Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0019163 (hepatitis B)
38,309 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Hepatitis B virus (HBV) has been reported in association with the nephrotic syndrome from different parts of the world, but its role as a cause of the pathological findings of nephrotic syndrome is still controversial. We report seven nephrotic children with positive hepatitis B markers in which members of their families were also positive for the markers but without clinical, renal or hepatic involvement. Four showed haematuria at onset and three developed hypertension later in the course of the disease. Only two were responsive to steroid therapy. Renal biopsy was performed in four, of whom three showed membranous nephropathy and the other showed mesangioproliferative glomerulonephritis. Four patients developed end-stage renal disease. We conclude that in our environment HBV, when detected in children with nephrotic syndrome, should not be considered as a chance finding, but may have a definite role in its pathogenesis. Moreover, the prognosis of HBV-associated nephrotic syndrome appears poor.
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PMID:Hepatitis B surface antigen associated nephrotic syndrome. 246 Nov 51

Of 61 boys and girls with relapsing or steroid-resistant nephrotic syndrome admitted for renal biopsy, 22 had persistent hepatitis B virus surface antigenaemia despite normal liver function and an absence of previous transfusion. The prevalence of hepatitis B virus surface antigenaemia amongst nephrotic patients is significantly higher than that of the general population. Membranous nephropathy remains the commonest glomerulopathy associated with hepatitis B virus antigenaemia, and boys predominate.
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PMID:High prevalence of hepatitis B surface antigenaemia in nephrotic syndrome in Hong Kong. 247 44

A 9-year-old boy with hepatitis B-associated glomerulonephritis and nephrotic syndrome underwent antiviral combination therapy including interferon and acyclovir. Pretreatment evaluation showed that active hepatitis B virus replication with HBsAg, HBeAg, HBV-DNA and DNA-polymerase had occurred for a period of at least 4 years. Signs of liver disease were minimal; serum amino transferases were normal and liver histology showed chronic persistent hepatitis with positive HBcAg, HBeAg and HBsAg immunofluorescence. A kidney biopsy revealed membranous glomerulonephritis with deposition of HBcAg, HBeAg, IgG, C3, C1q and, on electron microscopy, virus-like particles. After 8 weeks of therapy, active viral replication ceased, HBe seroconversion occurred and the nephrotic syndrome disappeared. One year after treatment, the boy was asymptomatic. No viral markers could be detected in the kidney, but low-grade membranous glomerulonephritis persisted with deposition of C1q, IgG and C3, but not HBeAg, HBsAg or HBcAg. Liver histology showed a minimal aspecific portal infiltrate with weak membrane-bound HBsAg immunofluorescence; no HBcAg could be detected. For patients with active viral replication and deposition of HBc, HBe immune complexes in the kidney, antiviral therapy can be beneficial, even in the absence of active liver disease.
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PMID:Improvement of hepatitis B-associated glomerulonephritis after antiviral combination therapy. 247 23

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

Immunoelectron microscopy was used to localize membrane attack complex (MAC) and hepatitis B e (HBe) antigen in renal tissue specimens from a total of 9 patients with membranous nephropathy (MN); 6 with MN associated with a hepatitis B virus (HBV) infection, 2 with idiopathic MN, and 1 with lupus nephritis. All the patients were proteinuric, and 2 patients were classified as stage I-II, 6 as stage II, and 1 as stage IV. MAC, along with IgG and C3, was distributed within the subepithelial electron dense deposits in all the stages. MAC was also stained in the striated membranous structures within the glomerular basement membrane and mesangial matrix of some patients. In HBV-associated MN, HBe antigen was localized in the subepithelial electron dense deposits of 5 patients, while it was absent from the subepithelial deposits in a patient that was sero-positive for hepatitis B s antigen but negative for HBe antigen. This patient also lacked MAC deposition in these loci. These results suggest that MAC is associated with the formation of subepithelial deposits and proteinuria in MN. In HBV-associated MN, HBe antigen-antibody immune complex makes up the subepithelial deposits and is likely to activate the terminal components of complement in situ.
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PMID:Immunoelectron microscopic localization of membrane attack complex and hepatitis B e antigen in membranous nephropathy. 249 20

Eighty-two consecutive Caucasian adults (52 males, 30 females, aged 17-86 years) with membranous glomerulonephritis were prospectively evaluated for possible aetiological factors 1-4 weeks after renal biopsy. Presumed causes were identified in 17 patients (21%) as follows: drugs in five (D-penicillamine 3, captopril 1, fenoprofen 1); malignancy in four; chronic thyroiditis in three; systemic lupus erythematosus (SLE) in two; secondary syphilis in one; hepatitis B virus (HBV) infection in one and non-insulin-dependent diabetes mellitus in one patient. Except for age (patients with secondary membranous glomerulonephritis were older), clinical presentation and histological stage distribution did not differ between the secondary and the primary groups. Ten out of the 17 patients with secondary membranous glomerulonephritis (59%) achieved complete clinical remission within 12 months. The incidence of associated conditions in adults with membranous glomerulonephritis in this study corresponds with that reported in the few previous series. Although membranous glomerulonephritis is deemed to be idiopathic in most cases, it seems warranted to search for medication, malignancy, SLE, HBV infection, syphilis and thyroiditis as possible aetiological factors. Further evaluation should be orientated by the clinical context. An improved outcome of membranous glomerulonephritis may be expected insofar as the underlying condition is controlled.
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PMID:Aetiology of membranous glomerulonephritis: a prospective study of 82 adult patients. 251 87

