Libyan Journal of Medical Sciences

: 2022  |  Volume : 6  |  Issue : 1  |  Page : 1--6

Hepatitis B virus-related nephropathy: Review and update

Elmukhtar Habas1, Fahim Khan1, Khalifa Farfar2, Aml Habas3, Aisha Al Aldab1, Mehdi Errayes4, Eshrak Habas5, Ijaz Kamal4, Amnna Rayani3, Abdel-Naser Elzouki6,  
1 Internal Medicine, Hamad General Hospital, Doha-, Qatar
2 Alwakar Hospital, Alwakra, Alwakra-, Qatar
3 Department of Medical, Tripoli Medical Center, Tripoli-, Libya
4 Internal Medicine, Hamad General Hospital, Doha, Qatar
5 Tripoli Medical Center, Tripoli University, Tripoli, Libya
6 Hamad Medical Corporation

Correspondence Address:
Prof. Elmukhtar Habas
Internal Medicine, Hamad General Hospital, Doha


Viral-associated nephropathy indicates the direct pathogenic relationship between viral status and the development of nephropathy. Hepatitis B virus (HBV) infection (especially chronic) causes different glomerular, tubular, and interstitium damages. Membranous and membranoproliferative are the common HBV-associated nephropathy. The pathogenesis of HBV-associated nephropathy is primarily immune complex mediated; however, direct tubular damage may occur. The virus load and activity are essential risk factors in HBV-associated nephropathy development. Decreasing virus load and early treatment reduce the risk of HBV-associated nephropathy and may prevent the disease progression. Prevention of HBV infection by a worldwide vaccination program governed by the World Health Organization is the prime target to prevent hepatic and extrahepatic HBV-related complications. The authors searched the EMBASE, Google Scholar, Scopus, and Google search engines for articles about HBV-associated nephropathy using phrases, texts, and keywords such as chronic HBV infection and kidney, HBV-associated glomerulonephritis, nephritis in HBV infection, viral nephropathy, and HBV vaccination. Following multiple meetings and discussions, each author was given a section on the topic to search and summarize. Then, this narrative review manuscript has been written and revised to update HBV-associated nephropathy pathogenesis and treatment.

How to cite this article:
Habas E, Khan F, Farfar K, Habas A, Al Aldab A, Errayes M, Habas E, Kamal I, Rayani A, Elzouki AN. Hepatitis B virus-related nephropathy: Review and update.Libyan J Med Sci 2022;6:1-6

How to cite this URL:
Habas E, Khan F, Farfar K, Habas A, Al Aldab A, Errayes M, Habas E, Kamal I, Rayani A, Elzouki AN. Hepatitis B virus-related nephropathy: Review and update. Libyan J Med Sci [serial online] 2022 [cited 2023 Mar 30 ];6:1-6
Available from:

Full Text


Despite significant advancements in vaccination and antiviral therapy for hepatitis B virus (HBV), more than 30% of the global population shows serological evidence of a previous or present HBV infection.[1] The chronic kidney disease (CKD) global burden is increasing and will become the 5th most common cause of death worldwide by 2040,[2],[3] with the burden of CKD growing faster in low- and middle-income countries.[4] CKD is a condition affecting >10% of the general population, equating to >800 million people worldwide.[5] Another report in 2010 noted a prevalence range between 10.5% and 13.1%.[6] CKD has become one of the first five leading causes of death and morbidity in the 21st century. In 2017, an estimated 843.6 million people were diagnosed with CKD.[5] This increase is attributed to the increased number of patients with risk factors, such as hypertension, obesity, and diabetes mellitus.[7] The number of people having renal replacement therapy exceeds 2.5 million. It is projected to double to 5.4 million by 2030.[8] A forecasting analysis suggested that by 2040, the number of disability-adjusted life years due to CKD will be 52.5 million, up from about 26 million in 2016. Also, the number of deaths will rise to 3.1 million.[8] Although mortality in people with end-stage renal disease (ESRD) has decreased,[2] CKD has become the most significant cause of increased morbidity, hospitalization, and death worldwide.[9]

