverse effects of oral antiviral therapy in chronic hepatitis B[J]. World J Hepatol, 2017, 9(5): 227-241. DOI: 10.4254/wjh.v9.i5.227.
    [8]
    BOCK P, NEL K, FATTI G, et al. Renal dysfunction by baseline CD4 cell count in a cohort of adults starting antiretroviral treatment regardless of CD4 count in the HIV Prevention Trials Network 071[HPTN 071; Population Effect of Antiretroviral Therapy to Reduce HIV Transmission (PopART)] study in South Africa[J]. HIV Med, 2019, 20(6): 392-403. DOI: 10.1111/hiv.12729.
    [9]
    WENG Q, ZHOU Q, TONG J, et al. New risk score for predicting steroid resistance in patients with focal segmental glomerulosclerosis or minimal change disease[J]. Clin Proteomics, 2020, 17: 18. DOI: 10.1186/s12014-020-09282-x.
    [10]
    ZHANG H, LI X, XU H, et al. The significance of the hemalexin C1q, RBP, and urinary NAG levels in the diagnosis and prognosis of children with purpura nephritis[J]. Am J Transl Res, 2021, 13(6): 7065-7070.
    [11]
    HOJS R, EKART R, BEVC S, et al. Biomarkers of renal disease and progression in patients with diabetes[J]. J Clin Med, 2015, 4(5): 1010-1024. DOI: 10.3390/jcm4051010.
    [12]
    KIM YJ, CHO HC, SINN DH, et al. Frequency and risk factors of renal impairment during long-term adefovir dipivoxil treatment in chronic hepatitis B patients[J]. J Gastroenterol Hepatol, 2012, 27(2): 306-312. DOI: 10.1111/j.1440-1746.2011.06852.x.
    • Relative Articles
    • Supplements(0)
    • Cited By
  • 加载中

Catalog

    通讯作者: 陈斌, bchen63@163.com
    • 1. 

      沈阳化工大学材料科学与工程学院 沈阳 110142

    1. 本站搜索
    2. 百度学术搜索
    3. 万方数据库搜索
    4. CNKI搜索

    Tables(10)

    Get Citation
    PDF
    XML

    Article Metrics

    Article views (538) PDF downloads(44) Cited by()
    Proportional views
    Related
        

    The first journal specializing in hepatobiliary and pancreatic diseases in China

    Supervisor：Ministry of Education of the People's Republic of China

    Sponsor：Jilin University

    Academic Support: Chinese Society of Hepatology，Chinese Medical Association

    Address: 461 Xinjiang Road, Changchun

    Submit：0431-88782044

    Peer review：0431-88783542

    Email：lcgdb@vip.163.com

    About Journal

    Submission Guideline

    Journal Online

    Hepatobiliary College

    Guidelines

    YesterdayIP[]YesterdayPV[]TodayIP[]TodayPV[]Online[]

    Website Design © 2020 Editorial Board of Journal of Clinical Hepatology 吉ICP备10000617号-1 Supported by: Beijing Renhe Information Technology Co. Ltd  

    /

    DownLoad:  Full-Size Img  PowerPoint
    Return
    Return