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Wiese J, Derian NA, Turki M, Joshi T, Alsanani A, Satoskar A. Rapidly Progressive Glomerulonephritis Associated With IgA Nephropathy and C3 Deposits in a Patient With Chronic Hepatitis B. Cureus 2024; 16:e70619. [PMID: 39483559 PMCID: PMC11526628 DOI: 10.7759/cureus.70619] [Citation(s) in RCA: 0] [Impact Index Per Article: 0] [Reference Citation Analysis] [Abstract] [Key Words] [Track Full Text] [Figures] [Journal Information] [Subscribe] [Scholar Register] [Accepted: 09/25/2024] [Indexed: 11/03/2024] Open
Abstract
Hepatitis B-associated glomerulonephritis (GN) has been recognized for decades. However, only a few cases of IgA nephropathy (IgAN) in a setting of rapidly progressive glomerulonephritis (RPGN) associated with chronic hepatitis B virus (HBV) have been described. Herein, we report the case of a 42-year-old Asian female with a past medical history significant for chronic HBV on entecavir, hypertension, chronic kidney disease, and newly diagnosed breast cancer, who underwent elective bilateral mastectomy and breast augmentation. Post-operatively, she developed non-oliguric acute kidney injury and proteinuria. Renal biopsy revealed active focal crescentic and necrotizing GN with IgA and C3 deposits. Systemic autoimmune-associated and other infection-related GN were ruled out. IgAN in a setting of RPGN associated with chronic HBV was suspected.
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Affiliation(s)
- Jennifer Wiese
- Internal Medicine, Marshall University Joan C. Edwards School of Medicine, Huntington, USA
| | - Nayiri A Derian
- Internal Medicine, Marshall University Joan C. Edwards School of Medicine, Huntington, USA
| | - M'hamed Turki
- Gastroenterology, Marshall University Joan C. Edwards School of Medicine, Huntington, USA
| | - Tejas Joshi
- Gastroenterology and Hepatology, Marshall University Joan C. Edwards School of Medicine, Huntington, USA
| | - Ahlim Alsanani
- Nephrology, Marshall University Joan C. Edwards School of Medicine, Huntington, USA
| | - Anjali Satoskar
- Pathology, The Ohio State University College of Medicine, Columbus, USA
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Hoxha E, von Haxthausen F, Wiech T, Stahl RAK. Membranous nephropathy-one morphologic pattern with different diseases. Pflugers Arch 2017; 469:989-996. [PMID: 28555350 DOI: 10.1007/s00424-017-2000-4] [Citation(s) in RCA: 13] [Impact Index Per Article: 1.6] [Reference Citation Analysis] [Abstract] [Key Words] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Received: 04/25/2017] [Revised: 05/14/2017] [Accepted: 05/16/2017] [Indexed: 01/05/2023]
Abstract
Since the discovery of the phospholipase A2 receptor 1 (PLA2R1) and thrombospondin type-1 domain-containing 7A (THSD7A) as endogenous antigens involved in the development of membranous nephropathy (MN) in over 80% of adult patients, substantial progress in the diagnosis, prognosis, and therapy of MN has been made. In most cases of patients with MN, it is now possible to specifically define the responsible pathogenic mechanisms of disease and make a diagnosis even without a renal biopsy. Moreover, the presence of antibodies in the blood and the detection of the antigens in renal biopsies allow the definite diagnosis without the morphologic uncertainties, which now still apply for only about 20% of all renal biopsies showing MN. The discovery that the expression of THSD7A in malignant tumors might serve as the site of primary antigen recognition for the immune system to start MN might lead to a better understanding of not only tumor-associated MN, which accounts for up to 10% of all patients with MN, but also of the pathomechanisms relevant for MN development in general.
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Affiliation(s)
- Elion Hoxha
- III. Medizinische Klinik, Universitätsklinikum Hamburg-Eppendorf, Hamburg, Germany.,SFB 1192, Universitätsklinikum Hamburg-Eppendorf, Martinistrasse 52, 20246, Hamburg, Germany
| | | | - Thorsten Wiech
- SFB 1192, Universitätsklinikum Hamburg-Eppendorf, Martinistrasse 52, 20246, Hamburg, Germany.,Sektion Nephropathologie, Institut für Pathologie, Universitätsklinikum Hamburg-Eppendorf, Hamburg, Germany
| | - Rolf A K Stahl
- SFB 1192, Universitätsklinikum Hamburg-Eppendorf, Martinistrasse 52, 20246, Hamburg, Germany.
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4
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Dupuy JM, Dulac O, Dupuy C, Alagille D, Michalak T, Nowoslawski A. Severe Hyporegenerative Viral Hepatitis in Children. Proc R Soc Med 2016. [DOI: 10.1177/003591577707000404] [Citation(s) in RCA: 3] [Impact Index Per Article: 0.3] [Reference Citation Analysis] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Indexed: 12/13/2022]
Affiliation(s)
| | - O Dulac
- Hôpital d'Enfants, Bicêtre, France
| | | | | | - T Michalak
- National Institute of Hygiene, Warsaw, Poland
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Pugh RNH, Bell DR, Gilles HM. Malumfashi Endemic Diseases Research Project, XV. ANNALS OF TROPICAL MEDICINE AND PARASITOLOGY 2016. [DOI: 10.1080/00034983.1980.11687393] [Citation(s) in RCA: 26] [Impact Index Per Article: 2.9] [Reference Citation Analysis] [Track Full Text] [Subscribe] [Scholar Register] [Indexed: 12/28/2022]
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Mareddy AS, Rangaswamy D, Vankalakunti M, Attur RP, Nagaraju SP, Koti N. Immune mediated crescentic MPGN secondary to HBV infection: A rare presentation for a common infection. Australas Med J 2016; 9:12-6. [PMID: 26913086 DOI: 10.4066/amj.2015.2568] [Citation(s) in RCA: 0] [Impact Index Per Article: 0] [Reference Citation Analysis] [Abstract] [Key Words] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Indexed: 11/09/2022]
Abstract
Hepatitis B virus (HBV) infection presenting as crescentic glomerulonephritis in the absence of cryoglobulinemia is an extremely rare phenomenon. We report a case of a 44-year-old male with HBV infection, who underwent kidney biopsy for rapidly progressive renal failure and nephrotic range proteinuria. Histopathological evaluation of the kidney biopsy was consistent with immune complex mediated crescentic membranoproliferative glomerulonephritis (MPGN). The patient achieved complete renal and virological remission with steroids, plasmapheresis and antiviral therapy. This case report summarises the importance of early initiation of immunosuppression and plasmapheresis under antiviral coverage for improved clinical outcomes.
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Affiliation(s)
| | - Dharshan Rangaswamy
- Department of Nephrology, Kasturba Medical College, Manipal University, Mangalore, India
| | | | - Ravindra Prabhu Attur
- Department of Nephrology, Kasturba Medical College, Manipal University, Mangalore, India
| | | | - Neeraja Koti
- Department of Medicine, Kasturba Medical College, Manipal University, Mangalore, India
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Sarin SK, Kumar M, Lau GK, Abbas Z, Chan HLY, Chen CJ, Chen DS, Chen HL, Chen PJ, Chien RN, Dokmeci AK, Gane E, Hou JL, Jafri W, Jia J, Kim JH, Lai CL, Lee HC, Lim SG, Liu CJ, Locarnini S, Al Mahtab M, Mohamed R, Omata M, Park J, Piratvisuth T, Sharma BC, Sollano J, Wang FS, Wei L, Yuen MF, Zheng SS, Kao JH. Asian-Pacific clinical practice guidelines on the management of hepatitis B: a 2015 update. Hepatol Int 2016; 10:1-98. [PMID: 26563120 PMCID: PMC4722087 DOI: 10.1007/s12072-015-9675-4] [Citation(s) in RCA: 1879] [Impact Index Per Article: 208.8] [Reference Citation Analysis] [Abstract] [Key Words] [MESH Headings] [Track Full Text] [Download PDF] [Figures] [Journal Information] [Submit a Manuscript] [Subscribe] [Scholar Register] [Received: 05/20/2015] [Accepted: 09/14/2015] [Indexed: 02/06/2023]
Abstract
Worldwide, some 240 million people have chronic hepatitis B virus (HBV), with the highest rates of infection in Africa and Asia. Our understanding of the natural history of HBV infection and the potential for therapy of the resultant disease is continuously improving. New data have become available since the previous APASL guidelines for management of HBV infection were published in 2012. The objective of this manuscript is to update the recommendations for the optimal management of chronic HBV infection. The 2015 guidelines were developed by a panel of Asian experts chosen by the APASL. The clinical practice guidelines are based on evidence from existing publications or, if evidence was unavailable, on the experts' personal experience and opinion after deliberations. Manuscripts and abstracts of important meetings published through January 2015 have been evaluated. This guideline covers the full spectrum of care of patients infected with hepatitis B, including new terminology, natural history, screening, vaccination, counseling, diagnosis, assessment of the stage of liver disease, the indications, timing, choice and duration of single or combination of antiviral drugs, screening for HCC, management in special situations like childhood, pregnancy, coinfections, renal impairment and pre- and post-liver transplant, and policy guidelines. However, areas of uncertainty still exist, and clinicians, patients, and public health authorities must therefore continue to make choices on the basis of the evolving evidence. The final clinical practice guidelines and recommendations are presented here, along with the relevant background information.
