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)

The most well-described renal disease associated with hepatitis B virus (HBV) infection is membranous glomerulonephritis; membranoproliferative glomerulonephritis is described much less frequently. The course of HBV-associated renal disease after liver transplantation has not been described to date. We present a 15-year-old girl with HBV-associated membranoproliferative glomerulonephritis and end-stage liver disease, in whom, after cadaver liver transplantation, clinical and histological resolution of renal disease was observed. Resolution was associated with diminution of circulating HBV surface antigen levels.
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PMID:Resolution of hepatitis B virus-related membranoproliferative glomerulonephritis after orthotopic liver transplantation. 858 18

In children with hepatitis B-associated membranous glomerulonephritis, the time of onset of the infection and the duration of the carrier state before diagnosis of the renal disease are always unknown. Moreover, follow-up is usually short. We report the unique observation of a French girl who was infected with hepatitis B virus by her mother who had acute hepatitis during the immediate postpartum period; the girl developed proteinuria at 6 years of age. The onset of the infection in the perinatal period, the mild liver abnormalities, and the absence of nephrotic syndrome did not justify any treatment. Spontaneous seroconversion to anti-HBe antibody positive occurred at 12 years of age. Proteinuria gradually diminished and was absent at 18 years. However, HBs antigenemia persists.
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PMID:Membranous nephropathy following perinatal transmission of hepatitis B virus infection--long-term follow-up study. 861 64

We studied direct and indirect methods of measuring membrane charge by detecting fixed anionic sites with polyethylenimine (PEI) on the glomerular basement membrane (GBM) and Alcian blue on red blood cell (RBC) membrane (ABRBC), respectively, in 40 children with nephrotic syndrome (NS). Size selectivity of the GBM was measured indirectly by fine analysis of urinary proteins with sodium dodecyl sulfate-polyacrylamide gel electrophoresis in 22 of these children. Correlation between ABRBC and PEI was strongest (r = 0.79; p = 0.0037) in 11 children with steroid-responsive NS (SRNS), moderate (r = 0.31) in 10 children with focal glomerulosclerosis (FGS), and absent in 14 children with hepatitis B antigen membranous nephropathy (MGN) and 5 with mesangioproliferative glomerulonephritis (MPGN). ABRBC and PEI were reduced in the group as a whole as compared with their controls (ABRBC: 44.53 +/- 9.81 vs 71.54 +/- 12.14, p < 0.05; PEI: 16.31 +/- 4.34 vs 33.3 +/- 1.09, p < 0.005). This reduction was greater in SRNS (26.35 +/- 7.15 p = 0.004) but was also detected in the remainder of the group taken together (52.31 +/- 26.07, p < 0.001). Excretion of glomerular proteins was restricted by size (< or = 80 kd) in SRNS but unrestricted (< or = 80 kd plus > 80 kd) in FGS, MGN, and MPGN. The main cause of proteinuria is likely to be depletion of negative charge on the GBM in SRNS, and distortion of capillary pore size in MGN and MPGN, with probable overlap of these mechanisms in each disease, especially in FGS. Basement membrane injury appears widespread in SRNS but confined to the kidney in MGN and MPGN.
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PMID:Direct and indirect tests of pore size and charge selectivity in nephrotic syndrome. 863 48

We report a 58-year-old woman with classical rheumatoid arthritis (RA) who developed a membranous glomerulonephritis (MGN). She had never been treated with gold or D-penicillamine; other connective tissue diseases as well as hepatitis B were excluded. We suggest that the responsible cause of MGN is RA.
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PMID:Membranous glomerulonephritis in rheumatoid arthritis unrelated to gold, D-penicillamine or other connective tissue disease. 885 74

Glomerular deposition of hepatitis B virus (HBV) antigens are observed in chronic HBsAg carriers with different glomerulonephritides yet the etiologic role of HBV remains uncertain. We examined the paraffin section of kidney biopsies from 40 chronic HBsAg carriers with membranous nephropathy (MGN), mesangiocapillary glomerulonephritis (MCGN) or IgA nephropathy (IgAN) for HBV DNA and HBV RNA using in situ hybridization (ISH). Glomerular HBV antigens were present in all biopsies by immunofluorescence. HBsAg or HBcAg mRNA was also studied in RNA extracted from frozen renal tissue using a two-step polymerase chain reaction (PCR) following reverse transcription (RT). HBcAg DNA was not easily detected with ISH alone, but was readily found in 31 biopsies (78%) following PCR. HBV DNA was detected mainly in the cytoplasm of proximal tubular epithelia but not in glomerular cells. HBsAg and/or HBcAg mRNA were detected by RT-PCR in extracted RNA from 13 biopsies (33%). The PCR findings were further confirmed by (a) Southern blot hybridization using a cloned HBV probe and (b) absence of PCR product following treating RNA with RNase or omitting the RT. It is plausible that HBV DNA in renal tubules represents endocytosis of HBV DNA in the urinary filtrate and the HBV RNA extracted from kidney biopsies could derive from infiltrating cells bearing HBV RNA. Hence, ISH with specific HBV core gene RNA probe was performed subsequently. HBcAg RNA, localized in the nuclei and cytoplasm of glomerular and tubular cells, was detected in 56%, 20%, and 36% of renal biopsies in chronic HBsAg carriers with MGN, MCGN, and IgAN, respectively. Our findings indicate the presence of viral transcription in glomerular cells and renal tubular epithelia, supporting an etiological role of HBV in some chronic HBsAg carriers who develop coexisting glomerulonephritides.
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PMID:Detection of hepatitis B virus DNA and RNA in kidneys of HBV related glomerulonephritis. 894 80