HBV prevalence differs according to continent and region. It was noted that it is unknown whether these prevalence differences impact the HBV-associated nephropathy syndrome or not.[10] HBV infection is one of the causes of kidney injuries that can proceed to CKD and may cause ESRD.[11] However, it was reported that the relationship is unclear enough between chronic HBV infection and the increased risk of CKD.[12] Chronic HBV-induced nephropathy is mostly immune complex mediated, but a direct injury to tubules and glomeruli occurs.[13]

The first described lesion associated with HBV infection is membranous glomerulonephritis (MGN), mainly due to Australian–antigen-containing immune complex deposition in the glomeruli.[14] Later, MGN in two children showed HBeAg with IgG and β1C deposits along the glomerular capillary wall. Other glomerular lesions were reported in HBV carriers, although the most common is MGN.[6] HBV-induced nephropathies such as membranoproliferative glomerulonephritis (MPGN) and polyarteritis nodosa (PAN) occur.[11]

 Chronic Hepatitis B Virus Infection-Associated Nephropathies

Chronic HBV cases are increasing progressively. It was estimated that >350 million HBV carriers worldwide, of whom about 6 million die annually due to HBV-associated liver disease.[10] In 2019, about 248 million persons were chronic HBV surface antigen (HBsAg) carriers worldwide.[15] Approximately 240 million individuals have detected HBsAg in their serum,[16] and 20%–30% of those in the inactive HBsAg carrier status can experience spontaneous reactivation of hepatitis B during follow-up.[10] HBV-nephropathy (HBV-GN) is one of the extrahepatic symptoms in patients with persistent HBV infection and nonsymptomatic HBV carriers.[17] In addition to the hepatic complications of chronic and acute HBV, extrahepatic involvement occurs in about 3%–5% of cases, of which 3%–5% may have renal disease, mainly the MGN.[18]

Serologic evidence of persistent HBV infection (HBsAg, HBeAg, or HB core antigen) and the presence of glomerular immune complex deposits are often required to diagnose HBV-GN. The common glomerular pathologies are MGN, MPGN, mesangial proliferative glomerulonephritis, minimal change disease, IgA nephropathy, lupus-associated nephritis, and focal segmental glomerulosclerosis [Table 1].[19]{Table 1}

 Membranous Glomerulonephritis

MGN was described firstly during the 19th century,[20] and then, Gilbert and Wiggelinkhuizen and others demonstrated that MGN has a strong relationship with chronic HBV infection, particularly in children.[21] MGN-associated HBV resolves spontaneously in children, typically in conjunction with the development of free anti-HBeAb in the circulation.[22] However, in adults, MGN cure is uncommon, and most MGNs tend to progress.[22]

MGN is a pathological condition characterized by the thickening of the glomerular basement membrane involving the whole glomerulus. As demonstrated by the presence of HBV DNA and hepatitis B antigen, MGN is typically associated with active viral replication. At the MGN diagnosis, liver enzyme levels may be normal or modestly increased. In almost all cases of MGN, the pathogenesis is mediated by autoantibodies directed against phospholipase A2 receptor or, more seldom, thrombospondin type-1 domain-containing 7A.[23],[24]

MGN is classified into primary and secondary MGNs. Primary MGN accounts for around 70% of MGN cases. The remaining third of the patients usually have secondary MGN. Secondary MGN has usually defined as underlying causes such as medications, cancer, autoimmune diseases, and viral infections such as hepatitis B and C. The clinical presentation of primary and secondary MGN is usually identical; however, the recognized feature of the primary disease is also present. Differentiation between the primary and secondary MGN is essential. It must be based not only on the patient's history and clinical symptoms but also on immunofluorescence and electron microscopy analysis of the renal biopsy and identifying the circulating antibodies. Furthermore, identifying the pathologic processes underlying secondary MGN is essential, as removal of the etiological causes may be followed by remission or cure of secondary MGN.