In an attempt to find a parameter for the differentiation of membranous nephropathy with hepatitis B surface antigenemia (HBVMN) and other types of nephrotic syndrome (NS) in HBsAg (+) carriers, we measured the urinary neopterin in 20 HBVMN patients, other types of NS in HBsAg (+) carriers, asymptomatic HBsAg (+) carriers and HBsAg (-) controls, during the active nephrotic phase and in remission. The urinary neopterin excretion was found to be significantly elevated only in the HBVMN during NS or heavy proteinuria. It progressively decreased and corresponded with the amount of proteinuria. In patients with deteriorated renal function, initially, urinary neopterin excretion was significantly higher than in others and it remained significantly elevated during the follow-up period. In vitro when a patient's mononuclear cells were stimulated with lymphoblastoid cell line, the release of neopterin content in supernatant was increased during the acute phase. There was a significant correlation between supernatant and urinary neopterin level. These results suggest that urinary neopterin may be a new biochemical marker for the differential diagnosis of HBVMN and may be used to monitor the course of HBVMN and serve as a prognostic indicator. However, the specificity is not clear.
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PMID:Urinary neopterin as a new biochemical marker for the monitoring of disease activity and prognosis in membranous nephropathy associated with hepatitis B surface antigenemia. 251 33

In an attempt to clarify the relationship between hepatitis B virus (HBV) infection and glomerulonephritis (GN), and to explore the significance and possible mechanisms of HBV deposition in kidney, renal biopsy specimens obtained from 69 HBV carriers with various forms of GN and 69 age-, sex-, and renal histology-matched controls were studied with 4-layer PAP immunoperoxidase and indirect immunofluorescence techniques using monoclonal antibodies to HBV surface (HBsAg), core (HBcAg) and e antigen (HBeAg). The 3 HBV associated antigens were detected in the kidney in 18/18 patients with membranous nephropathy and in 21/26 (80.8%) patients with lupus nephritis regardless of whether HBV antigenemia was present or not. In certain types of primary GN, including IgA nephropathy, mesangial proliferative GN and membrano-proliferative GN, HBsAg in the kidney was more common in patients with HBs antigenemia than in those without it (49.1% vs 26.4%, P less than 0.05). No significant difference was observed between patients with and without HBV antigenemia in terms of HBcAg or HBeAg deposition in kidney. Immunopathological studies showed granular deposition of HBV antigens in exactly the same pattern as that of Ig(s) and complement components, and the characteristics of HBV deposition in the kidney were closely correlated with the extent of immune deposits. We conclude that the deposition of HBV-associated antigens in the kidney is often non-specific, although HBsAg is more commonly seen in some HBsAg carriers with GN.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Is there a hepatitis B virus-associated glomerulonephritis? Identification of HBsAG, HBcAG and HBeAG in kidney with monoclonal antibodies. 251 65

To assess the pathogenic significance of hepatitis B virus (HBV) in glomerulonephritis (GN), 98 patients with histopathologically proven glomerulonephropathies were screened for HBV markers, complement components and levels of circulating immune complexes (CICs); and renal biopsies from 31 of them were examined for the presence of hepatitis B surface antigen (HBsAg), and its location, by immunoperoxidase staining. The HBsAg positive rate in the patients (who came from a population with 10% HBsAg positivity) ranged from 51.9% in minimum change nephrotic syndrome (MCNS) to 81.8% in patients with proliferative glomerulonephritis (PGN). Whereas 24.5% of the cases were positive for HBsAg only, 10.2% had anti-HBcIgM with HBsAg, 13.3% had HBeAg with HBsAg and 9.2% had HBsAg, HBeAg and anti-HBcIgM. Complement component C3 levels were decreased in all groups of GN studied, but C4 levels varied. CIC levels were significantly increased (p less than 0.01) only in HBsAg-positive MCNS, focal glomerulosclerosis (FGS) and membranous glomerulonephritis (MGN). Of the 31 renal biopsies examined for the deposition of HBsAg, 4 (12.9%) were found to be positive for HBsAg in situ; 64.5% of biopsied patients were seropositive for HBsAg and 77.4% had CICs. All the four in-situ HBsAg-positive cases were seropositive for HBsAg, HBeAg and anti-HBcIgM with significantly high CIC levels (p less than 0.01). HBsAg deposition was intracytoplasmic in the mesangial cells of the glomeruli, in the glomerular basement membrane or in the tubules, or in a combination of these sites.
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PMID:Serum and tissue positivity for hepatitis B virus markers in histopathologically proven glomerulonephropathies. 254 53

A case of hepatitis B virus (HBV)-associated membranous nephropathy (MN) is presented in an 18-year-old Korean male, whose renal disease had begun 9 years previously. He was positive for hepatitis B surface antigen (HBsAg), hepatitis B e antigen (HBeAg) and antibody to hepatitis B core antigen (anti-HBc) in the serum. By immunofluorescence, HBeAg staining was noted in glomerular deposits in association with IgG, C3 and Clq, while neither HBsAg nor HBcAg was found in the glomerular deposits. The presence of glomerular HBeAg staining by FITC-monoclonal anti-HBe F(ab')2 fragments has been reported before, but never in non-Japanese patients. The demonstration of HBeAg in both the glomerular deposits and serum in this case supports the causal relationship of HBeAg and HBV-associated MN.
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PMID:Hepatitis B e antigen-associated membranous nephropathy. 267 64


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