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Affiliation(s)
- S K Sarin
- Department of Hepatology, Institute of Liver and Biliary Sciences, New Delhi, India.
| | - M Kumar
- Department of Hepatology, Institute of Liver and Biliary Sciences, New Delhi, India
| | - G K Lau
- Division of Gastroenterology and Hepatology, Humanity and Health Medical Centre, Hong Kong SAR, China
- The Institute of Translational Hepatology, Beijing, China
| | - Z Abbas
- Department of Hepatogastroenterlogy, Sindh Institute of Urology and Transplantation, Karachi, Pakistan
| | - H L Y Chan
- Institute of Digestive Disease, The Chinese University of Hong Kong, Hong Kong, China
| | - C J Chen
- Genomics Research Center, Academia Sinica, National Taiwan University, Taipei, Taiwan
| | - D S Chen
- Department of Internal Medicine, National Taiwan University College of Medicine, Taipei, Taiwan
| | - H L Chen
- Graduate Institute of Clinical Medicine, National Taiwan University College of Medicine, Taipei, Taiwan
| | - P J Chen
- Department of Internal Medicine, National Taiwan University Hospital, Taipei, Taiwan
| | - R N Chien
- Liver Research Unit, Chang Gung Memorial Hospital and University, Chilung, Taiwan
| | - A K Dokmeci
- Department of Gastroenterology, Ankara University School of Medicine, Ankara, Turkey
| | - Ed Gane
- New Zealand Liver Transplant Unit, Auckland City Hospital, Auckland, New Zealand
| | - J L Hou
- Department of Infectious Diseases and Hepatology Unit, Nanfang Hospital, Guangzhou, China
| | - W Jafri
- Department of Medicine, Aga Khan University, Karachi, Pakistan
| | - J Jia
- Beijing Friendship Hospital, Capital Medical University, Beijing, China
| | | | - C L Lai
- Department of Medicine, University of Hong Kong, Hong Kong, China
| | - H C Lee
- Internal Medicine Asan Medical Center, Seoul, Korea
| | - S G Lim
- Division of Gastroenterology and Hepatology, National University Health System, Singapore, Singapore
| | - C J Liu
- Graduate Institute of Clinical Medicine, National Taiwan University College of Medicine, Taipei, Taiwan
| | - S Locarnini
- Research and Molecular Development, Victorian Infectious Diseases Reference Laboratory, Melbourne, Australia
| | - M Al Mahtab
- Bangabandhu Sheikh Mujib Medical University, Dhaka, Bangladesh
| | - R Mohamed
- Department of Medicine, Faculty of Medicine, University Malaya, Kuala Lumpur, Malaysia
| | - M Omata
- Yamanashi Hospitals (Central and Kita) Organization, 1-1-1 Fujimi, Kofu-shi, Yamanashi, 400-8506, Japan
| | - J Park
- Department of Internal Medicine, Institute of Gastroenterology, Yonsei University College of Medicine, Seoul, Korea
| | - T Piratvisuth
- NKC Institute of Gastroenterology and Hepatology, Prince of Songkla University, Songkhla, Thailand
| | - B C Sharma
- Department of Gastroenterology, G.B. Pant Hospital, New Delhi, India
| | - J Sollano
- Department of Medicine, University of Santo Tomas, Manila, Philippines
| | - F S Wang
- Treatment and Research Center for Infectious Diseases, Beijing 302 Hospital, Beijing, China
| | - L Wei
- Peking University Hepatology Institute, Beijing, China
| | - M F Yuen
- Division of Gastroenterology and Hepatology, Department of Medicine, University of Hong Kong, Pofulam, Hong Kong
| | - S S Zheng
- Department of Hepatobiliary and Pancreatic Surgery, Collaborative Innovation Center for Diagnosis and Treatment of Infectious Diseases, Key Laboratory of Combined Multi-organ Transplantation, Ministry of Public Health, First Affiliated Hospital, Zhejiang University School of Medicine, Hangzhou, 310003, Zhejiang Province, China
| | - J H Kao
- Graduate Institute of Clinical Medicine and Hepatitis Research Center, National Taiwan University College of Medicine, National Taiwan University Hospital, Taipei, Taiwan
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Abstract
Viral infections associate temporally with the onset of many glomerular diseases, particularly in children. In other cases of glomerulonephritis, when infection is clinically silent, viral syndromes can still be implicated as a trigger. However, strong evidence for viral causality in most glomerular disease is still lacking. While numerous case reports in children document the occurrence of specific forms of glomerular disease after seroconversion to a wide range of viruses, relatively few reports provide pathologic evidence of viral infection associated with glomerular lesions on kidney biopsy. Strong associations between hepatitis viruses and glomerular injury have been acknowledged in adults, but hepatitis C virus appears not to be an etiology in children. In the context of treating glomerular diseases, when diagnosed, the treatment of hepatitis B virus, cytomegalovirus and human immunodeficiency virus in children with membranoproliferative, membranous and collapsing glomerulopathy plays an important role. Otherwise, there is no evidence suggesting that the identification of a viral infection in a child with glomerulopathy should change the management of the infection or the glomerulonephritis. Therefore, additional research into this topic is very much needed.
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Qi X, Wang JY, Mao RC, Zhang JM. Impact of nucleos(t)ide analogues on the estimated glomerular filtration rate in patients with chronic hepatitis B: a prospective cohort study in China. J Viral Hepat 2015; 22:46-54. [PMID: 25402626 DOI: 10.1111/jvh.12229] [Citation(s) in RCA: 21] [Impact Index Per Article: 2.1] [Reference Citation Analysis] [Abstract] [Key Words] [Track Full Text] [Journal Information] [Submit a Manuscript] [Subscribe] [Scholar Register] [Received: 10/20/2013] [Accepted: 12/12/2013] [Indexed: 01/09/2023]
Abstract
Chronic hepatitis B therapy with nucleos(t)ide analogues, particularly tenofovir or adefovir, may affect renal function. To date, there has not been a head-to-head controlled study to assess estimated glomerular filtration rate (eGFR) fluctuations in nucleos(t)ide-treated CHB patients. We aimed to evaluate the long-term effects of nucleos(t)ide on eGFR in Chinese patients with chronic hepatitis B. This prospective cohort study included 275 patients. Patient subgroups included those treated with lamivudine (n = 50), adefovir (n = 60), telbivudine (n = 68) and entecavir (n = 61); untreated patients (n = 36) served as control. After an average follow-up duration of 23 months, eGFR calculated by Cockcroft-Gault and Modification of Diet in Renal Disease formulas increased by 18.35 mL/min and 19.34 mL/min (P < 0.0001) in the telbivudine group, respectively, and decreased by 10.95 mL/min and 12.17 mL/min (P = 0.0001) in the adefovir group, respectively. Even if renal function was normal or mildly impaired at baseline, eGFR increased significantly more in the telbivudine group than in the other groups (P < 0.001). More patients in the adefovir group (23%) had a ≥20% decrease in eGFR than the other groups (P < 0.0001). More patients in the telbivudine group (31%) had a ≥20% increase in eGFR than the other groups (P < 0.0001). In conclusion, prolonged telbivudine therapy resulted in improved eGFR, while adefovir therapy was associated with decreased eGFR. Lamivudine and entecavir therapy did not significantly influence eGFR.