MGN is the most common cause of proteinuria and nephrotic syndrome.[25] MGN is the most common form of HBV-related nephropathy, occurring in 35% of chronic HCV-infected patients.[26] It was reported that HBV-related MGN histologic changes are challenging to differentiate from the idiopathic MGN because both types have subepithelial immune complex deposits on electron microscopy. However, the MGN-related HBV immune deposits consist of one or more of the three potential viral particles (HBsAg, HBcAg, or HBeAg).[27] Furthermore, the idiopathic MGN patients have circulating anti-phospholipase A2 receptor (anti-PLA2R) antibodies and IgG subtype in the glomerular basement membrane as IgG4;[28] whereas, in HBV-induced MGN, the IgG1 class is the main IgG subtype.[18] Another study reported that immunofluorescent staining and electron microscopy reveal granular IgG, C3, and some IgM staining in the subepithelial region within the glomerular basement membrane. Furthermore, the podocyte foot processes and viral particles in various locations within the glomerulus detected extensive effacements.[29] A minor percentage (<5%) of HBV-related MGN has positive anti-PLA2R;[23] however, another study reported 64% of HBV patients to have anti-PLA2R.[30] Hence, the subside of anti-PLA2R to differentiate between the HBV-related and idiopathic MGNs is not substantiated yet. Tubular reticular inclusions are frequently reported in HBV.[31] The presence of tubular reticular inclusions confirms the upregulation of the local interferon, making the idiopathic MGN unlikely. In adults, about 25%–35% of HBV-related MGNs progress to ESRD adults, while in children, ESRD develops in about <5%.[32]

Mild and nephrotic syndrome range proteinuria is the most common manifestation of HBV-related MGN in adults. Adults with HBV-associated MGN from places where HBV is not common are more likely than children who have a history of acute hepatitis. This might be related to intravenous drug consumption[33] or acquired immunodeficiency syndrome.[34] HBeAg has an essential pathogenetic role in a chronic HBV infection patient who has MGN. Most reported cases are among chronic HBV-infected children, but HBV-related MGNs were also observed in adults.[26],[35] HBV-related MGN course is endemic and is not benign even with active treatment, and has a slowly but persistently progressive clinical course in almost a third of adult patients.[27] After systemic HBeAg clearance, a kidney biopsy detected spontaneous improvement of MGN lesions in children.[36]

 Membranoproliferative Glomerulonephritis

HBV-associated MPGN is an immune complex-mediated glomerulopathy.[37] In chronic HBV infection, MPGN is characterized by circulating antigen–antibody complex deposition in the mesangial and subendothelial space. MPGN has been classified into three subtypes according to the locations of electron antigen–antibody complex dense deposits.[38] Types 1 and III occur in chronic HBV infection, but type II (dense deposit disease) was not reported in HBV-associated nephropathy.[39] The deposits are mainly IgG and C3.[40] HBeAg and HBsAg were implicated in MPGN-related HBV infection, although their exact role remains uncertain.[37] HBV-related MPGN is rarely due to mixed cryoglobulinemia compared to HCV infection.[41]

MPGN is the second most common nephropathy related to HBV carriers. It affects both adults and children. MPGN characterizes by basement membrane splitting and mesangial, subendothelial, and even subepithelial layers of the glomerulus deposits. IgG can only stick to HBsAg and deposits in the subendothelial space.[42] Chronic HBV carriers have both type 1 and type 3 MPGNs. It is marked by the nephritic syndrome with or without nephrotic range proteinuria and decreased levels of serum C, primarily because of the complement classic pathway activation manifesting by low serum C3 and C4.[27]

Mixed cryoglobulinemia is a cause of type 1 MPGN in HBV carriers. Most of these patients (75%) present with mostly type 3 cryoglobulinemia (polyclonal IgM and IgG) after 10 years of HBV infection. In contrast, type 2 cryoglobulinemia (monoclonal IgM and polyclonal IgG) is likely to happen with type 1 MPGN in people who have had chronic HCV infection for more than 10–15 years.[38] Patients with HBV who have cryoglobulinemia may develop nephrotic syndrome, acute kidney injury, and systemic vasculitis along with low C4 (92%) and low C3 (58%). While HBV does not move through the lymph system, the underlying mechanisms that stimulate B-cells to synthesize the cryoglobulin are unknown. Because of this new link between HBV and cryoglobulinemia, it is essential to rule out co-infection with hepatitis C as a cause of MPGN in HBV carriers. Up to 10% of patients worldwide have both viral infections, and the treatment will depend on which virus is causing the renal lesion.[18] HBV-MPGN has a poor prognosis in adults, with an increased mortality rate and ESRD development.[36]

