Viral nephropathy

Lai, Agnes Yuen Kwan; Lai, Kar Neng

doi:10.1038/ncpneph0166

Cited by 83 publications

(77 citation statements)

References 56 publications

(28 reference statements)

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“…In case of HBV-MN, remission of proteinuria was associated with seroconversion to anti-HBeAg. 17,18 In this study, although seroconversion to anti-HBeAg occurred in all patients receiving anti-viral therapy, the slope of renal function decline and urinary protein excretion did not differ between patients with and without anti-viral therapy. Thus, anti-viral therapy did not appear to benefit patients with HBs-IgAN in our study.…”

Section: Discussionmentioning

confidence: 95%

Clinical Characteristics and Treatment of Patients with IgA Nephropathy and Hepatitis B Surface Antigen

et al. 2013

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Background: The aim of this study is to investigate the clinical characteristics and our experience of treating patients with IgA nephropathy (IgAN) and IgA nephropathy with hepatitis B surface antigen (HBs-IgAN). Methods: From 1996 to 2011, biopsy-proven IgAN was diagnosed in 477 patients and 22 (4.6%) had hepatitis B surface antigen (HBsAg). Of these, we included 360 patients who had more than 6-month follow-up period, and compared clinical characteristics and renal function decline between the patients with IgAN and HBs-IgAN. Results: Of 360 patients, 22 were classified as HBs-IgAN. There were no differences in the clinical characteristics and renal function decline between idiopathic IgAN and HBs-IgAN (-0.01 vs. -0.17 mL/min per 1.73 m 2 /month, p ¼ 0.319). Of 22 patients with HBs-IgAN, nine had hepatitis B virus (HBV) replication marker (RM), of which six were treated with anti-viral agents. However, there were no differences in renal function decline and urinary protein excretion between patients who did or did not receive anti-viral therapy. Five patients with HBs-IgAN received corticosteroid therapy. Of these, three without HBV RM and one with HBV RM who received entecavir did not exhibit active viral replication, whereas the other patients with HBV RM experienced viral replication after lamivudine was discontinued. Conclusion: There were no differences in the clinical characteristics and prognosis between the patients with IgAN and HBs-IgAN. Further, there were no differences in renal function decline and urinary protein excretion between patients with and without anti-viral therapy. Anti-viral therapy may be considered for treating patients with HBs-IgAN receiving immunosuppressants according to HBV RM.

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Section: Discussionmentioning

confidence: 95%

Clinical Characteristics and Treatment of Patients with IgA Nephropathy and Hepatitis B Surface Antigen

et al. 2013

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“…Viral infections often cause the onset or worsening of glomerulonephritis (Lai and Lai 2006). Glomerular mesangial cells are involved in the immune and inflammatory reactions in the kidney by producing a variety of functional molecules.…”

mentioning

confidence: 99%

Melanoma Differentiation-Associated Gene 5 Regulates the Expression of a Chemokine CXCL10 in Human Mesangial Cells: Implications for Chronic Inflammatory Renal Diseases

Imaizumi

Aizawa-Yashiro

Tsuruga

et al. 2012

Tohoku J. Exp. Med.

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Mesangial cells play an important role in inflammatory reactions in kidney. Although viral infections often trigger the worsening of chronic inflammatory renal diseases, the mechanisms are largely unknown. Melanoma differentiation-associated gene 5 (MDA5) is a member of RNA helicase family with a conserved Asp-Glu-x-His (DExH) box. In the present study, we examined the effect of polyinosinic-polycytidylic acid (poly IC), an authentic double-stranded RNA (dsRNA) that mimics viral dsRNAs, on MDA5 expression using primary culture of human mesangial cells. The cells were simply treated or transfected with poly IC; the former procedure is a model of cells exposed to viral dsRNA released from dying cells, and the latter is a model of entry of RNA virus into the cytoplasm. Expression levels of MDA5 mRNA in mesangial cells were increased about 70-100 fold in response to either treatment or transfection with poly IC. MDA5 protein expression was significantly induced as well. RNA interference experiments revealed that poly IC treatment induced MDA5 expression via Toll-like receptor 3 (TLR3) and interferon (IFN)-β, and that poly IC trasnfection induced MDA5 expression via another DExH box RNA helicase, retinoic acid-inducible gene-I (RIG-I), and IFN-β. Moreover, MDA5 induced by poly IC, in turn, increased the expression of a chemokine CXCL10. In addition, immunohistochemical staining demonstrated a high level of MDA5 expression in glomeruli, mainly in mesangial cells, of patients with severe lupus nephritis or proteinuric IgA nephropathy. MDA5 may be involved not only in physiological antiviral reactions but also in chronic inflammation in glomerular mesangial cells.

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“…1 Viral infections activate systemic antiviral immunity, which may contribute to disease flares of glomerulonephritis by enhancing autoantibody production, immune complex formation, or by systemic interferon (IFN) release. 2 In fact, rapid production of type I IFN is a central element of antiviral immunity because type I IFNs inhibit viral replication in the infected cells and have pleiotrophic immunomodulatory effects on macrophages, T cells, and natural killer cells.…”

mentioning

confidence: 99%

Viral RNA Induces Type I Interferon-Dependent Cytokine Release and Cell Death in Mesangial Cells via Melanoma-Differentiation-Associated Gene-5

Flür¹,

Allam²,

Zecher³

et al. 2009

The American Journal of Pathology

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Viral nephropathy

Cited by 83 publications

References 56 publications

Clinical Characteristics and Treatment of Patients with IgA Nephropathy and Hepatitis B Surface Antigen

Clinical Characteristics and Treatment of Patients with IgA Nephropathy and Hepatitis B Surface Antigen

Melanoma Differentiation-Associated Gene 5 Regulates the Expression of a Chemokine CXCL10 in Human Mesangial Cells: Implications for Chronic Inflammatory Renal Diseases

Viral RNA Induces Type I Interferon-Dependent Cytokine Release and Cell Death in Mesangial Cells via Melanoma-Differentiation-Associated Gene-5

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