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Affiliation(s)
- X Qi
- Department of Infectious Diseases, Huashan Hospital, Fudan University, Shanghai, China; Key laboratory of Medical Molecular Virology of the Ministries of Education and Health (MOH&MOE), Fudan University, Shanghai, China; Department of Hepatitis Diseases, Shanghai Public Health Clinical Center, Fudan University, Shanghai, China
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Du W, Zheng Z, Han S, Ma S, Chen S. HBV reactivation in an occult HBV infection patient treated with prednisone for nephrotic syndrome: case report and literature review. BMC Infect Dis 2013; 13:394. [PMID: 23977980 PMCID: PMC3765334 DOI: 10.1186/1471-2334-13-394] [Citation(s) in RCA: 10] [Impact Index Per Article: 0.8] [Reference Citation Analysis] [Abstract] [Track Full Text] [Download PDF] [Figures] [Journal Information] [Subscribe] [Scholar Register] [Received: 05/28/2013] [Accepted: 08/21/2013] [Indexed: 01/05/2023] Open
Abstract
Background Reactivation of hepatitis B virus (HBV), characterized by increased levels of serum HBV DNA, abnormal liver function and hepatic failure, is a frequent complication of immunosuppressive therapy and chemotherapy in patients with HBV infection. However, reactivation of occult HBV infection with immunosuppressive therapy or chemotherapy is rare. Case presentation A 77-year-old man was diagnosed with nephrotic syndrome and IgM nephropathy with unclear pathogenesis. Liver function was normal, HBV-related serum markers were negative and HBV DNA titer was below the upper limits of normal. Two months following the start of prednisone therapy for his nephrotic syndrome, laboratory tests revealed a substantial increase in serum transaminase levels (ALT: 490 IU/L; AST: 149 IU/L) and an elevation of HBV DNA level (3.42×106 copies/ml). We tested stored kidney tissue for HBsAg and HBcAg using immunohistochemistry and found the sample to be HBcAg positive, allowing us to confirm the etiology of nephropathy as an occult HBV infection. The cause of the hepatitis was thought to be HBV reactivation, so we immediately administered lamivudine. One month after the initiation of daily lamivudine treatment, laboratory tests revealed that serum levels of transaminases had improved (ALT: 35 IU/L; AST: 17 IU/L). Patient examination one year later showed that HBeAg had decreased with a concomitant increase of HBeAb, the quantity of HBV DNA was undetectable, and liver function and renal function had stabilized. Conclusion This is the first report describing HBV reactivation in an occult HBV infection patient treated with oral prednisone for nephrotic syndrome. HBV-associated antigen should be regularly tested for in patients with unknown etiological glomerulonephritis in areas with high HBV viral popular and even in those with no clinical evidence for diagnosis of HBV.
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Affiliation(s)
- Wenjun Du
- Department of Liver Disease, Jinan Infectious Disease Hospital, Shandong University School of Medicine, Jinan 250021, China
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Li X, Huang A, Zhou P, Dang X, Mo S, Yi Z, He Q. Differences in Tissue Expression of HBV Markers in Children with HBV-Associated Glomerulonephritis. Ren Fail 2011; 33:885-91. [DOI: 10.3109/0886022x.2011.605979] [Citation(s) in RCA: 1] [Impact Index Per Article: 0.1] [Reference Citation Analysis] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Indexed: 11/13/2022] Open
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Elewa U, Sandri AM, Kim WR, Fervenza FC. Treatment of hepatitis B virus-associated nephropathy. Nephron Clin Pract 2011; 119:c41-9; discussion c49. [PMID: 21677438 DOI: 10.1159/000324652] [Citation(s) in RCA: 38] [Impact Index Per Article: 2.7] [Reference Citation Analysis] [Abstract] [Journal Information] [Subscribe] [Scholar Register] [Indexed: 01/28/2023] Open
Abstract
Epidemiological studies have shown a relationship between hepatitis B virus (HBV) infection and development of proteinuria in some patients (most commonly children), with a predominance for male gender and histological findings of membranous nephropathy on renal biopsy. The presence of immune complexes in the kidney suggests an immune complex basis for the disease, but a direct relation between HBV and membranous nephropathy (or other types of glomerular diseases) remains to be proven. Clearance of HBV antigens, either spontaneous or following antiviral treatments results in improvement in proteinuria. Thus, prompt recognition and specific antiviral treatment are critical in managing patients with HBV and renal involvement. The present review focuses on treatment of HBV with special emphasis given to antiviral therapies, its complications, and dosing in patients with HBV-associated kidney disease.
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Affiliation(s)
- Usama Elewa
- New Kasr Al-Aini Teaching Hospital, Cairo University, Egypt
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Xu G, Huang T. Hepatitis B virus-associated glomerular nephritis in East Asia: progress and challenges. Eur J Intern Med 2011; 22:161-6. [PMID: 21402246 DOI: 10.1016/j.ejim.2010.11.005] [Citation(s) in RCA: 14] [Impact Index Per Article: 1.0] [Reference Citation Analysis] [Abstract] [MESH Headings] [Track Full Text] [Journal Information] [Submit a Manuscript] [Subscribe] [Scholar Register] [Received: 08/18/2010] [Revised: 10/18/2010] [Accepted: 11/16/2010] [Indexed: 12/30/2022]
Abstract
BACKGROUND Hepatitis B virus-associated glomerular nephritis (HBV-GN) is the most common secondary glomerulonephritis in East Asia. Part of the patients developed to renal insufficiency within 10 years, which cause a great burden for patients' family and society. METHODS We reviewed basic and clinical research work in China, Japan, Korea, and Mongolia, eastern part of Asia. Comparisons between data from East Asia and those from other regions were made. RESULTS The genetic variations conferring susceptibility to HBV-GN and disease progression as well as the pathogenic role in HBV-GN progression were investigated. Clinical features of HBV-GN in East Asia were different from that of other regions in the world. Clinical trials showed that treatment with anti-viral agents was effective to promote the disease remission. CONCLUSION HBV-GN remains a great challenge to East Asian nephrologists. In-depth basic studies and multi-centered clinical trials are needed in the future.
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Affiliation(s)
- Gaosi Xu
- Department of Nephrology, Second Affiliated Hospital, Nanchang University, China.
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14
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Ren J, Wang L, Chen Z, Ma ZM, Zhu HG, Yang DL, Li XY, Wang BI, Fei J, Wang ZG, Wen YM. Gene expression profile of transgenic mouse kidney reveals pathogenesis of hepatitis B virus associated nephropathy. J Med Virol 2006; 78:551-60. [PMID: 16555286 DOI: 10.1002/jmv.20575] [Citation(s) in RCA: 36] [Impact Index Per Article: 1.9] [Reference Citation Analysis] [Abstract] [MESH Headings] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Indexed: 12/18/2022]
Abstract
Hepatitis B virus (HBV)-associated nephritis has been reported worldwide. Immune complex deposition has been accepted as its pathogenesis, although the association between the presence of local HBV DNA and viral antigen and the development of nephritis remains controversial. To understand better the roles played by HBV protein expression in the kidney, the global gene expression profile was studied in the kidney tissue of a lineage of HBV transgenic mouse (#59). The mice expressed HBsAg in serum, and HBsAg and HBcAg in liver and kidney, but without virus replication. Full-length HBV genome (adr subtype, C genotype) isolated from a chronic HBV carrier was used to establish the transgenic mice #59. Similarly manipulated mice that did not express HBV viral antigens served as controls. Southern blotting, hybridization with HBV probe, and immuno-histochemical staining were used to study HBV gene expression. mRNA extracted from the kidney tissue was analyzed using Affymetrix microarrays. HBsAg and HBcAg were located mainly in the cytoplasm of tubular epithelium. Altogether 520 genes were "up-regulated" more than twofold and 76 genes "down-regulated" more than twofold in the kidney. The complement activation, blood coagulation, and acute-phase response genes were markedly "up-regulated". Compared to the controls, the level of serum C3 protein was decreased in #59 mice, while the level of C3 protein from kidney extract was increased. Results indicate that expression of HBsAg and HBcAg in tubular epithelial cells of the kidney per se can up-regulate complement-mediated inflammatory gene pathways, in addition to immune complex formation.