 Mesangioproliferative Glomerulonephritis

Mesangioproliferative GN was reported with predominant mesangial IgA deposits and persistent hepatitis B surface antigenemia.[43] In IgA nephropathy, glomerular HBeAg deposits were not found in renal biopsies, but HBsAg mesangial deposits similar to the IgA immunostaining distribution were noticed in 40% and 21% of renal biopsies by polyclonal and monoclonal antibodies, respectively.[43],[44] Further studies reported a strong association between chronic HBV infection and mesangial IgA nephropathy.[45] Later, Bhimma et al. reported that 26% of the 23 studied children with HBV-associated glomerular disease other than MGN had mesangial proliferative GN.[11] Circulating immune complexes, particularly the large circulating immune complexes, are deposited principally in the mesangial regions and subendothelial space.[46] It is unclear whether IgA present in glomeruli has a specific anti-HBs antibody activity. Lai et al. demonstrated HBcAg by immune peroxidase within the nuclei of mesangial cells in patients with HBV-associated IgA nephropathy.[45] The association may be incidental as the prevalence of the HBsAg carrier state among patients with this lesion is much lower compared to those with MGN or MPGN.

 Polyarteritis Nodosa

HBV-associated PAN shares the same characteristic features as idiopathic PAN. Chronic HBV infection is sometimes accidentally associated with focal segmental glomerulosclerosis and minimal change nephropathy.[46] Chronic HBV infection is reported in approximately 15%–25% of PAN patients. HBV was the cause of up to 30% of PAN cases.[47] Global use of the hepatitis B vaccine has significantly reduced the HBV-PAN incidence, which is recently estimated to account for <8% of all PAN cases.[48]

HBV-associated PAN typically occurs within 4–6 months after the onset of HBV infection;[48] however, it may occur at any time during HBV infection clinical course.[49] HBV infection induces the deposition of antigen–antibody complexes in the medium-sized arteries.[50] The presence of HBV-associated disease is suggested by the findings of HBsAg, HBeAg, and HBV DNA (an indicator of viral replication) in the serum. The deposition of circulating antigen–antibody immune complexes in the medium-sized artery wall triggers downstream inflammatory processes.[17],[39] Renal disease is due to the local inflammatory process of medium-sized arteritis, leading to glomerular ischemia,[51] by a direct effect on the blood vessel wall,[49] and endothelial dysfunction that induces inflammation via the production of adhesion molecule and cytokine.[52] PAN causes different types of GN, including diffuse proliferative and membranous[53] and mesangial proliferative GNs.[54] The activity of HBV-associated PAN is not parallel to the degree of hepatitis, and the presenting symptoms are almost identical to idiopathic PAN. In small studies, there were more gastrointestinal manifestations, malignant hypertension, renal infarction, and orchiepididymitis reported in HBV-PAN than in idiopathic PAN.[49]

The standard PAN treatments, including steroids and cyclophosphamide, improve the disease activity control and prognosis. Nevertheless, these therapies can induce persistent HBV infection and delay the seroconvert of HBs-AB and HBeAg antibodies. Thus, antiviral medications are required in the treatment of these patients. Guillevin et al. studied therapeutic strategies, including steroids, antivirals, and plasma exchange (plasmapheresis), and they concluded that these regimens are not entirely successful in HBV-associated PAN.[55]

Other types of HBV-associated nephropathy are reported. HBV viral transcripts have been found in patients with IgA nephropathy and renal mesangial cells of patients with focal segmental glomerulosclerosis, implying that HBV could cause both disorders.[56] In anecdotal cases, antiviral medication resulted in glomerular disease remission, substantiating the putative causal involvement of HBV in a subset of IgA and focal segmental glomerulosclerosis patients. Furthermore, case reports of minimal change disease in children with HBV who achieved clinical remission only with antiviral medication suggest a new kidney lesion with possible linkage to persistent HBV viremia.[57]

 Treatment of Hepatitis B Virus-Related Nephropathy

The Food and Drug Administration approved different agents for HBV therapy for adults. The effect of these agents is to lower the serum level of HBV. Nucleoside/nucleotide analogs such as interferon-(standard interferon-2b and longer-acting peginterferon-2a) (lamivudine, adefovir, entecavir, tenofovir, and telbivudine) are approved in the USA. Emtricitabine is readily in use in Europe.

