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Query: UMLS:C0019158 (hepatitis)
 30,205 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Renal histology in 163 Japanese children, aged 3 to 15, with proteinuria and/or haematuria showed that 11 had membranous nephropathy (M.N) and the rest had various other renal diseases. Hepatitis-B-virus surface antigen (HBsAg) was identified, by a reversed passive haemagglutination method, in the serum of all the patients with M.N. but in only 4.6% of the patients with other renal diseases. 6 of the 11 mothers of the children with M.N. were positive for HBsAg, and 1 was positive for antibody to HBsAg (anti-HBs). These findings suggest that M.N. in Japanese children is mainly, if not exclusively, caused by hepatitis-B virus and that in most instances the virus is transmitted from mother to child.
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PMID:Strong association between membranous nephropathy and hepatitis-B surface antigenaemia in Japanese children. 8 85

The paper presents a female patient in whom the penicillamine therapy for aggressive hepatitis triggered off the development of nephrotic syndrome. Histological findings revealed membranous glomerulonephritis. After the withdrawal of penicillamine therapy, the laboratory results returned to normal. The authors concluded that penicillamine should only be administered in conditions in which other means of therapy prove inefficient (i.e. Wilson's disease, cystinuria associated with calculi).
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PMID:Nephrotic syndrome induced by D-penicillamine therapy. 53 82

The authors report a case of chronic aggressive hepatitis associated with persisting HBs (Australia) antigenaemic nephrosis. The disease proved to be membranous glomerulonephritis. Immune fluorescence revealed granular type IgG, IgM, C3 and HBs antigen deposits along the glomerular basement membrane. The IgA deposit was partly linear, partly granular. Subepithelial deposits were noted by electron microscopy along the glomerular basement membrane. It is supposed that the deposition in the glomeruli of HBs antigen-antibody immune complex was responsible for the diffuse membraneous glomerulonephritis.
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PMID:Membraneous glomerulonephritis induced by HB (Australia) antigen-antibody complexes. 80 16

Authors describe a case of chronic aggressive hepatitis with persistent HBs (Australia) antigenaemia and nephrosis syndrome. The renal process microscbically appeared to be membranous glomerulonephritis. By immunofluorescent method antigen deposits IgG, IgM, C3 and HBs of the granular type have been revealed on the glomerular basal membranes. Deposits of the IgA were partially of granular, partially of linear type. Electronmicroscopically on the glomerular basale membrane subepithelial deposits were seen. The results of this study indicate that in the case reported diffuse membranus glomerulonephritis occurred due to HBs antigen-antibody immuno-deposits on the glomerular basal membrane.
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PMID:[Membranous glomerulonephritis caused by HBs (Australia) antigen-antibody complexes]. 85 50

This is a case report of a 35-year-old female who showed a relatively short clinical course of severe liver cirrhosis and proteinuria. On light microscopical studies of autopsy material, besides active postnecrotic type liver cirrhosis, typical membranous glomerulonephritis was found. Immunofluorescent study disclosed not only clustered HBsAg (hepatitis type B surface antigen) in occasional hepatic cells but also beaded granular type deposition of HBsAg, IgG, IgM, IgA and complement C3 along renal glomerular basement membrane (GBM). Electron microscopical study disclosed multiple particulated material in occasional inclusion bodies of hepatic cells and in subepithelial and subendothelial dense deposits along the GBM. Enzymatic immunoelectron microscopical study confirmed these particles especially along the GBM being HBsAg themselves. It was concluded that HBsAg-Ab (antibody) complex was the pathogenetic factor responsible for the glomerular change of this particular case. Although HBsAg and Ab were examined to be negative in serum throughout the patient's clinical course, the possibility of the presence of circulating HBsAg-Ab complex in serum was discussed.
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PMID:Membranous glomerulonephritis associated with active liver cirrhosis both involved by HBs antigen. 127 84

Retrospective analysis of necropsy findings of 705 woodchucks was performed to determine the prevalence and morphology of immune-mediated glomerulonephritis, its relationship to woodchuck hepatitis virus (WHV) infection, and the presence of major WHV antigens. Twenty-six woodchucks had glomerular lesions. Renal tissue of the 26 animals was evaluated histologically and immunohistochemically for immune-mediated glomerulonephritis. Of these 26 animals, immune-mediated glomerulonephritis was diagnosed in six, all of which were chronic WHV carriers. Membranous glomerulonephritis was identified in three animals, two of which also had mesangial proliferation. Host immunoglobulin was present within the mesangium and along capillary loops in all three. Woodchuck hepatitis virus core antigen (WHcAg) was present along capillary loops of two of these animals, one membranous and one mixed, and in the mesangium of all three. Woodchuck hepatitis virus surface antigen (WHsAg) deposition was similar to WHcAg deposition but was only present along capillaries in those animals with mixed nephritis. The remaining three animals had mesangial proliferation. WHsAg and host immunoglobulin deposition were predominately mesangial; WHcAg was not detected. Transmission electron microscopy showed thickening of the capillary loop basement membranes and subepithelial electron-dense deposits in animal one, and deposits in the mesangium in animal six.
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PMID:Immunopathology of glomerulonephritis associated with chronic woodchuck hepatitis virus infection in woodchucks (Marmota monax). 163 59