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Affiliation(s)
- J Ren
- Key laboratory of Medical Molecular Virology, Institute of Medical Microbiology, Shanghai Medical College, Fudan University, Shanghai, China
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Mason A, Theal J, Bain V, Adams E, Perrillo R. Hepatitis B virus replication in damaged endothelial tissues of patients with extrahepatic disease. Am J Gastroenterol 2005; 100:972-6. [PMID: 15784044 DOI: 10.1111/j.1572-0241.2005.41308.x] [Citation(s) in RCA: 48] [Impact Index Per Article: 2.4] [Reference Citation Analysis] [Abstract] [MESH Headings] [Track Full Text] [Journal Information] [Submit a Manuscript] [Subscribe] [Scholar Register] [Indexed: 12/11/2022]
Abstract
Hepatitis B virus (HBV) infection may be complicated by extrahepatic manifestations such as polyarteritis nodosa (PAN), glomerulonephritis, polymyositis, and dermatitis, but the etiology of these processes is not yet clear. HBV replication has been demonstrated in a variety of extrahepatic tissues and cell types, but the possible pathogenetic role of extrahepatic HBV replication has not been fully explored in patients with extrahepatic manifestations of HBV infection. In this case series, immunohistochemistry and in situ hybridization studies were performed on extrahepatic tissues from one HBsAg-positive patient with PAN and another HBsAg-positive patient with polymyositis, using HBsAg-seronegative control subjects with the same vasculitic disorders as controls. Tissue samples from the two study patients had detectable HBV RNA, replicative intermediates of HBV DNA, as well as HBsAg and HBcAg localized to vascular endothelium. In contrast, HBsAg-negative control patients had no tissue reactivity. Our results suggest that patients with HBV-related extrahepatic disease have evidence of viral replication in damaged extrahepatic endothelial tissues. While further studies would be required to support a hypothesis of causality, these findings suggest a role for both immune complex deposition and viral replication within diseased endothelial tissue in the pathogenesis of these poorly understood extrahepatic disorders.
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Affiliation(s)
- Andrew Mason
- Division of Gastroenterology, University of Alberta, Edmonton, Alberta, Canada
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Wang NS, Wu ZL, Zhang YE, Liao LT. Existence and significance of hepatitis B virus DNA in kidneys of IgA nephropathy. World J Gastroenterol 2005; 11:712-6. [PMID: 15655828 PMCID: PMC4250745 DOI: 10.3748/wjg.v11.i5.712] [Citation(s) in RCA: 16] [Impact Index Per Article: 0.8] [Reference Citation Analysis] [Abstract] [Key Words] [MESH Headings] [Track Full Text] [Download PDF] [Journal Information] [Submit a Manuscript] [Subscribe] [Scholar Register] [Received: 04/24/2004] [Revised: 04/27/2004] [Accepted: 05/08/2004] [Indexed: 02/06/2023] Open
Abstract
AIM To investigate the existence and significance of hepatitis B virus (HBV) DNA in the pathogenesis of IgA nephropathy (IgAN). METHODS Fifty cases of IgAN with HBV antigenaemia and/or hepatitis B virus antigens (HBAg, or HBsAg, HBcAg) detected by immunohistochemistry in renal tissues were enrolled in our study. The distribution and localization of HBV DNA were observed using in situ hybridization. Southern blot analysis was performed to reveal the state of renal HBV DNA. RESULTS Among the 50 patients with IgAN, HBs antigenemia was detected in 17 patients (34%). HBAg in renal tissues was detected in 48 patients (96%), the positive rate of HBAg, HBsAg, and HBcAg was 82% (41/50), 58% (29/50), and 42% (21/50) in glomeruli, respectively; and was 94% (47/50), 56% (28/50) and 78% (39/50) in tubular epithelia, respectively. Positive HBV DNA was detected in 72% (36/50) and 82% (41/50) cases in tubular epithelia and glomeruli respectively by in situ hybridization, and the positive signals were localized in the nuclei of tubular epithelial cells and glomerular mesangial cells as well as infiltrated interstitial lymphocytes. Moreover, 68% (34/50) cases were proved to be HBV DNA positive by Southern blot analysis, and all were the integrated form. CONCLUSION HBV infection might play an important role in occurrence and progress of IgAN. In addition to humoral immune damages mediated by HBAg-HBAb immune complex, renal tissues of some IgAN are directly infected with HBV and express HBAg in situ, and the cellular mechanism mediated by HBV originating from renal cells in situ may also be involved in the pathogenesis of IgAN.
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Affiliation(s)
- Nian-Song Wang
- Department of Nephrology, the Sixth Affiliated Hospital of Shanghai Jiaotong University, 600 Yushan Road, Shanghai 200233, China.
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17
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Abstract
Several extrahepatic manifestations are associated with chronic HBV infection, many with significant morbidity and mortality. The cause of these extrahepatic manifestations is generally believed to be immune mediated. PAN is a rare, but serious, systemic complication of chronic HBV affecting the small- and medium-sized vessels. PAN is seen more frequently in North American and European patients and rarely in Asian patients. PAN ultimately involves multiple organ systems, some with devastating consequences, though the hepatic manifestations are often more mild. The optimal treatment of HBV-associated PAN is thought to include a combination of antiviral and immunosuppressive therapies. HBV-associated GN occurs mainly in children, predominantly males, in HBV endemic areas of the world, but is only occasionally reported in the United States. In children, GN is usually self-limited with only rare progression to renal failure. In adults, the natural disease course of GN may be more relentless, slowly progressing to renal failure. Immunosuppressive therapy in HBV-related GN is not recommended, but antiviral therapy with alpha-interferon has shown promise. The serum-sickness like "arthritis-dermatitis" prodrome is seen in approximately one third of patients acquiring HBV. The joint and skin manifestations are varied, but the syndrome spontaneously resolves at the onset of clinical hepatitis with few significant sequelae. Occasionally, arthritis following the acute prodromal infection may persist; however, joint destruction is rare. The association between HBV and mixed essential cryoglobulinemia remains controversial; but a triad of purpura, arthralgias, and weakness, which can progress to nephritis, pulmonary disease, and generalized vasculitis, has characterized the syndrome. Finally, skin manifestations of HBV infection typically present as palpable purpura. Though papular acrodermatitis of childhood has been reported to be caused by chronic HBV, this association remains controversial.
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Affiliation(s)
- Steven-Huy B Han
- Division of Digestive Diseases, Pfleger Liver Institute, David Geffen School of Medicine at UCLA, 200 Medical Plaza, Suite 214, Los Angeles, CA 90095-7302, USA.
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Wang NS, Wu ZL, Zhang YE, Guo MY, Liao LT. Role of hepatitis B virus infection in pathogenesis of IgA nephropathy. World J Gastroenterol 2003; 9:2004-8. [PMID: 12970894 PMCID: PMC4656662 DOI: 10.3748/wjg.v9.i9.2004] [Citation(s) in RCA: 30] [Impact Index Per Article: 1.4] [Reference Citation Analysis] [Abstract] [MESH Headings] [Track Full Text] [Download PDF] [Journal Information] [Submit a Manuscript] [Subscribe] [Scholar Register] [Indexed: 02/06/2023] Open
Abstract
AIM: To investigate the role of hepatitis B virus (HBV) in the pathogenesis of IgA nephropathy (IgAN).
METHODS: HBV antigens (HBAg, or HBsAg, HBcAg, and HBeAg) in renal tissues with IgAN were detected by immunohistochemical technique. The distribution and localization of HBV DNA were observed by using in situ hybridization. Southern blot analysis was performed to reveal the state of renal HBV DNA.
RESULTS: Among 100 patients with IgAN, HBs antigenemia was detected in 18 patients (18.00%). HBAg in renal tissues was detected in 31 patients (31.00%), the positive rate of HBAg, HBsAg and HBcAg was 64.52% (20/31), 32.26% (10/31), 32.26% (10/31), respectively in glomeruli. HBcAg was also found in tubular epithelia and interstitia, which was 45.16% (14/31) and 6.45% (2/31), respectively. Five out of six cases with positive HBV DNA by in situ hybridization were proved to be HBV DNA positive by Southern blot analysis, and all were of the integrated form. Eight specimens were demonstrated to be HBV DNA positive by in situ hybridization, which was localized in the nuclei of tubular epithelial cells and glomerular mesangial cells as well as in infiltrated interstitial lymphocytes.
CONCLUSION: There is a relationship between HBV infection and IgAN. In addition to the humoral immune damage mediated by HBAg-HBAb immune complex, the cellular mechanism mediated by HBV originating from renal cells in situ may be also involved in the pathogenesis of IgAN.
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Affiliation(s)
- Nian-Song Wang
- Department of Nephrology, the Sixth Affiliated Hospital of Shanghai Jiaotong University, 600 Yushan Road, Shanghai 200233, China.
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19
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Abstract
Hepatitis B (HBV) and C (HCV) viruses are well-recognized causes for chronic hepatitis, cirrhosis, and even for hepatocellular carcinoma. Apart from liver disease, these viral infections are known to be associated with a spectrum of extrahepatic manifestations. The prevalence of clinically significant extrahepatic manifestations is relatively low, but it can be associated with significant morbidity and even mortality. An awareness and recognition of these manifestations is of paramount importance in facilitating early diagnosis and in offering treatment. However, treatments are not necessarily effective, and patients may continue with disabling extrahepatic manifestations. Hepatitis B virus has been well recognized as causing a variety of manifestations that include skin rash, arthritis, arthralgia, glomerulonephritis, polyarteritis nodosa, and papular acrodermatitis. More recently, infection with hepatitis C virus has elicited considerable interest for its role in a spectrum of extrahepatic manifestations. Among the best-reported are cryoglobulinemia, glomerulonephritis, high titer of autoantibodies, idiopathic thrombocytopenic purpura, lichen planus, Mooren's corneal ulcer, Sjögren's syndrome, porphyria cutanea tarda, and necrotizing cutaneous vasculitis. The precise pathogenesis of these extrahepatic complications has not been determined, although the majority represent the clinical expression of autoimmune phenomena.
