Improvement of hepatitis B-associated glomerulonephritis after antiviral combination therapy

Man, Robert A. de; Schalm, Solko W.; Heijden, A. J. van der; Kate, F. W. J. Ten; Wolff, Eva; Heijtink, R. A.

doi:10.1016/0168-8278(89)90036-6

Cited by 28 publications

(6 citation statements)

References 14 publications

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“…Although deposition of HBeAg in renal tissues by immunostainings could not be confirmed, excess HBeAg originated from patients with high HBV-DNA level might influence the development of HBV-associated nephropathy. As reported previously, antiviral treatments such as IFN [Garcia et al, 1985;Mizushima et al, 1987;de Man et al, 1989;Lisker-Melman et al, 1989;Wong et al, 1992;Conjeevaram et al, 1995;Lin, 1995;Bhimma et al, 2002a,b] or lamivudine [Connor et al, 2003;Filler et al, 2003;Okuse et al, 2006] were effective for the HBVassociated nephropathy in this study.…”

Section: Genetic Characteristics Of Hbv Strains In the Patients With supporting

confidence: 66%

Virological features of hepatitis B virus‐associated nephropathy in Japan

Kusakabe

Tanaka

Kurbanov

et al. 2007

Journal of Medical Virology

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Hepatitis B virus (HBV)-associated nephropathy is considered as an immune-mediated disorder which is dependent on interactions between viral, host, and environmental factors. But there are few reports that investigated the relationship between the development of HBV-associated nephropathy and HBV genotypes and the mutations. To clarify the relationship between nephropathy and HBV genotype in Japan, six male patients with HBV-associated nephropathy were examined. The complete genome sequences of HBV were determined directly and the specific mutations associated with the development of HBV-associated nephropathy were examined by comparison of the alignments along with consensus sequences [HBV/A1 (Aa), A2 (Ae), B1 (Bj), B2 (Ba), C1 (Cs) and C2 (Ce)] retrieved from international database. The mean age of the six patients was 33.5 years. HBeAg was found in all patients and serum HBV-DNA levels were relatively high. Histological findings of renal tissues indicated five cases of membranous nephropathy and one membranoproliferative glomerulonephritis. HBV genotypes from the six patients were two HBV/A1, two A2 and two C2, suggesting HBV/A was predominant. G1862T mutation was observed in the two HBV/A1 patients, resulting in the pre-core amino acid substitution with a switch from valine (Val) to phenylalanine (Phe). Only one patient had core deletions. It is concluded that HBV/A may be associated with membranous nephropathy, but little relationship between HBV gene mutations and the development of HBV-associated nephropathy was observed.

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Section: Genetic Characteristics Of Hbv Strains In the Patients With supporting

confidence: 66%

Virological features of hepatitis B virus‐associated nephropathy in Japan

Kusakabe

Tanaka

Kurbanov

et al. 2007

Journal of Medical Virology

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“…37 However, in HBVMN, antiviral treatment may be associated with resolution of proteinuria and HBeAg seroconversion, even when serum transaminases are normal. 6 Our patient had moderately increased transaminases when treatment was introduced. These increased prior to seroconversion, then rapidly declined.…”

Section: Discussionmentioning

confidence: 66%

“…Previous studies showed improvement with alfa interferon (IFN) therapy. [1][2][3][4][5][6][7][8] Lamivudine is a nucleoside analogue inhibitor of HBV DNA polymerase, which has advantages over IFN for HBV treatment, having less frequent side effects and oral route of administration. To our knowledge, this is the first reported case of HBV associated nephrotic syndrome treated with lamivudine therapy.…”

mentioning

confidence: 99%

HBV associated nephrotic syndrome: resolution with oral lamivudine

Connor

Rosenberg²,

Kennedy³

et al. 2003

Archives of Disease in Childhood

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A 6 year old boy presenting with a five month history of fever, lethargy, and anorexia, was found to have hepatitis B associated membranous glomerulonephropathy and nephrotic syndrome. After two months treatment with oral lamivudine, his proteinuria cleared and serum albumin and aminotransferases normalised, associated with disappearance of hepatitis B e antigen (HBeAg) and appearance of anti-HBeAg antibodies. After 12 months, without side effects, lamivudine was discontinued. He remains well 11 months off treatment. W orldwide, hepatitis B (HBV) infection is an important cause of nephrotic syndrome. The typical renal lesion is membranous glomerulonephropathy (HBVMN). Previous studies showed improvement with alfa interferon (IFN) therapy. [1][2][3][4][5][6][7][8] Lamivudine is a nucleoside analogue inhibitor of HBV DNA polymerase, which has advantages over IFN for HBV treatment, having less frequent side effects and oral route of administration. To our knowledge, this is the first reported case of HBV associated nephrotic syndrome treated with lamivudine therapy. CASE REPORTThe patient, a child of mixed race (mother white, father white/Filipino), migrated to Australia from South Africa at 2 1 ⁄2 years of age. Before leaving South Africa, he had received childhood vaccinations at a community clinic and sutures for a minor laceration at a local hospital. He presented at 6 years, 3 months of age with a five month history of recurrent fever, lethargy, and anorexia. There was no other significant past medical or family history. He looked well, with weight 19.5 kg (25th percentile) and height 110 cm (3-10th percentile). There was mild digital clubbing, leuconychia, and palmar erythema, but no other peripheral stigmata of chronic liver disease. He was normotensive. The abdomen was soft and non-tender. Borderline hepatomegaly was present (liver span 9 cm), but there was no splenomegaly, renal mass, ascites, or peripheral oedema. Physical examination was otherwise unremarkable.Persistent heavy proteinuria (urinary albumin/creatinine ratio 390 mg/mmol (normal <5)) and intermittent microscopic haematuria were noted. Serum albumin was persistently decreased at 24-26 g/l. Urea and creatinine were normal. Complements were reduced: C3 0.63 g/l (normal range 0.89-1.73) and CH50 25% (normal range 56-174). Renal and abdominal ultrasound was normal. Mild elevations of serum aminotransferases were noted: alanine aminotransferase (ALT) 77 U/l (normal range 17-63), aspartate aminotransferase (AST) 61 U/l (normal range 15-45). Bilirubin, γ glutamyl transferase, alkaline phosphatase, and coagulation were normal. Autoantibodies (antinuclear, antineutrophil cytoplasmic, and antiglomerular basement membrane) were negative and he was seronegative for Epstein-Barr and cytomegalovirus. HBV infection was confirmed with positive HBV surface antigen (HBsAg), HBV e antigen (HBeAg), and HBV core antibody. Antibodies to HBeAg and HBsAg were negative. His mother and four siblings were HBV seronegative.Renal biopsy (fig 1) showed stage 2 membranous ...

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“…[3][4][5][6][7][8][9][10] Although the natural history of the disease tends often to remission with preservation of renal function, there is considerable morbidity and significant mortality. 1,2 Various therapeutic approaches have been used for HBV-associated GN including corticosteroids, [11][12][13] adenine arabinoside, 14 thymic estracts, 14 acyclovir, 15 interferon (IFN), 1 and lamivudine. 1 Only anti-viral therapy (IFN or lamivudine) 1 proved to be effective in clearing HBV antigens and abrogating proteinuria.…”

Section: Introductionmentioning

confidence: 99%