Since 1973, 15 patients, consisting of 8 boys and 7 girls, were diagnosed as having membranous nephropathy (MN). The average age at detection was 8.2 years (2-14 years). The presenting symptom was edema in 1, pyrexia in 1 and upper respiratory infection in 1 case, in the all other cases, abnormal urinalysis was detected by the school or chance urinalysis. Surface antigen of hepatitis B virus (HBs) was positive in 6 patients and negative in 9. Anti-nuclear antibody (ANA) was positive in 3 and negative in 11. In one patient, ANA was not tested. One patient who was negative for ANA was diagnosed as having SLE 4 years later. At the last follow-up, 10 patients continued to have urinary abnormalities. Among these was one case positive for HBs antigen who went into end-stage renal failure. In the other 14 patients, the serum creatinine level was below 1.4 mg/dl. All patients showed a normal mesangium or mild mesangial proliferation. The patient diagnosed as having SLE. 4 years later showed mesangial deposits at the first renal biopsy. In our experience, most patients with MN were detected by the school or chance urinalysis and six of the these had positive HBs antigen. Lupus nephritis must be ruled out in making a diagnosis of idiopathic MN.
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PMID:[Membranous nephropathy in Japanese children]. 901 80

To evaluate the therapeutic effect of recombinant human alpha-interferon (alpha-IFN) on hepatitis B virus associated glomerulonephritis (HBV-GN) and the relationship between the seroconversion of viral antigens and the change of proteinuria, the hepatitis B viral markers and urinary protein were monitored during alpha-IFN treatment in 8 male adult patients who (1) were positive in serum HBsAg and HBeAg, (2) had chronic hepatitis, (3) had persistent proteinuria > 1 g/day, and (4) showed glomerulonephritis on kidney biopsy. alpha-IFN was given at a dose of 3 million units, subcutaneously, three times a week for 6 months. Kidney biopsy specimens showed membranoproliferative glomerulonephritis (MPGN) in 4 patients, mesangial proliferative glomerulonephritis (MesPGN) in 2, and membranous glomerulonephritis (MGN) in 2 patients. Seven of the 8 patients received a 6-month course of alpha-IFN therapy; 1 patient with MGN quitted therapy 2 months after the initial dose because of side effects. In 5 of the 7 patients who received a 6-month therapy, serum HBeAg disappeared, and anti-HBe appeared during the therapy. In 2 of these 5 patients, HBeAg reappeared, in 1 during alpha-IFN therapy and in 1 9 months after the last dose of alpha-IFN. The hepatitis B viral markers of the patient who received a 2-month therapy did not change. HBs antigenemia persisted in all patients. In all 4 patients with MPGN, serum HBeAg was transiently or persistently converted to negative, but the proteinuria persisted. Both patients with MesPGN showed remission of proteinuria; however, only 1 patient had seroconversion of HBeAg. In 2 patients with MGN, proteinuria persisted. In conclusion, alpha-IFN at the doses given was not effective in MPGN type of HBV-GN. Improvement of proteinuria was achieved in MesPGN patients without disappearance of HBs antigenemia which is the finding against the possible role of HBsAg in the pathogenesis of this type of HBV-GN.
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PMID:Treatment of hepatitis B virus associated glomerulonephritis with recombinant human alpha interferon. 909 40