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Affiliation(s)
- N T Pyrsopoulos
- Division of Hepatology, Center for Liver Diseases, University of Miami School of Medicine, 1500 NW 12th Avenue, Suite 1100, Miami, FL 33136, USA
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20
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Antonovych TT, Sabnis SG, Broumand BB. A study of membranoproliferative glomerulonephritis in Iran. Ann Saudi Med 1999; 19:505-10. [PMID: 17277468 DOI: 10.5144/0256-4947.1999.505] [Citation(s) in RCA: 5] [Impact Index Per Article: 0.2] [Reference Citation Analysis] [Abstract] [Track Full Text] [Journal Information] [Submit a Manuscript] [Subscribe] [Scholar Register] [Indexed: 11/22/2022] Open
Abstract
BACKGROUND The aim of this study was to review the morphologic patterns of membranoproliferative glomerulonephritis (MPGN) in 100 Iranian patients using light microscopy (LM) and electron microscopy (EM), and to compare the treatment and outcome in 13 patients with two biopsies. PATIENTS AND METHODS A retrospective study of 713 kidney biopsies of Iranian patients received between 1981 to 1994 was carried out. Of the 713 kidney biopsies, MPGN (n=106) and membranous glomerulopathy (n=112) made up the highest numbers of cases. RESULTS Among 100 MPGN patients, 55 (55%) were MPGN type I, 10 were type II (10%), and 35 type III (35%). Eighty-three (83%) had nephrotic proteinuria, 39 (39%) had hematuria, and 52 (52%) were hypertensive. Complement levels were estimated in 58, with low C3 in 10. The glomerular involvement was irregular, with focal hypercellularity in 47 patients (47%), widely patent capillaries in 50 (50%), arteriosclerosis in 48 (48%), and with hyaline change in 25 (25%). Follow-up data (22-130 months) was available in 61 (61%) patients: 6 (10%) died after 14-56 months, 27 (44%) were on maintenance hemodialysis for 15-110 months, and three received transplants. Thirteen patients had detailed follow-up and a second biopsy after 24-120 months. All 13 presented with edema and nephrotic range proteinuria, with hematuria and hypertension in five and azotemia in four. Seven of the 13 patients received initial steroids, followed by antiplatelet or antihypertensive drugs. Four (type III) patients received antiplatelet and antihypertension drugs, and two (type III) received only antihypertensive drugs. In the first biopsy, glomerular changes by light microscopy were non-uniform in 7 of 10 (70%) type III MPGN cases. Vascular changes were absent or mild in 11, and moderate in two. In the second biopsies, 10 showed decrease in cellularity, with many open capillaries, persistence of deposits by EM in all, and progression of vascular sclerosis in eight, and tubulointerstitial changes in 10. Among the 13, six were clinically stable, another six received dialysis followed by transplant in three, and one had relapses with episodes of cryoglobulinemia. Three patients died. CONCLUSION There is a high incidence of MPGN in Iranian patients, with a substantial number of type III MPGN cases. Second biopsies showed decreased cellularity, but increase in chronic tubulointerstitial and vascular cases. Steroids did not appear to benefit the outcome in types I and III MPGN patients compared to patients who received antihypertensive and antiplatelet treatment without steroids.
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Affiliation(s)
- T T Antonovych
- Armed Forces Institute of Pathology, Division of Nephropathology, Washington, D.C., USA, and Iran University of Medical Sciences, Tehran, Iran
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21
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Gbadoé AD, Atakouma DY, Napo-Koura G, Gouna A, Akakpo-Maxwell O, Dogba MA, Tatagan-Agbi K, Késsié K, Assimadi JK. [Primary nephrotic syndrome in the black African child]. Arch Pediatr 1999; 6:985-9. [PMID: 10519035 DOI: 10.1016/s0929-693x(99)80594-6] [Citation(s) in RCA: 7] [Impact Index Per Article: 0.3] [Reference Citation Analysis] [Abstract] [MESH Headings] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Indexed: 11/15/2022]
Abstract
Idiopathic nephrotic syndrome (INS) in black African children differs from that of children in temperate areas. The main differences are the high rate of corticosteroid non-responders and the low rate of minimal change glomerulopathy in black African children, possibly related to a racial factor. The identification of a high corticosensibility in certain African regions (Togo and Ghana) can lead to the identification of an ethnic factor. Further genetic studies should be carried out in order to provide a better approach to INS in Africa.
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Affiliation(s)
- A D Gbadoé
- Service de pédiatrie, CHU de Lomé-Tokoin, Togo
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LIN CHINGYUANG. Clinical features, pathogenesis and treatment of hepatitis B virus-associated membranous nephropathy in children. Nephrology (Carlton) 1996. [DOI: 10.1111/j.1440-1797.1996.tb00146.x] [Citation(s) in RCA: 0] [Impact Index Per Article: 0] [Reference Citation Analysis] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Indexed: 11/28/2022]
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23
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ZHANG YE, MA X, FANG L, LIN S, WU Z, GU J. The existence and significance of hepatitis B virus DNA in glomerulonephritis. Nephrology (Carlton) 1996. [DOI: 10.1111/j.1440-1797.1996.tb00074.x] [Citation(s) in RCA: 2] [Impact Index Per Article: 0.1] [Reference Citation Analysis] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Indexed: 12/15/2022]
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24
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Nowicki MJ, Welch TR, Ahmad N, Kuramoto IK, Mendoza EC, Zeldis JB, Baroudy BM, Balistreri WF. Absence of hepatitis B and C viruses in pediatric idiopathic membranoproliferative glomerulonephritis. Pediatr Nephrol 1995; 9:16-8. [PMID: 7742214 DOI: 10.1007/bf00858957] [Citation(s) in RCA: 10] [Impact Index Per Article: 0.3] [Reference Citation Analysis] [Abstract] [MESH Headings] [Track Full Text] [Journal Information] [Submit a Manuscript] [Subscribe] [Scholar Register] [Indexed: 01/26/2023]
Abstract
The blood-borne hepatitis viruses, hepatitis B virus (HBV) and hepatitis C virus (HCV), have similar epidemiological features. The association of chronic HBV infection and glomerulonephritis is well established, particularly in children. Recent reports have shown an association between HCV infection and glomerulonephritis in adults. In order to assess the role of these hepatotropic viruses in membranoproliferative glomerulonephritis (MPGN) we screened 34 children with idiopathic MPGN for the presence of HBV and HCV infection using highly sensitive polymerase chain reaction techniques for the detection of HBV DNA and HCV RNA. Also, enzyme-linked immunosorbent assays were used to detect the presence of antibody to hepatitis B surface antigen and antibody to HCV. No evidence of HBV or HCV infection was demonstrated in any of the patients. We conclude that HBV and HCV are not significant causes of idiopathic MPGN in children in the United States.
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Affiliation(s)
- M J Nowicki
- Division of Pediatric Gastroenterology, Children's Hospital Research Foundation, Cincinnati, Ohio, USA
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25
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Nakopoulou L, Stefanaki K, Zeis PM, Boletis J, Papadakis J, Vosnides G, Davaris P. The frequency of hepatitis B virus infection in Greek patients with various types of glomerulonephritis. Eur J Epidemiol 1994; 10:737-42. [PMID: 7672056 DOI: 10.1007/bf01719291] [Citation(s) in RCA: 3] [Impact Index Per Article: 0.1] [Reference Citation Analysis] [Abstract] [MESH Headings] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Indexed: 01/26/2023]
Abstract
The frequency of hepatitis B surface antigen (HBsAg) was studied in the sera of 622 patients with glomerulonephritis (GN). The prevalence of HBs-antigenemia was 2.8% (18/622; eleven adults and seven children); the difference from 2.6% in the general population of Central and Southern Greece was not statistically significant (chi 2 = 0.01; p > 0.50). Two of the 11 HBsAg-seropositive adult patients with GN suffered from IgA nephropathy, one from IgA and membranous glomerulonephritis (MGN), four from diffuse proliferative GN, two from membranous GN and one each from crescentic GN and focal segmental glomerulosclerosis. Five children out of 12 with membranous glomerulonephritis, one out of 24 with IgA nephropathy and one out of 16 with focal segmental glomerulosclerosis had HBs-antigenemia. The frequency of HBs-antigenemia in children with MGN was 41.7%, which is significantly higher than in children with other types of GN (0.9%). All seropositive patients were asymptomatic HBsAg carriers, while one seropositive HBsAg child with MGN suffered from chronic persistent hepatitis. HBsAg was detected by the immunoperoxidase-antiperoxidase (PAP) method in the glomeruli of only 3 children with MGN and HBs antigenemia, while HBcAg was not detected in any case. Our study suggests that in the Greek population there is no increased prevalence of HBs-antigenemia in patients with glomerulonephritis. Moreover, HBsAg was not found to contribute in the pathogenesis of GN in adults but it may be associated with the pathogenesis of membranous GN in children.
