HBsAg IN RENAL DISEASE

Nagy, Judit; G, Bajtai; Brasch, H; Süle, T; Ambrus, M; Deák, Gy.; Hámori, A

doi:10.1016/s0140-6736(78)91716-6

Cited by 14 publications

(4 citation statements)

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“…Never theless, IgA nephropathy associated with HBV antigen emia has not been previously recognized as a distinct disease entity and yet, increased incidences of HBV sur face antigenemia have been reported in patients with IgA nephropathy [10,11], One could argue that the two disease entities are merely coincidental as HBV infection is lo cally endemic and IgA nephropathy is the commonest primary glomerulopathy in Chinese [5], However, the demonstration of the presence of HBsAg and HBcAg in the cytoplasm and nuclei of glomerular cells would sug gest a highly probable pathogenetic role of HBV antigen emia in a subset of IgA nephropathy. These findings were in accord with the previous observation by Nagy et al [10] that HBsAg was detected in renal biopsies of 10 of the 32 patients with IgA nephropathy. This glomerulopathy is speculated to be an immune complex glomerulonephritis as found in hepatitis-associated membranous glomeru lopathy [2] since IgA immune complexes has been re ported in the sera from patients with HBV hepatitis [12].…”

Section: Discussionmentioning

confidence: 99%

IgA Nephropathy Associated with Hepatitis B Virus Antigenemia

Lai

et al. 1987

Nephron

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The pathogenetic ability of hepatitis B virus (HBV) antigenemia to induce IgA nephropathy was examined in 10 patients with IgA nephropathy and HBV antigenemia. They had no previous history of liver diseases and their liver function tests were normal. All were positive for hepatitis + surface antigen (HBsAg) and antibody to hepatitis B core antigen (anti-HBcAg) with high titers, thereby indicating they were persistent carriers of HBV. Immunoperoxidase studies using monospecific polyclonal antibodies revealed HBcAg and HBsAg in the nuclei and cytoplasm of glomerular mesangial cells in 8 patients. These findings suggest immune complexes involving HBcAg and HBsAg may induce IgA nephropathy in persons who carry HBV.

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Section: Discussionmentioning

confidence: 99%

IgA Nephropathy Associated with Hepatitis B Virus Antigenemia

Lai

et al. 1987

Nephron

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“…Typical of its his tology is the predominance of IgA granular deposits in the glomeruli, primarily in the mesangium [2][3][4], The patho genesis of the disease is unknown, but an immune com plex etiology is most likely [3][4][5][6]; however, nonhomogenous immunopathogenicity has also been suggested [5,6]. Several authors have studied the role of viral and bacterial infections [7][8][9], bone marrow Ig synthesis [10], the im mune system (complement [11,12], cytokines [13], IgA disregulation [6,14]), mucosal immune protective capaci ty [ 15,16], and increased absorption of food antigens [ 17,18] in the development of the disease. In both children [ 15] and adults [ 19] with IgA NP.…”

Section: Introductionmentioning

confidence: 99%

Do Intestinal Hyperpermeability and the Related Food Antigens Play a Role in the Progression of IgA Nephropathy?

et al. 1996

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Intestinal permeability was investigated by using ⁵¹Cr-EDTA as a probe molecule in 29 patients with immunoglobulin A nephropathy (IgA NP) and 20 healthy controls in 1990. Intestinal permeability was significantly higher in the IgA NP patients than in the controls (IgA NP, 3.86 ± 0.29%; controls, 2.72 ± 0.23%, p < 0.005). There was a significant relation between the manifestations of the disease (proteinuria and/or microhematuria) and the increased intestinal permeability (p < 0.05). By 1994, after an interval of 4 years, average intestinal permeability in the 21 patients available for study had not changed (3.80 ± 0.36 vs. 4.57 ± 0.63%) and was significantly higher than in the controls (p < 0.02). In patients with elevated serum IgA levels (serum IgA > 3.2 g/l; n = 15) there was a significant correlation between serum IgA levels and the degree of intestinal permeability (p < 0.02). During the 4-year period, the patients’ kidney function deteriorated (n = 25; creatinine clearance in 1990, 92.4 ± 6.1 ml/min; in 1994,73.9 ± 7.6 ml/min; p < 0.0002), the deterioration being greater in patients with increased intestinal permeability. There was no relation between the histologic grade of the biopsy specimen, hypertension and intestinal permeability. These data collected over a 4-year period suggest that in IgA NP increased intestinal permeability may play a role in the pathogenesis of the disease and adversely influence its progression.

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“…The presence of hepatitis B surface antigen (HBsAg) in glomerular immune complexes has been reported in patients with renal disease of varying morphological patterns, including membranous, proliferative and mesangiocapillary glomerulonephritis and focal glomerulosclerosis (Combes et al 1971, Brzosko et al 1974, Knieser et al 1974, Kohler et al 1974. While many of these patients had evidence of co-existent liver disease (Combes et al , Knieser et al 1974, Kohler et al 1974, glomerular HBsAg immune complexes have also been found in patients subclinically infected with the hepatitis B virus (Brzosko et al 1974, Nagy et al 1978. Although chronic HBs antigenaemia in patients with systemic lupus erythematosus (SLE) has been reported (Alarcon-Segovia, Fishbein & Diaz-Jouanen 1972), there is no published information on the frequency of HBsAg immune deposits in lupus nephritis.…”

Section: Introductionmentioning

confidence: 99%

“…While many of these patients had evidence of co-existent liver disease (Combes et al , Knieser et al 1974, Kohler et al 1974, glomerular HBsAg immune complexes have also been found in patients subclinically infected with the hepatitis B virus (Brzosko et al 1974, Nagy et al 1978. Although chronic HBs antigenaemia in patients with systemic lupus erythematosus (SLE) has been reported (Alarcon-Segovia, Fishbein & Diaz-Jouanen 1972), there is no published information on the frequency of HBsAg immune deposits in lupus nephritis.…”

Section: Introductionmentioning

confidence: 99%

Hepatitis B virus surface antigen in glomerular immune complex deposits of patients with systemic lupus erythematosus

Looi

Prathap

1982

Histopathology

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In view of a high prevalence of hepatitis B virus infection in the Malaysian population, indirect immunofluorescence examination for hepatitis B surface antigen (HBsAg) was routinely performed on renal biopsy specimen at the University Hospital, Kuala Lumpur, over a 3-year period. Examination of renal tissue from 259 patients, including 47 with systemic lupus erythematosus (SLE), revealed 43 cases with HBsAg in glomerular immune complexes. A significantly high proportion (30/43) of these were SLE patients. The deposits were granular in nature, situated in both the capillary walls and mesangium and associated with immunoglobulin deposition. Morphological patterns of lupus nephritis involved were focal proliferative (one case), diffuse proliferative (23 cases) and membranous (six cases). None of these patients showed clinical evidence of liver disease. The significance of these findings remains uncertain, but the possibility exists that the hepatitis B virus may have a role in the pathogenesis of SLE in the tropics where both SLE and HBs antigenaemia are common.

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HBsAg IN RENAL DISEASE

Cited by 14 publications

References 3 publications

IgA Nephropathy Associated with Hepatitis B Virus Antigenemia

IgA Nephropathy Associated with Hepatitis B Virus Antigenemia

Do Intestinal Hyperpermeability and the Related Food Antigens Play a Role in the Progression of IgA Nephropathy?

Hepatitis B virus surface antigen in glomerular immune complex deposits of patients with systemic lupus erythematosus

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