Kidney Disease Improving Global Outcomes recommends IFN or oral antiviral medicines containing either nucleotide (tenofovir and adefovir) or nucleoside (lamivudine, entecavir, and telbivudine) reverse transcription inhibitors for HBV patients with MGN.[58] Lamivudine (a cytidine analog) has been the most often utilized medication in treating hepatitis B-associated MGN, with initial remission of viremia and complete clearance of the MGN lesion in 75%–80% of patients. On the other hand, lamivudine is associated with a 20% annual resistance rate due to a somatic mutation of the HBV reverse transcription gene at the YMDD motif (tyrosine [Y], methionine [M], aspartate [D], and aspartate [D]) motif of RNA-dependent DNA polymerase. As a result, either entecavir or tenofovir is currently recommended as first-line therapy, as neither is associated with clinically significant acquired resistance.[59] Steroids alone or combined with other immune-suppressive drugs are an ineffective treatment and may increase the risk of virus replication. They may increase the risk of HBV viremia and insignificantly affect morbidity or mortality rates.[60]

The treatment of HBV-related MPGN with type 3 cryoglobulinemia differs from the treatment of HCV type 2 cryoglobulinemia in that it focuses on HBV viremia control rather than direct-acting antivirals. Rituximab, plasmapheresis, and cytotoxic therapy are rarely utilized,[59] because cryoglobulinemia rarely occurs with HBV infection.

Treatment with pegylated interferon alpha-2b is reported to be effective in complete clinical remission of the nephrotic syndrome and nephrotic syndrome cases induced by HBV infection. HBV viremia load was lowered in some reported cases of IgA nephropathy caused by HBV the interferon therapy. Furthermore, the patients were in clinical remission for the following 5 years.[61]

HBV vaccination reduces HBV MGN caused by horizontal virus transmission. Still, it has no effect on HBV MGN caused by vertical HBV acquisition, which remains a vital transmission vector in third-world countries.[62]


Research studies have been scarce about HBV-associated pathogenesis in the recent 5 years. HBV infection during the acute and chronic phases can affect the kidneys and lead to kidney function abnormality. The pathogenesis is primarily due to an immune-mediated mechanism; however, direct damage to the glomeruli and tubular cells may happen. Different histopathological lesions were detected by renal biopsy in HBV patients, although the common lesions are MGN and MPGN. Worldwide HBV vaccination to prevent HBV infection is the prim method to prevent HBV-linked hepatic and extrahepatic complications. It seems therapies targeting HBV load are the cornerstone of kidney involvement prevention rather than treatment; however, some case reports noted improvement in kidney involvement following virus load reduction. Further research projects are needed to evaluate HBV-associated GN occurrence rate and their response to the available therapies.

Financial support and sponsorship


Conflicts of interest

There are no conflicts of interest.