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Affiliation(s)
- L Nakopoulou
- Department of Pathology, Medical School, University of Athens, Greece
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26
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27
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Gładysz A, Juszczyk J, Brzosko WJ. Influence of Padma 28 on patients with chronic active hepatitis B. Phytother Res 1993. [DOI: 10.1002/ptr.2650070307] [Citation(s) in RCA: 7] [Impact Index Per Article: 0.2] [Reference Citation Analysis] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Indexed: 11/07/2022]
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28
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Jonas MM, Ragin L, Silva MO. Membranous glomerulonephritis and chronic persistent hepatitis B in a child: treatment with recombinant interferon alfa. J Pediatr 1991; 119:818-20. [PMID: 1941393 DOI: 10.1016/s0022-3476(05)80310-5] [Citation(s) in RCA: 10] [Impact Index Per Article: 0.3] [Reference Citation Analysis] [MESH Headings] [Track Full Text] [Journal Information] [Submit a Manuscript] [Subscribe] [Scholar Register] [Indexed: 12/29/2022]
Affiliation(s)
- M M Jonas
- Department of Pediatrics, University of Miami School of Medicine, Florida
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29
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Wrzołkowa T, Zurowska A, Uszycka-Karcz M, Picken MM. Hepatitis B virus-associated glomerulonephritis: electron microscopic studies in 98 children. Am J Kidney Dis 1991; 18:306-12. [PMID: 1882821 DOI: 10.1016/s0272-6386(12)80088-6] [Citation(s) in RCA: 11] [Impact Index Per Article: 0.3] [Reference Citation Analysis] [Abstract] [MESH Headings] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Indexed: 12/29/2022]
Abstract
Ninety-eight children with glomerulonephritis concomitant with hepatitis B surface HBs antigenemia were studied, the antigenemia being first documented at the clinical onset of glomerulopathy. Initial diagnoses, based on examination of the paraffin sections, varied, membrano-proliferative, mesangial, and membranous glomerulonephritis being most frequently considered. However, electron microscopic examination showed that 77 children had a uniform type of glomerulopathy, irrespective of the light microscopic appearance. This type was diagnosed as secondary membranous glomerulonephritis. The clinical course of this nephropathy was relatively indolent and short. Moreover, in many children, elimination of some hepatitis B virus (HBV) antigens from the circulation was also associated with clinical remission of glomerulopathy. The remaining 21 children with HBs antigenemia had various morphological forms of glomerulonephritis, these being similar to their idiopathic counterparts in both morphology and clinical course. The distinct clinical and morphological picture of secondary membranous glomerulonephritis with HBs antigenemia occurring in 77 of 98 children supports the hypothesis that HBsV-associated glomerulonephritis is of the secondary membranous type. Thus, we conclude that in children HBV antigenemia associated with glomerulonephritis other than secondary membranous is coincidental.
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Affiliation(s)
- T Wrzołkowa
- Laboratory of Electron Microscopy, Medical School Gdansk, Poland
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30
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Affiliation(s)
- S P Sylvan
- Elias Bengtsson Research Unit, Department of Infectious Diseases, Karolinska Institute, Roslagstull Hospital, Stockholm, Sweden
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31
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Hong SY, Yang DH, Park JM. Circulating HBsAg/IgG complexes in idiopathic chronic glomerulonephritis. Korean J Intern Med 1991; 6:21-6. [PMID: 1742252 PMCID: PMC4535014 DOI: 10.3904/kjim.1991.6.1.21] [Citation(s) in RCA: 0] [Impact Index Per Article: 0] [Reference Citation Analysis] [Abstract] [Key Words] [MESH Headings] [Track Full Text] [Download PDF] [Figures] [Journal Information] [Submit a Manuscript] [Subscribe] [Scholar Register] [Indexed: 12/28/2022] Open
Abstract
We measured HBsAg/IgG complexes (CX) quantitatively by ELISA from HBsAg positive serum of 35 liver disease patients, 15 patients with glomerular diseases (8 membranous glomerulonephritis (MGN) 7 membranoproliferative glomerulonephritis (MPGN), and 50 healthy carriers of HBsAg. HbsAg/IgG CX was detected in 26 out of 35 liver disease patients (74.3%), 5 out of 50 healthy carriers (10%), and one of both 8 MGN patients (12.5%) and 7 MPGN patients (14.3%). HBsAg/IgG CX was big in size and wide spread in the liver disease groups but negligible in the healthy carrier group (41 +/- 2.6 ng/ml, n = 5) and MGN (50 ng/ml, n = 1) and MPGN (42 ng/ml, n = 1) group. In the liver disease group, no one suffered from glomerulopathy even with a wide spectrum of HBsAg/IgG CX. These results suggest that HBsAg/IgG CX in plasma is non causative of MGN and MPGN.
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Affiliation(s)
- S Y Hong
- Department of Internal Medicine, Soonchunhyang University Chunan Hospital, Chungnam, Korea
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32
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33
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Hepatitis B Virus Infection and Primary Glomerular Disease. Nephrology (Carlton) 1991. [DOI: 10.1007/978-3-662-35158-1_76] [Citation(s) in RCA: 0] [Impact Index Per Article: 0] [Reference Citation Analysis] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Indexed: 11/26/2022]
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34
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35
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Johnson RJ, Couser WG. Hepatitis B infection and renal disease: clinical, immunopathogenetic and therapeutic considerations. Kidney Int 1990; 37:663-76. [PMID: 1968522 DOI: 10.1038/ki.1990.32] [Citation(s) in RCA: 175] [Impact Index Per Article: 5.0] [Reference Citation Analysis] [MESH Headings] [Grants] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Indexed: 12/29/2022]
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36
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Hsu HC, Wu CY, Lin CY, Lin GJ, Chen CH, Huang FY. Membranous nephropathy in 52 hepatitis B surface antigen (HBsAg) carrier children in Taiwan. Kidney Int 1989; 36:1103-7. [PMID: 2689751 DOI: 10.1038/ki.1989.307] [Citation(s) in RCA: 42] [Impact Index Per Article: 1.2] [Reference Citation Analysis] [Abstract] [MESH Headings] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Indexed: 01/02/2023]
Abstract
To elucidate the prognosis and the causative viral antigens of hepatitis B virus (HBV)-associated childhood membranous nephropathy (MN), the clinical course and glomerular HBV antigens were studied in 52 HBsAg carrier children with MN (40 boys, 12 girls). With Fab fragments of monoclonal antibodies, hepatitis Be antigen (HBeAg) was detected in the glomerular deposits in 41 (95%) of 43 cases but HBsAg and hepatitis B core antigen (HBcAg) in none. HBeAg was detected in sera from 43 (93%) of 46 children examined. These results suggest that HBeAg plays an important role in the development of MN in HBsAg carrier children. During the follow-up period (mean, 4 years), complete remission was found in 64% and 92% of the patients followed for one and seven years, respectively; only one child had mild renal function impairment. These findings suggest a favorable outcome of HBsAg-associated childhood MN. The patient's age, disease duration, amount of glomerular deposit, focal sclerosis and disease stage appeared to affect the clinical course. HBsAg seroconversion to HBsAg-negative occurred in seven cases, and all (100%) had quick remission in two years. In patients with persistent HBsAg carriage, serum HBeAg status alone did not correlate with remission rate and remission occurred usually before the HBeAg seroconversion to anti-HBe. These findings, together with the predominant horizontal infection in these children in contrast to the frequent vertical (perinatal) transmission from HBsAg carrier mothers in HBsAg carriers in Taiwan, suggest that factors other than HBeAg per se may also play important roles.
