Circulating Immune Complex in Glomerulonephropathy Associated with Hepatitis B Virus Infection

Furuse, Akio; Hattori, Shinzaburo; Terashima, Takanori; Karashima, Shinnyo; Matsuda, Ichiro

doi:10.1159/000182649

Cited by 35 publications

(11 citation statements)

References 15 publications

(26 reference statements)

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“…Corticosteroid therapy used in primary MN has been administered to some patient with HBV-associated nephropathy as a therapeutic trial for symptomatic relief of proteinuria [80, 88]. However, corticosteroids given at the onset of nephrotic syndrome in HBVMN do not seem to have an ameliorative effect on the nephrotic state or lead to clearance of the virus [89].…”

Section: Treatment Of Hbvmnmentioning

confidence: 99%

Hepatitis B Virus-Associated Nephropathy

Bhimma

Coovadia²

2004

Am J Nephrol

209

165

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A direct causal association between hepatitis B virus (HBV) infection and the development of nephropathy remains controversial. Epidemiological studies have shown that chronic carriage of HBV in some individuals (particularly children) leads to the development of nephrotic syndrome with a strong male predominance, the commonest histological type being membranous nephropathy (MN). Spontaneous clearance of HBV antigens (particularly the HBeAg) leads to abrogation of proteinuria. The isolation of immune complexes in the kidney suggests that the pathogenesis of the disease may have an immune-complex basis. Recent studies showing expression of HBV viral antigens in kidney tissue suggest direct viral-induced pathological alterations and chronic immunologic injury. Biosocial studies have detected no correlation between HBV carriage and proteinuria using both quantitative and qualitative urinary protein analysis. Genetic studies of HLA class I and II genes showed a predisposition to MN but no similar correlation in those with milder degrees of proteinuria. These findings suggest that milder proteinuria is unrelated to HBV carriage or genetic factors but the development of nephropathy, particularly MN, in patients with chronic HBV carriage (HBsAg and/or HBV DNA positive) is based on an interaction of virus and host factors. Although the natural history of the disease tends to remission with preservation of renal function, there is considerable morbidity and a small but significant mortality. Use of naturally occurring cytokines (such as interferon-α2b) and other candidate therapies accelerates clearance of the virus and proteinuria. The most effective tool in reducing the incidence of the disease is the use of HBV vaccines.

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Section: Treatment Of Hbvmnmentioning

confidence: 99%

Hepatitis B Virus-Associated Nephropathy

Bhimma

Coovadia²

2004

Am J Nephrol

209

165

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“…It has been demonstrated by immunofluorescence in cases of HBV-associated MGN that IgG, C3 and HBe antigen are present in a granular fashion along the glo merular capillary walls [3][4][5]8]. Circulating immune complexes in sera from these patients can be evidenced by the C 1 q-binding assay and by the protein A precipita tion test [5], Two kinds of HBe antigen, i.e., both free HBe antigen and IgG-associated HBe antigen, have been detected in the sera [3).…”

Section: Discussionmentioning

confidence: 99%

“…Circulating immune complexes in sera from these patients can be evidenced by the C 1 q-binding assay and by the protein A precipita tion test [5], Two kinds of HBe antigen, i.e., both free HBe antigen and IgG-associated HBe antigen, have been detected in the sera [3). After the appearance of serum anti-HBe antibody (seroconversion), urinary findings normalized, and the glomerular immune deposits were no longer detectable [4], All these observations support the possibility that the disease is caused by HBe antigenanti-HBe immune complex deposition.…”

Section: Discussionmentioning

confidence: 99%

“…Immunohistopathological studies of MGN revealed the presence of the HBe anti gen, IgG, and C3 in the glomerular capillary basement membrane, thereby suggesting a HBe antigen-anti-HBe immune complex disease [3][4][5]. Maggiore et al [7] ex pressed serious doubt about the specificity of immuno fluorescent staining for HBV-associated antigens in glo merular immune deposits.…”

Section: Introductionmentioning

confidence: 99%

See 1 more Smart Citation

Presence of HBe Antibody in Glomerular Deposits in Membranous Glomerulonephritis Is Associated with Hepatitis B Virus Infection

Hattori

Furuse²,

Matsuda³

1988

Am J Nephrol

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The specificity of IgG on the glomerular capillary wall was investigated in 3 patients with hepatitis B virus associated membranous glomerulonephritis. The immune deposits on the capillary walls were stained by immunofluorescent antibody against HBe antigen and IgG. The eluted fluid (0.02 M citrate buffer, pH 3.2) from renal biopsy slices contained significant activity of HBe antibody, but not of HBs and HBe antibodies. After elution, the disappearance of IgG on the capillary walls was confirmed by immunofluorescence. Heterologous complement activation with fresh guinea pig complement was positive in the glomerular capillary walls from all 3 patients. Our observations support the notion that this disease is caused by HBe antigen-anti-HBe immune complexes.

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“…Immune complexes (ICs) have been demonstrated in numerous conditions, in health and disease. The presence of ICs has been demonstrated in hepatitis B (Almeida and Waterson, 1969;Araki et al, 1982) and certain diseases related to hepatitis B virus (HBV) infection (Alpert et al, 197 1 ;Prince and Trepo, 197 1 ;Carella et al, 1977 ;Furuse et al, 1982).…”

Section: Introductionmentioning

confidence: 99%