1European Association for The Study of The Liver. EASL clinical practice guidelines: Management of chronic hepatitis B virus infection. J Hepatol 2012;57:167-85.
2Li PK, Garcia-Garcia G, Lui SF, Andreoli S, Fung WW, Hradsky A, et al. Kidney health for everyone everywhere-from prevention to detection and equitable access to care. J Ren Care 2020;46:4-12.
3Foreman KJ, Marquez N, Dolgert A, Fukutaki K, Fullman N, McGaughey M, et al. Forecasting life expectancy, years of life lost, and all-cause and cause-specific mortality for 250 causes of death: Reference and alternative scenarios for 2016-40 for 195 countries and territories. Lancet 2018;392:2052-90.
4Stanifer JW, Muiru A, Jafar TH, Patel UD. Chronic kidney disease in low- and middle-income countries. Nephrol Dial Transplant 2016;31:868-74.
5Kovesdy CP. Epidemiology of chronic kidney disease: An update 2022. Kidney Int Suppl (2011) 2022;12:7-11.
6James MT, Hemmelgarn BR, Tonelli M. Early recognition and prevention of chronic kidney disease. Lancet 2010;375:1296-309.
7Couser WG, Remuzzi G, Mendis S, Tonelli M. The contribution of chronic kidney disease to the global burden of major noncommunicable diseases. Kidney Int. 2011;80:1258-70.
8Fraser SD, Roderick PJ. Kidney disease in the Global Burden of Disease Study 2017. Nat Rev Nephrol 2019;15:193-4.
9Vos T, Lim SS, Abbafati C, Abbas KM, Abbasi M, Abbasifard M, et al. Global burden of 369 diseases and injuries in 204 countries and territories, 1990-2019: A systematic analysis for the Global Burden of Disease Study 2019. Lancet 2020;396:1204-22.
10Tseng TC, Huang LR. Immunopathogenesis of hepatitis B virus. J Infect Dis 2017;216:S765-70.
11Bhimma R, Coovadia HM, Adhikari M. Hepatitis B virus-associated nephropathy in black South African children. Pediatr Nephrol 1998;12:479-84.
12Hong YS, Ryu S, Chang Y, Caínzos-Achirica M, Kwon MJ, Zhao D, et al. Hepatitis B virus infection and development of chronic kidney disease: A cohort study. BMC Nephrol 2018;19:353.
13Lai KN, Ho RT, Tam JS, Lai FM. Detection of hepatitis B virus DNA and RNA in kidneys of HBV related glomerulonephritis. Kidney Int 1996;50:1965-77.
14Combes B, Shorey J, Barrera A, Stastny P, Eigenbrodt EH, Hull AR, et al. Glomerulonephritis with deposition of Australia antigen-antibody complexes in glomerular basement membrane. Lancet 1971;2:234-7.
15Makhlouf NA, Morsy KH, Mahmoud AA. Hepatitis D virus infection among hepatitis B virus surface antigen positive individuals in Upper Egypt: Prevalence and clinical features. J Infect Public Health 2019;12:350-6.
16Schweitzer A, Horn J, Mikolajczyk RT, Krause G, Ott JJ. Estimations of worldwide prevalence of chronic hepatitis B virus infection: A systematic review of data published between 1965 and 2013. Lancet 2015;386:1546-55.
17Johnson RJ, Couser WG. Hepatitis B infection and renal disease: Clinical, immunopathogenetic and therapeutic considerations. Kidney Int 1990;37:663-76.
18Kupin WL. Viral-associated GN: Hepatitis B and other viral infections. CJASN 2017;12:1529-33.
19Zhang L, Meng H, Han X, Han C, Sun C, Ye F, et al. The relationship between HBV serum markers and the clinicopathological characteristics of hepatitis B virus-associated glomerulonephritis (HBV-GN) in the northeastern Chinese population. Virol J 2012;9:200.
20Brzosko WJ, Krawczyński K, Nazarewicz T, Morzycka M, Nowoslawski A. Glomerulonephritis associated with hepatitis-B surface antigen immune complexes in children. Lancet 1974;2:477-82.
21Gilbert RD, Wiggelinkhuizen J. The clinical course of hepatitis B virus-associated nephropathy. Pediatr Nephrol 1994;8:11-4. Bhimma R, Coovadia HM. Hepatitis B virus-associated nephropathy. Am J Nephrol 2004;24:198-211.