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Affiliation(s)
- H C Hsu
- Department of Pathology, College of Medicine, National Taiwan University, Taipei, Republic of China
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37
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Abstract
Acute or chronic hepatitis B virus infection is often associated with symptoms which are probably caused by immune complexes, such as vasculitis, glomerulonephritis and arthritis. The immune complexes found in such patients contain excessive viral proteins. The functions of these proteins and the immune response to them during various states of infection are discussed.
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Affiliation(s)
- K H Heermann
- Department of Medical Microbiology, University of Göttingen, Federal Republic of Germany
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38
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de Man RA, Schalm SW, van der Heijden AJ, ten Kate FW, Wolff ED, Heijtink RA. Improvement of hepatitis B-associated glomerulonephritis after antiviral combination therapy. J Hepatol 1989; 8:367-72. [PMID: 2471723 DOI: 10.1016/0168-8278(89)90036-6] [Citation(s) in RCA: 25] [Impact Index Per Article: 0.7] [Reference Citation Analysis] [Abstract] [MESH Headings] [Track Full Text] [Journal Information] [Submit a Manuscript] [Subscribe] [Scholar Register] [Indexed: 01/01/2023]
Abstract
A 9-year-old boy with hepatitis B-associated glomerulonephritis and nephrotic syndrome underwent antiviral combination therapy including interferon and acyclovir. Pretreatment evaluation showed that active hepatitis B virus replication with HBsAg, HBeAg, HBV-DNA and DNA-polymerase had occurred for a period of at least 4 years. Signs of liver disease were minimal; serum amino transferases were normal and liver histology showed chronic persistent hepatitis with positive HBcAg, HBeAg and HBsAg immunofluorescence. A kidney biopsy revealed membranous glomerulonephritis with deposition of HBcAg, HBeAg, IgG, C3, C1q and, on electron microscopy, virus-like particles. After 8 weeks of therapy, active viral replication ceased, HBe seroconversion occurred and the nephrotic syndrome disappeared. One year after treatment, the boy was asymptomatic. No viral markers could be detected in the kidney, but low-grade membranous glomerulonephritis persisted with deposition of C1q, IgG and C3, but not HBeAg, HBsAg or HBcAg. Liver histology showed a minimal aspecific portal infiltrate with weak membrane-bound HBsAg immunofluorescence; no HBcAg could be detected. For patients with active viral replication and deposition of HBc, HBe immune complexes in the kidney, antiviral therapy can be beneficial, even in the absence of active liver disease.
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Affiliation(s)
- R A de Man
- Department of Internal Medicine II, Erasmus University, Rotterdam, The Netherlands
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39
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Cupps TR, Hoofnagle JH, Ellis RW, Miller WJ, Seeff L, Guerrera A, Gerin JL, Haas-Smith SA. In vitro immune responses to hepatitis B surface antigen (Pre-S2 and S) following remote infection by hepatitis B virus in humans. J Clin Immunol 1989; 9:229-41. [PMID: 2768432 DOI: 10.1007/bf00916819] [Citation(s) in RCA: 3] [Impact Index Per Article: 0.1] [Reference Citation Analysis] [Abstract] [MESH Headings] [Grants] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Indexed: 01/02/2023]
Abstract
In this report we evaluate the human immune response to hepatitis B surface antigen (HBsAg) following remote infection with hepatitis B virus (HBV). HBsAg-reactive lymphocytes can be readily demonstrated in the peripheral blood of individuals with established immunity following infection with HBV. In vitro stimulation with small doses of plasma-derived HBsAg, yeast-derived HBsAg (S region) or pre-S2 peptide will induce specific IgG to HBsAg (anti-HBs) in the absence of a polyclonal increase in total IgG. The pre-S2 peptide will stimulate, in a T cell-dependent fashion, the in vitro production of anti-HBs with specificity for the S domain. This anti-HBs production is mediated by pre-S2-stimulated soluble T-cell factors. Peripheral blood mononuclear cells from individuals with established immunity proliferate to the yeast-derived HBsAg but not to the plasma-derived HBsAg or pre-S2 peptide. The chronic HBsAg carriers do not produce anti-HBs following stimulation with HBsAg regardless of the source or component of antigen used. Different study protocols failed to demonstrate HBsAg-specific responses in the peripheral blood mononuclear cells of chronic carriers.
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Affiliation(s)
- T R Cupps
- Department of Medicine, Georgetown University Medical Center, Washington, DC 20007
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40
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Lee HS, Choi Y, Yu SH, Koh HI, Kim MJ, Ko KW. A renal biopsy study of hepatitis B virus-associated nephropathy in Korea. Kidney Int 1988; 34:537-43. [PMID: 3199674 DOI: 10.1038/ki.1988.215] [Citation(s) in RCA: 30] [Impact Index Per Article: 0.8] [Reference Citation Analysis] [Abstract] [MESH Headings] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Indexed: 01/04/2023]
Abstract
The pathogenic role of the hepatitis B virus (HBV) infection for glomerulonephritis (GN) is not clear. The frequency of HBsAg has been studied in sera of 732 consecutive patients who have glomerular diseases by using radioimmunoassay. The frequency of HBs antigenemia was 11.9%, which was not different from that in the general population of South Korea. Of the 87 HBsAg seropositive patients with GN, 29 cases with membranoproliferative GN (MPGN) and eighteen with membranous nephropathy (MN) were diagnosed as having HBV-associated nephropathy. Eighty-seven and one-half percent of the adults with MPGN and 80% of the children with MN were HBsAg carries. The morphologic findings and laboratory data in cases with HBV-associated MPGN and MN did not differ significantly from those observed in patients with MPGN and MN without circulating HBsAg. Yet mesangial deposits were more frequently noted in patients with HBV-associated MN when compared to others with idiopathic MN. Glomerular deposits of HBsAg were not detected using indirect immunofluorescence technique. Even though HBsAg was not demonstrable within the glomeruli, HBV infection seems to play an important role in the pathogenesis of MPGN in Korean adults and MN in children.
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Affiliation(s)
- H S Lee
- Department of Pathology, College of Medicine, Seoul National University, Korea
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41
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Elidrissy AT, Abdurrahman MB, Ramia S, Lynch JB. Hepatitis B surface antigen associated nephrotic syndrome. ANNALS OF TROPICAL PAEDIATRICS 1988; 8:157-61. [PMID: 2461151 DOI: 10.1080/02724936.1988.11748560] [Citation(s) in RCA: 13] [Impact Index Per Article: 0.4] [Reference Citation Analysis] [Abstract] [MESH Headings] [Track Full Text] [Subscribe] [Scholar Register] [Indexed: 01/01/2023]
Abstract
Hepatitis B virus (HBV) has been reported in association with the nephrotic syndrome from different parts of the world, but its role as a cause of the pathological findings of nephrotic syndrome is still controversial. We report seven nephrotic children with positive hepatitis B markers in which members of their families were also positive for the markers but without clinical, renal or hepatic involvement. Four showed haematuria at onset and three developed hypertension later in the course of the disease. Only two were responsive to steroid therapy. Renal biopsy was performed in four, of whom three showed membranous nephropathy and the other showed mesangioproliferative glomerulonephritis. Four patients developed end-stage renal disease. We conclude that in our environment HBV, when detected in children with nephrotic syndrome, should not be considered as a chance finding, but may have a definite role in its pathogenesis. Moreover, the prognosis of HBV-associated nephrotic syndrome appears poor.
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Affiliation(s)
- A T Elidrissy
- Department of Paediatrics, College of Medicine, Riyadh, Saudi Arabia
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42
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Affiliation(s)
- J Zarconi
- Division of Nephrology, Akron City Hospital, OH 44304
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Onwubalili JK. Fulminant hepatic failure in nephrotic syndrome related to withdrawal of immunosuppressive therapy. Postgrad Med J 1988; 64:325-7. [PMID: 3186580 PMCID: PMC2428506 DOI: 10.1136/pgmj.64.750.325] [Citation(s) in RCA: 15] [Impact Index Per Article: 0.4] [Reference Citation Analysis] [Abstract] [MESH Headings] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Indexed: 01/04/2023]
Abstract
Two patients with nephrotic syndrome developed fatal fulminant hepatitis B following withdrawal of prednisolone or cyclophosphamide. Immunosuppressive therapy probably enhanced hepatitis B virus (HBV) replication and widespread infection of hepatocytes; its withdrawal permitted a return of immune competence resulting in massive destruction of infected hepatocytes. Prior screening of all patients for hepatitis B surface antigen, gradual withdrawal of immunosuppressive drugs with careful monitoring, and prompt intervention with corticosteroids at the first clinical or biochemical signs of liver cell damage may prevent this complication.
