» Articles » PMID: 15655828

Existence and Significance of Hepatitis B Virus DNA in Kidneys of IgA Nephropathy

Overview
Specialty Gastroenterology
Date 2005 Jan 19
PMID 15655828
Citations 11
Authors
Affiliations
Soon will be listed here.
Abstract

Aim: To investigate the existence and significance of hepatitis B virus (HBV) DNA in the pathogenesis of IgA nephropathy (IgAN).

Methods: Fifty cases of IgAN with HBV antigenaemia and/or hepatitis B virus antigens (HBAg, or HBsAg, HBcAg) detected by immunohistochemistry in renal tissues were enrolled in our study. The distribution and localization of HBV DNA were observed using in situ hybridization. Southern blot analysis was performed to reveal the state of renal HBV DNA.

Results: Among the 50 patients with IgAN, HBs antigenemia was detected in 17 patients (34%). HBAg in renal tissues was detected in 48 patients (96%), the positive rate of HBAg, HBsAg, and HBcAg was 82% (41/50), 58% (29/50), and 42% (21/50) in glomeruli, respectively; and was 94% (47/50), 56% (28/50) and 78% (39/50) in tubular epithelia, respectively. Positive HBV DNA was detected in 72% (36/50) and 82% (41/50) cases in tubular epithelia and glomeruli respectively by in situ hybridization, and the positive signals were localized in the nuclei of tubular epithelial cells and glomerular mesangial cells as well as infiltrated interstitial lymphocytes. Moreover, 68% (34/50) cases were proved to be HBV DNA positive by Southern blot analysis, and all were the integrated form.

Conclusion: HBV infection might play an important role in occurrence and progress of IgAN. In addition to humoral immune damages mediated by HBAg-HBAb immune complex, renal tissues of some IgAN are directly infected with HBV and express HBAg in situ, and the cellular mechanism mediated by HBV originating from renal cells in situ may also be involved in the pathogenesis of IgAN.

Citing Articles

Hepatitis B Virus Status and Clinical Outcomes in IgA Nephropathy.

Gao M, Xu L, Li Y, Wang X, Chen P, Shi S Kidney Int Rep. 2024; 9(4):1057-1066.

PMID: 38765575 PMC: 11101714. DOI: 10.1016/j.ekir.2024.01.009.


Unmasking the tissue-resident eukaryotic DNA virome in humans.

Pyoria L, Pratas D, Toppinen M, Hedman K, Sajantila A, Perdomo M Nucleic Acids Res. 2023; 51(7):3223-3239.

PMID: 36951096 PMC: 10123123. DOI: 10.1093/nar/gkad199.


IFI16 induces inflammation in hepatitis B virus-associated glomerulonephritis by regulating the Caspase-1/ IL-1 ß pathway.

Liu L, Xie S, Li C, Guo Y, Liu X, Zhao X Diagn Pathol. 2022; 17(1):39.

PMID: 35459254 PMC: 9034479. DOI: 10.1186/s13000-022-01220-9.


Clinicopathological features, risk factors, and outcomes of immunoglobulin A nephropathy associated with hepatitis B virus infection.

Wang K, Yu Z, Huang Y, Yang K, He T, Xiao T J Nephrol. 2021; 34(6):1887-1896.

PMID: 33683672 DOI: 10.1007/s40620-021-01004-2.


Secondary IgA nephropathy.

Saha M, Julian B, Novak J, Rizk D Kidney Int. 2018; 94(4):674-681.

PMID: 29804660 PMC: 6981247. DOI: 10.1016/j.kint.2018.02.030.


References
1.
Zhang Y, Guo M, Ying Y . [Further study on the immunopathology of hepatitis B virus associated glomerulonephritis]. Zhonghua Nei Ke Za Zhi. 1990; 29(9):526-9, 574. View

2.
Endo Y, Kanbayashi H . Etiology of IgA nephropathy syndrome. Pathol Int. 1994; 44(1):1-13. DOI: 10.1111/j.1440-1827.1994.tb02579.x. View

3.
Thyagarajan S, Thirunalasundari T, Subramanian S, Panchanadam M, Nammalwar B, Prabha V . Serum and tissue positivity for hepatitis B virus markers in histopathologically proven glomerulonephropathies. J Med Microbiol. 1989; 29(4):243-9. DOI: 10.1099/00222615-29-4-243. View

4.
Wang N, Wu Z, Zhang Y, Guo M, Liao L . Role of hepatitis B virus infection in pathogenesis of IgA nephropathy. World J Gastroenterol. 2003; 9(9):2004-8. PMC: 4656662. DOI: 10.3748/wjg.v9.i9.2004. View

5.
Zhang Y, Fang L, Ma X . [Hepatitis B virus infection and pathogenesis of glomerulonephritis]. Zhonghua Bing Li Xue Za Zhi. 1995; 24(6):341-4. View