22Lai KN, Li PK, Lui SF, Au TC, Tam JS, Tong KL, et al. Membranous nephropathy related to hepatitis B virus in adults. N Engl J Med 1991;324:1457-63.
23Beck LH Jr., Bonegio RG, Lambeau G, Beck DM, Powel DW, Cummins TD, et al. M-type phospholipase A2 receptor as target antigen in idiopathic membranous nephropathy. N Engl J Med 2009;361:11-20.
24Tomas NM, Beck LH Jr., Meyer-Schwesinger C, Seitz-Polski B, Ma H, Zahner G, et al. Thrombospondin type-1 domain-containing 7A in idiopathic membranous nephropathy. N Engl J Med 2014;371:2277-87.
25Moroni G, Ponticelli C. Secondary membranous nephropathy. A narrative review. Front Med (Lausanne) 2020;7:611317.
26Lai KN, Lai FM, Chan KW, Chow CB, Tong KL, Vallance-Owen J. The clinico-pathological features of hepatitis B virus-associated glomerulonephritis. Q J Med 1987;63:323-33.
27Li P, Wei RB, Tang L, Wu J, Zhang XG, Chen XM. Clinical and pathological analysis of hepatitis B virus-related membranous nephropathy and idiopathic membranous nephropathy. Clin Nephrol 2012;78:456-64.
28Obrisca B, Ismail G, Jurubita R, Baston C, Andronesi A, Mircescu G. Antiphospholipase A2 receptor autoantibodies: A step forward in the management of primary membranous nephropathy. Biomed Res Int 2015;2015:249740.
29Chan TM. Hepatitis B and renal disease. Curr Hepat Rep 2010;9:99-105.
30Xie Q, Li Y, Xue J, Xiong Z, Wang L, Sun Z, et al. Renal phospholipase A2 receptor in hepatitis B virus-associated membranous nephropathy. Am J Nephrol 2015;41:345-53.
31Lee CJ, Suh KS, Kim KH, Chang YK, Na KR, Lee KW. The clinicopathologic significance of endothelial tubuloreticular inclusions in glomerular diseases. Ultrastruct Pathol 2013;37:386-94.
32Ozdamar SO, Gucer S, Tinaztepe K. Hepatitis-B virus associated nephropathies: A clinicopathological study in 14 children. Pediatr Nephrol 2003;18:23-8.
33Knieser MR, Jenis EH, Lowenthal DT, Bancroft WH, Burns W, Shalhoub R. Pathogenesis of renal disease associated with viral hepatitis. Arch Pathol 1974;97:193-200.
34Guerra IL, Abraham AA, Kimmel PL, Sabnis SG, Antonovych TT. Nephrotic syndrome associated with chronic persistent hepatitis B in an HIV antibody positive patient. Am J Kidney Dis 1987;10:385-8.
35Lai KN, Lai FM, Tam JS, Chow CB, Au TC. High prevalence of hepatitis B surface antigenaemia in nephrotic syndrome in Hong Kong. Ann Trop Paediatr 1989;9:45-8.
36Bhimma R, Coovadia HM. Hepatitis B virus-associated nephropathy. Am J Nephrol 2004;24:198-211.
37Takekoshi Y, Tochimaru H, Nagata Y, Itami N. Immunopathogenetic mechanisms of hepatitis B virus-related glomerulopathy. Kidney Int Suppl 1991;35:S34-9.
38Li SJ, Xu ST, Chen HP, Zhang MC, Xu F, Cheng SQ, et al. Clinical and morphologic spectrum of renal involvement in patients with HBV-associated cryoglobulinaemia. Nephrology (Carlton) 2017;22:449-55.
39Lai KN, Lai FM. Clinical features and natural history of hepatitis B virus-related glomerulopathy in adults. Kidney Int 1991;25 (Suppl):40-5.
40Abbas NA, Pitt MA, Green AT, Solomon LR. Successful treatment of hepatitis B virus (HBV)-associated membranoproliferative glomerulonephritis (MPGN) with alpha interferon. Nephrol Dial Transplant 1999;14:1272-5.
41Enríquez R, Sirvent AE, Andrada E, Escolano C, Rodríguez JC, Millán I, et al. Cryoglobulinemic glomerulonephritis in chronic hepatitis B infection. Ren Fail 2010;32:518-22.
42Venkataseshan VS, Lieberman K, Kim DU, Thung SN, Dikman S, D'Agati V, et al. Hepatitis-B-associated glomerulonephritis: Pathology, pathogenesis, and clinical course. Medicine (Baltimore) 1990;69:200-16.