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Affiliation(s)
- J K Onwubalili
- Department of Medicine, University of Nigeria Teaching Hospital, Enugu
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Ishihara T, Akamatsu A, Takahashi M, Yamashita Y, Yokota T, Nagasawa T, Gondo T, Kawano H, Kawamura S, Uchino F. Ultrastructure of kidney from three patients with HBeAg-associated nephropathy with special reference to virus-like particles in the glomerular tufts. ACTA PATHOLOGICA JAPONICA 1988; 38:339-50. [PMID: 3394523 DOI: 10.1111/j.1440-1827.1988.tb02306.x] [Citation(s) in RCA: 3] [Impact Index Per Article: 0.1] [Reference Citation Analysis] [Abstract] [MESH Headings] [Track Full Text] [Subscribe] [Scholar Register] [Indexed: 01/05/2023]
Abstract
The biopsied kidneys from three patients with hepatitis Be antigen (HBeAg)-associated nephropathy were observed by light microscopy, immunohistochemistry and electron microscopy. By an indirect technique utilizing horseradish peroxidase-conjugated antisera, HBeAg was found to be deposited in a diffuse granular fashion along the glomerular capillary wall. No deposition of hepatitis Bs or hepatitis Bc antigen was detected. The three cases were diagnosed as HBeAg-associated nephropathy. Ultrastructurally, there were finely granular electron-dense deposits in the subendothelial area, basement membrane, mesangial area and subepithelial area of the glomerular tufts. In all three cases, virus-like particles between 30 and 70 nm in diameter were also found in such areas of the glomerular tufts, and rarely in the glomerular capillary lumen and space of Bowman. They occasionally formed clusters in the phagosomes of mesangial cells. In addition, tubulo-reticular structures were noted in the cytoplasm of endothelial cells in the glomerular capillaries. The presence of HBeAg both in the serum and in the kidney and of virus-like particles in the glomerular tufts suggests that HBeAg is causally related to the development of HBeAg-associated nephropathy.
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Affiliation(s)
- T Ishihara
- First Department of Pathology, Yamaguchi University School of Medicine, Ube, Japan
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Takeda S, Kida H, Katagiri M, Yokoyama H, Abe T, Hattori N. Characteristics of glomerular lesions in hepatitis B virus infection. Am J Kidney Dis 1988; 11:57-62. [PMID: 3276172 DOI: 10.1016/s0272-6386(88)80176-8] [Citation(s) in RCA: 14] [Impact Index Per Article: 0.4] [Reference Citation Analysis] [Abstract] [MESH Headings] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Indexed: 01/05/2023]
Abstract
In an attempt to clarify a participation of hepatitis B virus (HBV) in the development of hepatic glomerulopathy in adults, kidney specimens obtained from 151 patients with liver diseases were studied. Although mesangial proliferation was more severe in patients with chronic hepatitis or liver cirrhosis than in those with acute hepatitis, no significant difference was observed between 82 serum hepatitis B surface antigen (HBsAg)-positive (HBV-related group) and 69 negative patients (HBV-nonrelated group). However, double contours of the glomerular capillary walls were observed more often in the former group (18/82, P less than .01), especially in the HBeAg-positive subgroup (8/24, P less than .001), than in the latter (3/69). In addition, glomerular capillary spike formation or a bubblelike appearance was observed in seven patients of the former group. Of these, all five patients examined were HBeAg-positive in their serum. By electron microscopic studies, subendothelial dense deposits and mesangial interpositions were observed more frequently in the HBV-related group, and subepithelial deposits were found only in the HBeAg-positive subgroup. The immunofluorescence study revealed IgA-dominant mesangial deposition in both HBV-related and nonrelated groups. As for the capillary wall deposits, however, IgG was dominant in 13 of the HBV-related group, but only one of the nonrelated group (P less than .01). Furthermore, one patient in the HBV-related group showed capillary wall-dominant HBeAg combined with IgG deposition.(ABSTRACT TRUNCATED AT 250 WORDS)
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Affiliation(s)
- S Takeda
- First Department of Internal Medicine, School of Medicine, Kanazawa University, Japan
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Steciwko A. Viral infections, their influence on some parts of the immune system and glomerulonephritis development. Int Urol Nephrol 1987; 19:433-9. [PMID: 3323103 DOI: 10.1007/bf02550362] [Citation(s) in RCA: 0] [Impact Index Per Article: 0] [Reference Citation Analysis] [Abstract] [MESH Headings] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Indexed: 01/05/2023]
Abstract
Glomerulonephritis complicates the course of various viraemias. Aetiopatho-mechanism leading to the development of a particular form of glomerulonephritis on this background is differentiated and multifactorial. Viraemias affect the immune system, provoking a number of alterations of functional nature, discriminating both humoral and cellular responses. It also seems that neuraminidase enclosed in certain viruses plays a role in the aetiopathogenesis of glomerulonephritis.
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Affiliation(s)
- A Steciwko
- Department of Nephrology, Medical Academy Wroclaw, Poland
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Abstract
Immune disorders of the gastrointestinal tract and hepatobiliary systems comprise a diverse group of illnesses which share in common certain overlapping and yet distinctive expressions of cellular and humoral immunity. As is evident from material contained in this article, controversy and disparate results frequently characterize the study of immune mechanisms in a given disease process. Nonetheless, advances in quantitation of specific immunocyte function and phenotypic expression have greatly facilitated the depth of understanding of the immune process related to these disorders. Challenges for future clinical investigation of these disorders are to characterize cell-specific target antigens to which immunologic attack is directed and to unravel the immunogenetic mechanisms that trigger and direct immune-mediated injury to host tissues. It is anticipated that continued investigation of immune disorders of the gastrointestinal tract and liver will clarify pathogenetic mechanisms and thus permit formulation of rational and effective therapies.
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Cadrobbi P, Bortolotti F, Zacchello G, Rinaldi R, Armigliato M, Realdi G. Hepatitis B virus replication in acute glomerulonephritis with chronic active hepatitis. Arch Dis Child 1985; 60:583-5. [PMID: 4015177 PMCID: PMC1777370 DOI: 10.1136/adc.60.6.583] [Citation(s) in RCA: 16] [Impact Index Per Article: 0.4] [Reference Citation Analysis] [Abstract] [MESH Headings] [Track Full Text] [Journal Information] [Submit a Manuscript] [Subscribe] [Scholar Register] [Indexed: 01/08/2023]
Abstract
A 3 year old boy who had chronic active hepatitis type B with features of ongoing liver damage and active virus replication, developed acute membranous glomerulonephritis two years after the clinical onset of liver disease, when both hepatitis B e antigen and antibody were detectable in serum. After withdrawal of short term steroid treatment and resolution of hepatitis B virus replication, both glomerulonephritis and chronic hepatitis went into remission. Some months later hepatitis B surface antigen was no longer found in serum.
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Hepatitis B surface antigenemia in North American children with membranous glomerulonephropathy. Southwest Pediatric Nephrology Study Group. J Pediatr 1985; 106:571-8. [PMID: 3981311 DOI: 10.1016/s0022-3476(85)80074-3] [Citation(s) in RCA: 52] [Impact Index Per Article: 1.3] [Reference Citation Analysis] [Abstract] [MESH Headings] [Track Full Text] [Journal Information] [Submit a Manuscript] [Subscribe] [Scholar Register] [Indexed: 01/08/2023]
Abstract
We describe 11 North American children with hepatitis B-associated membranous glomerulonephropathy (MGN). The children are predominantly black boys (seven of 11) and younger (mean age 5.3 years) than children with idiopathic MGN (10.6 years) or lupus-associated MGN (13.4 years). Most of the patients (10 of 11) had nephrotic syndrome, and although clinical evidence of liver disease was present in only one child, eight of 10 patients had elevated aspartate amino transferase levels. Liver biopsies performed in three children revealed chronic persistent hepatitis in two and chronic active hepatitis in one. Hepatitis B surface antigen was found in the serum of one of the parents of five patients and in the brother of one patient. Low serum C3 values were observed in all 11 children at some stage of their illness. Renal biopsy specimens revealed stage II or III glomerular capillary wall changes, and immunofluorescence studies revealed three or more glomerular immunoreactants in 10 of 11 biopsies. One patient developed end-stage renal disease 9 years after presentation of nephrotic syndrome; the duration of follow-up of the other 10 patients is limited at this time. We conclude from these data that hepatitis B-associated MGN is more frequent in North American children than previous reports have suggested, is most commonly seen in young black boys, and is characterized by low serum C3 levels. It appears, therefore, to be a distinct clinicopathologic entity.
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