Existence and significance of hepatitis B virus DNA in kidneys of IgA nephropathy

Wang, Niansong; Wu, Zhao‐Long; Zhang, Yue-E; lutan, liao

doi:10.3748/wjg.v11.i5.712

Cited by 31 publications

(19 citation statements)

References 25 publications

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“…Beaufils et al [12] undertook a systematic study of kidney in deceased AIDS patients using light and immunofluorescence microscopy and found that 7.75% showed diffuse mesangial IgA deposits. Wang et al [13] detected hepatitis B virus antigens by immunohistochemistry in renal tissues in 50 cases of IgAN; it was amazing to find that the positive rate of HBAg, HBsAg, and HBcAg was 82, 58 and 42% in glomeruli, respectively. However, the cellular mechanism mediated by virusin situ, which involved in the pathogenesis of IgAN, remains to be elucidated.…”

Section: Introductionmentioning

confidence: 99%

Synthetic Double-Stranded RNA Poly(I:C) Aggravates IgA Nephropathy by Triggering IgA Class Switching Recombination through the TLR3-BAFF Axis

He¹,

Peng²,

Wang³

et al. 2015

Am J Nephrol

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Background: Immunoglobulin class-switch recombination (CSR) is crucial for the expression of IgA, and it plays a vital role in the physiopathology of IgA nephropathy (IgAN). The aim of the study is to investigate the effect of polyriboinosinic:polyribocytidylic acid (poly(I:C)) in modulating toll-like receptor (TLR) 3-B-cell-activating factor belonging to the TNF family (BAFF) axis activation, which in turn promotes IgA CSR of IgAN patients and the IgAN rat model. Methods: Blood samples and tonsillar tissue specimens were obtained from 24 patients with IgAN and 26 patients with chronic tonsillitis as control. We also used the IgAN rat model to investigate the relationship between viral infection and IgA CSR. Results: Immunohistochemical and ELISA western blotting examination revealed that the TLR3/BAFF axis is activated in IgAN patients when compared to controls. Synthetic double-stranded RNA poly(I:C) stimulation upregulates the TACI/TLR3/TRIF/TRAF6 expression and promotes IgA CSR and BAFF productions in tonsil mononuclear cells. TLR3 or BAFF siRNA decreases IgA expression. In IgAN rat models, TLR3/BAFF signaling was highly activated. With 200 μg poly(I:C) sodium salt into the left naris for 8 weeks, IgA was highly deposited on glomeruli. It also revealed that poly(I:C) activated TLR3/BAFF axis and IgA CSR in vivo. Conclusion: These data points toward the role of TLR3/BAFF axis in IgA CSR of IgAN, and the data also support the notion that mucosal immunization with virus infection results in impaired mucosal and systemic IgA responses.

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Section: Introductionmentioning

confidence: 99%

Synthetic Double-Stranded RNA Poly(I:C) Aggravates IgA Nephropathy by Triggering IgA Class Switching Recombination through the TLR3-BAFF Axis

He¹,

Peng²,

Wang³

et al. 2015

Am J Nephrol

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“…3 The association of membranous nephropathy (MN) with HBs antigenemia has been well established in endemic regions, 4 although the etiological role of hepatitis B virus (HBV) antigenemia and HBV antigen deposition in IgAN remains speculative. 5,6 Researchers who suggest a strong association between IgAN and HBs antigenemia indicate that mesangial and subendothelial trapping of circulating immune complexes and subendothelial deposits results in the onset of IgA nephropathy with hepatitis B surface antigen (HBs-IgAN). [7][8][9] In case of HBV-associated membranous nephropathy (HBV-MN), unlike the prognosis in affected children, that in adults is not favorable.…”

Section: Introductionmentioning

confidence: 99%

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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“…Thus, cellular mechanism mediated by HBV originating from renal cells in situ might also be involved in the pathogenesis of IgAN. 10 In a retrospective study, Lai and coworkers reported 21 patients with hepatitis B surface antigenemia and IgAN; clinical presentations included macroscopic hematuria in four patients (19%), nephrotic syndrome in four patients (19%), microscopic hematuria in five patients (24%), asymptomatic proteinuria and hematuria in three patients (14%), and chronic kidney disease in one patient (5%); 19% of these patients developed progressive renal failure over a mean follow-up period of 40 months. 13 The role of HBV in the pathogenesis of different types of glomerulonephritis has yet to be clearly elucidated.…”

Section: Discussionmentioning

confidence: 99%

“…Various studies have shown that HBV infection might play an important role in both occurrence and progression of IgAN. [10][11][12] Wang et al 10 have shown that in addition to the humoral immune-mediated damage by HBV antigen-antibody immune complex, the renal tissues of some IgAN cases are directly infected with HBV and express HBV antigens in situ. Thus, cellular mechanism mediated by HBV originating from renal cells in situ might also be involved in the pathogenesis of IgAN.…”

Section: Discussionmentioning

confidence: 99%

Complete Remission of Hepatitis B Virus-Associated Nephrotic Syndrome from IgA Nephropathy Following Peginterferon Therapy

2012

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Hepatitis B virus (HBV) infection is a major cause of acute and chronic hepatitis, cirrhosis, and hepatocellular carcinoma. HBV has also been associated with various common and uncommon glomerular diseases, including IgA nephropathy (IgAN). We report a patient with chronic HBV infection who presented with atypical features of IgAN with management and long-term follow-up. Much of the data on the treatment of HBV-associated glomerular diseases come from patients with membranous nephropathy, whereas the information on treatment of other glomerulopathies remains largely anecdotal. To the best of our knowledge, treatment of an adult patient with HBV-associated nephrotic syndrome from IgAN with pegylated interferon has not been previously reported. Treatment with pegylated interferon alfa-2b in our patient resulted in complete clinical remission of the nephrotic syndrome as well as a dramatic decrease in HBV viral load. Patient continued to remain in clinical remission 5 years after treatment.

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Existence and significance of hepatitis B virus DNA in kidneys of IgA nephropathy

Cited by 31 publications

References 25 publications

Synthetic Double-Stranded RNA Poly(I:C) Aggravates IgA Nephropathy by Triggering IgA Class Switching Recombination through the TLR3-BAFF Axis

Synthetic Double-Stranded RNA Poly(I:C) Aggravates IgA Nephropathy by Triggering IgA Class Switching Recombination through the TLR3-BAFF Axis

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

Complete Remission of Hepatitis B Virus-Associated Nephrotic Syndrome from IgA Nephropathy Following Peginterferon Therapy

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