Human immunodeficiency virus-associated nephropathy (HIVAN), characterized by heavy proteinuria, rapidly progressive renal failure, "collapsing" glomerulopathy, and tubulointerstitial abnormalities, is the most common finding in HIV-infected patients undergoing a renal biopsy and predominantly affects blacks. We describe the clinical features and renal pathologic findings of 12 intravenous drug users (IVDUs) coinfected with HIV and hepatitis C virus (HCV) who were selected for renal biopsy because they presented with features different from typical HIVAN, including hypertension, microscopic hematuria, and cryoglobulinemia. There were seven black and five Hispanic patients. Eleven patients had immune complex glomerulonephritis (ICGN); one had glomerulosclerosis with immune complex deposits. Ten individuals had evidence of past hepatitis B viral infection, but none had persistent hepatitis B surface antigenemia. No other underlying cause for immune complex glomerulonephritis was identified. Renal biopsy showed membranoproliferative glomerulonephritis in five patients, mesangial proliferative glomerulonephritis in five, membranous nephropathy in one, and "collapsing" glomerulopathy with immune complex deposits in one. Hepatitis C virus RNA was detected by reverse transcription-polymerase chain reaction (RT-PCR) in the renal tissue and/or serum of nine of the 11 patients tested, and also in the renal biopsy tissue of four of eight patients with clinical and pathologic features of typical HIVAN without immunofluorescence evidence of immune complex deposits. One patient presented with renal failure, five patients developed end-stage renal disease (ESRD) requiring hemodialysis (mean time, 6.5 months), and six had stable renal function after a mean follow-up of 29.1 months (range, 2 to 72 months). Liver function abnormalities were present in seven of the 12 individuals, including four of the six patients who developed renal failure. These findings indicate that in some patients coinfected with HIV and HCV, the development of ICGN may dominate the clinical course of the disease. The occurrence of ICGN among black patients at risk for HIVAN may be related to the relatively high prevalence of HCV infection among IVDUs in this group.
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PMID:Immune complex glomerulonephritis in patients coinfected with human immunodeficiency virus and hepatitis C virus. 910 39

To elucidate the questions of why not all patients with hepatitis B virus (HBV) infection develop HBV membranous nephropathy (HBVMN), we first measured serum HBe circulating immune complex (CIC) during the acute nephrotic phase of HBVMN and in HBV carriers. We found that the level of HBe CIC was low in the HBVMN patients and absent either in HBsAg+/HBeAg+ patients without HBVMN or HBsAg+/HBeAg- asymptomatic carriers. Second, we needed to characterize the cellular immune response to HBV in patients with HBVMN. However, lack of a suitable autologous effector/target cell system makes a precise study of HBVMN pathogenesis difficult. In the present study, we established a model system by using autologous HBcAg-expressing Epstein-Barr-virus-immortalized lymphoblastoid cell lines (LCL) as stimulator/target cells. Both proliferative response after stimulation with HBcAg and cytotoxic activity against autologous HBcAg-expressing LCL of the peripheral blood T cells obtained from the HBVMN patients and HBsAg carriers could be measured. Using autologous HBcAg-expressing LCL as stimulator/target cells for the study of HBcAg-specific cytotoxic T lymphocytes, we found that HBVMN patients had lower cytotoxic activity than did both HBV carriers and HBsAg-/HBsAb+, HBeAg-/HBeAb+ children. From the in vitro cytokine production study of peripheral blood T cells after stimulation with HBcAg, we found that T-helper-cell-1-related IL-2 and IFN-gamma productions were very low in HBVMN patients but T-helper-cell-2-related IL-10 production was higher in HBsAg+/HBeAg+ patients with HBVMN than in those without HBVMN. Based on these findings, we conclude that HBVMN children seem to have an inadequate cellular immune response to HBcAg.
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PMID:Defect of cell-mediated immune response against hepatitis B virus: an indication for pathogenesis of hepatitis-B-virus-associated membranous nephropathy. 920 Apr 9

We report the case of a patient with acquired immunodeficiency syndrome (AIDS) who developed nephrotic syndrome and progressive renal failure mimicking human immunodeficiency virus (HIV)-associated focal segmental glomerulosclerosis (FSGS) who required initiation of hemodialysis and was found on renal biopsy to have membranous nephropathy. Hepatitis B and C serologies were negative. Although she required hemodialysis, she was treated with prednisone and experienced a progressive decline in her serum creatinine from 10.1 mg/dL to 1.9 mg/dL, which permitted the discontinuation of hemodialysis. After she abruptly discontinued prednisone, her creatinine level increased to 4.8 mg/dL, and she experienced marked worsening of her nephrotic syndrome. Resumption of prednisone resulted in normalization of serum creatinine and reduction in urine protein excretion. No adverse effects of prednisone occurred during this time. She remains off of hemodialysis for 1 year with a serum creatinine level of 1.0 mg/dL and urine protein excretion of 0.4 g/d. Although most patients with HIV infection, nephrotic-range proteinuria, and renal failure have FSGS, a minority may have membranous nephropathy. Although typically not a steroid-responsive lesion in the setting of advanced renal failure, membranous nephropathy may be a highly steroid-responsive lesion in the HIV-infected patient, and treatment may help avert the need for dialysis in a patient population that generally has a poor outcome on dialysis.
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PMID:AIDS-associated membranous nephropathy with advanced renal failure: response to prednisone. 921 10


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