Sera from 54 children (mean age 5.8 years) with chronic hepatitis B virus (HBV) infection were investigated for the presence of immune complexes containing HBV proteins. Clinical diagnosis was established by histology and biochemical markers and included chronic persistent (36 cases) or chronic aggressive (seven) hepatitis, liver cirrhosis (six) and HBV-mediated membranous glomerulonephritis (five). Circulating immune complexes were precipitated with 2.5% polyethylene glycol and analysed by immune blot using monoclonal antibodies against S, pre-S2 glycopeptide, pre-S1 and HBe/c epitopes. All sera, including those from 11 healthy HBV-negative blood donors contained PEG-precipitable substances, but the amount of precipitate did not correlate with the presence or amount of HBV proteins. The great majority (36 out of 40) of HBeAg-positive patients contained HBs proteins in immune complexes, but no detectable HBe protein. The immune complexes usually contained more pre-S1 than the free HBsAg particles from the same patient. The precipitates of anti-HBe-positive patients rarely contained HBV proteins (two out of 14) and, if so, in low amounts. During follow up of six patients we found that high levels of HBs-containing immune complexes may be correlated with subsequent elimination of HBV. This elimination is possibly initiated by binding of anti-pre-S1 antibodies to HBV and HBs particles.
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PMID:Analysis of viral proteins in circulating immune complexes from chronic carriers of hepatitis B virus. 204 31

Hepatitis-B-associated glomerulonephritis (HBGN) is a distinct entity occurring frequently in hepatitis-B-prevalent areas of the world. The disease affects both adults and children who are chronic hepatitis-B-virus (HBV) carriers with or without a history of overt liver disease. The diagnosis is established by serologic evidence of HBV antigens/antibodies, presence of an immune complex glomerulonephritis, immunohistochemical localization of 1 or more HBV antigens, and pertinent clinical history, when available. In this study we present clinicopathologic and follow-up findings in 12 patients (7 children, 5 adults) with hepatitis-B-associated glomerulonephritis. Twelve patients provided 15 renal biopsies and 1 specimen of kidney tissue, obtained at autopsy; these were examined by light microscopy, electron microscopy, and immunohistochemical methods. Membranous glomerulonephritis (MGN) with or without mesangial proliferation was noted in 7 biopsies, mesangiocapillary (membranoproliferative) glomerulonephritis (MCGN) in 5 biopsies, and proliferative glomerulonephritis with or without membranous changes in 2 biopsies. Tubulointerstitial changes were minimal except in 3 adults, in whom they were attributable to arterionephrosclerosis. Ultrastructural findings included the presence of considerable amounts of focal or diffuse granular electron-dense deposits in the glomeruli, in the subepithelial, subendothelial, and mesangial locations, occasionally destroying or replacing the lamina densa of the basement membrane. Variable mesangial proliferation was also observed, with interposition, with focal irregular reduplication of the basement membranes and rare clusters of spherical particles, probably representing viral particles in the deposits. In addition, granular deposits along tubular basement membranes were seen in 1 case. The glomerular deposits stained for 2 or more immunoglobulins, the predominant one being IgG, and variably also for complement components (C3, C4 and C1q). Hepatitis B viral antigens (HBsAg, HBcAg, HBeAg) were demonstrated using acid elution techniques in the deposits in all biopsies where frozen tissue was available, singly or in a variety of combinations and intensities. There were deposits of IgG, C3, C1q, and HBsAg along the tubular basement membranes in 1 case. Follow-up biopsies in 2 cases, 2 and 5 years apart, showed a transformation from a diffuse MGN to MCGN with segmental membranous features. Follow-up biopsy after 3 years in the third patient, who went into clinical remission, revealed partially resolving glomerular lesions. Renal lesions secondary to chronic liver disease, parasitic diseases, certain tropical nephropathies, and lupus nephritis are some of the diseases that may morphologically resemble HBGN. Recognition and differentiation of HBGN from other entities may have significant prognostic and therapeutic implications.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Hepatitis-B-associated glomerulonephritis: pathology, pathogenesis, and clinical course. 214 48

The therapeutic effect of corticosteroid in hepatitis B virus (HBV) related membranous nephropathy was investigated in a 29-year-old chronic HBV carrier. Prednisolone (60 mg/day) was given for eight weeks and gradually reduced over the subsequent four months. In the renal biopsies taken before and after corticosteroid therapy, light microscopy revealed progression of sclerosis. Immunofluorescent staining showed glomerular capillary deposition of hepatitis B core antigen (HBcAg) by polyclonal antisera and hepatitis B e antigen (HBeAg) by monoclonal antibodies. Electron microscopy revealed 40-50 nm diameter virus-like particles in the glomeruli only from the biopsy performed after corticosteroid therapy. The serum concentrations of alanine aminotransferase, HBeAg, and HBV DNA increased with corticosteroid therapy suggesting active viral replication despite the absence of overt clinical hepatitis. Renal function did not improve and corticosteroid therapy was apparently not helpful in this patient. Our results conflict with the earlier notion that short-term corticosteroid does not interfere with a favorable outcome of the infection of the related renal disease.
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PMID:Replication of hepatitis B virus with corticosteroid therapy in hepatitis B virus related membranous nephropathy. 249 7

Eight children with chronic HBV hepatitis and glomerular disease were studied. There were seven males and one female, with ages between one and nine years old. Three had CPH and five CAH. All patients with CPH had membranous nephropathy, and those with CAH three had MNG. one membranoproliferative glomerulonephritis and one mesangial glomerulonephritis. Only six patients had moderate liver enlargement. In all, the diagnosis of HBV infection was performed by investigation of the etiology of their nephropathy. Liver function test showed signs of moderate necrobiosis with impaired biliary acid metabolism. All were HBsAg (+), antiHBc (+), six were antiHBe (+) and two were HBeAg (+). In one case renal deposit of HBsAg was found. Due to the frequent association of HBsAg and glomerulonephritis (GN) in children, an investigation of liver function is highly recommended in those patients with GN a HBV infection.
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PMID:[Chronic hepatitis caused by B virus and glomerulonephritis in children]. 265 15


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