43Nagy J, Bajtai G, Brasch H, Sule T, Ambrus M, Deak G, et al. The role of hepatitis N surface antigen in the pathogenesis of glomerulonephritis. Clin Nephrol 1979;12:109-16.
44Lai KN, Lai FM, Lo S, Ho CP, Chan KW. IgA nephropathy associated with hepatitis B virus antigenemia. Nephron 1987;47:141-3.
45Lai KN, Lai FM, Tam JS. IgA nephropathy associated with chronic hepatitis B virus infection in adults: The pathogenetic role of HBsAG. J Pathol 1989;157:321-7.
46Lai KN, Lai FM, Tam JS. Comparison of polyclonal and monoclonal antibodies in determination of glomerular deposits of hepatitis B virus antigens in hepatitis B virus-associated glomerulonephritides. Am J Clin Pathol 1989;92:159-65.
47Mahr A, Guillevin L, Poissonnet M, Aymé S. Prevalences of polyarteritis nodosa, microscopic polyangiitis, Wegener's granulomatosis, and Churg-Strauss syndrome in a French urban multiethnic population in 2000: A capture-recapture estimate. Arthritis Rheum 2004;51:92-9.
48Guillevin L, Lhote H, Cohen P, Sauvaget F, Jarrousse B, Lortholary O, et al. Polyarteritis nodosa related hepatitis B virus. A prospective study with long-term observation of 41 patients. Medicine (Baltimore) 1998;74:238.
49Trepo C, Guillevin L. Polyarteritis nodosa and extrahepatic manifestations of HBV infection: The case against autoimmune intervention in pathogenesis. J Autoimmun 2001;16:269-74.
50Sharma A, Sharma K. Hepatotropic viral infection associated systemic vasculitides-hepatitis B virus associated polyarteritis nodosa and hepatitis C virus associated cryoglobulinemic vasculitis. J Clin Exp Hepatol 2013;3:204-12.
51Gerber MA, Brodin A, Steinberg D, Vernace Y, Yang CP, Paronetto F. Periarteritis nodosa, Australia antigen and lymphatic leukaemia. N Engl J Med 1972;286:14-7.
52Colmegna I, Maldonado-Cocco JA. Polyarteritis nodosa revisited. Curr Rheumatol Rep 2005;7:288-96.
53Michalak T. Immune complexes of hepatitis B surface antigen in the pathogenesis of periarteritis nodosa. A study of seven necropsy cases. Am J Pathol 1978;90:619-32.
54Duffy J, Lidsky MD, Sharp JT, Davis JS, Person DA, Hollinger FB, et al. Polyarthritis, polyarteritis and hepatitis B. Medicine (Baltimore) 1976;55:19-37.
55Guillevin L, Lhote F, Sauvaget F, Deblois P, Rossi F, Levallois D, et al. Treatment of polyarteritis nodosa related to hepatitis B virus with interferon-alpha and plasma exchanges. Ann Rheum Dis 1994;53:334-7.
56Sun IO, Hong YA, Park HS, Choi SR, Chung BH, Park CW, et al. Clinical characteristics and treatment of patients with IgA nephropathy and hepatitis B surface antigen. Ren Fail 2013;35:446-51.
57Zhou TB, Jiang ZP. Is there an association of hepatitis B virus infection with minimal change disease of nephrotic syndrome? A clinical observational report. Ren Fail 2015;37:459-61.
58Kidney Disease: Improving Global Outcomes (KDIGO) Glomerulonephritis Work Group. KDIGO Clinical Practice Guideline for Glomerulonephritis. Kidney Int Suppl. 2012;2:139-274.
59Elewa U, Sandri AM, Kim WR, Fervenza FC. Treatment of hepatitis B virus-associated nephropathy. Nephron Clin Pract 2011;119:c41-9.
60Zheng XY, Wei RB, Tang L, Li P, Zheng XD. Meta-analysis of combined therapy for adult hepatitis B virus-associated glomerulonephritis. World J Gastroenterol 2012;18:821-32.
61Shah HH, Patel C, Jhaveri KD. Complete remission of hepatitis B virus-associated nephrotic syndrome from IgA nephropathy following peginterferon therapy. Ren Fail 2013;35:295-8.
62Liao MT, Chang MH, Lin FG, Tsai IJ, Chang YW, Tsau YK. Universal hepatitis B vaccination reduces childhood hepatitis B virus-associated membranous nephropathy. Pediatrics 2011;128:e600-4.