Membranoproliferative glomerulonephritis associated with hepatitis C virus infection

Johnson, Richard J.; Gretch, David R.; Yamabe, Hideaki; Hart, Jaime; Bacchi, Carlos E.; Hartwell, Peter; Couser, William G.; Corey, Lawrence; Wener, Mark H.; Alpers, Charles E.; Willson, Richard A.

doi:10.1007/bf00852534

Cited by 87 publications

(137 citation statements)

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“…These observations support the concepts that a persistent viremia can continuously stimulate production of monoclonal and poly clonal immunoglobulins and that the pres ence of cirrhosis can facilitate emergence of the syndrome by impairing the clearance of circulating immune complexes and cryoglob ulins [34], Glomerulonephritis is another immune complex disease that can occur with or with out features of vasculitis or polyarteritis in patients with either chronic hepatitis B or C [64][65][66]. The disease is rare, but [66]. These patients frequently have seropositivity for IgM rheumatoid factor and in patients with chronic hepatitis C. HCV RNA and IgG anti-HCV can be found in crvoprecipitates [66].…”

Section: Foreign Antigen-driven I Mm It Ne Processessupporting

confidence: 67%

“…p < 0.01), and cirrhosis (55 versus 29%, p < 0.01) than in counterparts without these features [34]. These observations support the concepts that a persistent viremia can continuously stimulate production of monoclonal and poly clonal immunoglobulins and that the pres ence of cirrhosis can facilitate emergence of the syndrome by impairing the clearance of circulating immune complexes and cryoglob ulins [34], Glomerulonephritis is another immune complex disease that can occur with or with out features of vasculitis or polyarteritis in patients with either chronic hepatitis B or C [64][65][66]. The disease is rare, but [66].…”

Section: Foreign Antigen-driven I Mm It Ne Processessupporting

confidence: 65%

“…The disease is rare, but [66]. These patients frequently have seropositivity for IgM rheumatoid factor and in patients with chronic hepatitis C. HCV RNA and IgG anti-HCV can be found in crvoprecipitates [66].…”

Section: Foreign Antigen-driven I Mm It Ne Processesmentioning

confidence: 99%

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Extrahepatic Immunologic Features of Chronic Viral Hepatitis

Czaja¹

1997

Dig Dis

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Patients with chronic viral hepatitis commonly have immunologic manifestations, including autoantibodies and concurrent immune diseases. These immunologic findings may resemble those of autoimmune hepatitis and they are not disease specific. High titer autoantibodies (titers ≧ 1:320) are uncommon in chronic viral hepatitis as are multiple concurrent autoantibodies. These findings reflect an autoimmune-predominant disorder in which the viral infection may be coincidental or facilitative. Concurrent immunologic disorders may be viral antigen-driven and associated with immune complex deposition (cryoglobulinemia, glomerulonephritis, cutaneous vasculitis, and polyarteritis) or autoantigen-driven (autoimmune thyroiditis and Sjögren’s syndrome) and associated with host- rather than virus-specific factors. Genetic predispositions influence immunologic expression. Seropositivity for antinuclear antibodies is associated with HLA A1-B8-DR3, and concurrent immunologic diseases are associated with the DR4 allele. Interferon therapy is appropriate for patients with viral antigen-driven processes that depend on immune complex deposition and for patients with mild background autoimmune expressions. Corticosteroid therapy should be considered for those unusual patients with predominant autoantigen-driven processes since interferon treatment may exacerbate immune-mediated diseases. Patients with chronic hepatitis B and C can have similar immune features, but patients with chronic hepatitis C more commonly have autoantigen-driven processes.

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Section: Foreign Antigen-driven I Mm It Ne Processessupporting

confidence: 67%

Section: Foreign Antigen-driven I Mm It Ne Processessupporting

confidence: 65%

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Extrahepatic Immunologic Features of Chronic Viral Hepatitis

Czaja¹

1997

Dig Dis

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“…Other, less frequent symptoms are nausea, poor appeof the EMC. Glomerulonephritis can also occur with hepatitis C 40 ; it usually represents the renal involvement of HCV-tite, muscle aches, arthralgias, feverishness, weakness, and weight loss. Symptoms are rarely incapacitating, but they can related EMC.…”

Section: Of Disease Severitymentioning

confidence: 99%

Hepatitis C: The clinical spectrum of disease

1997

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Hepatitis C virus (HCV) accounts for approximately 20% resembles other forms of acute viral hepatitis with onset of malaise, nausea, and right upper quadrant pain followed by of cases of acute hepatitis, 70% of chronic hepatitis, and 30% of end-stage liver disease in the United States. The acute dark urine and jaundice. The mean incubation period to onset of symptoms is 7 weeks (range, 3-20 weeks). 2,3 Howinfection has an incubation period of 7 weeks (range, 4-20 weeks) and is symptomatic and icteric in only one third of ever, long before onset of symptoms, viral markers of infection appear: HCV RNA becomes detectable in serum within patients. Serum aminotransferase levels generally increase greater than 10-fold elevated and as symptoms and signs re-1 to 2 weeks of exposure ( Fig. 1) 4,5 and increases to levels of 10 6 to 10 8 genomes/mL. 6 After several weeks, serum alanine solve decrease into the normal range. Antibody to HCV is usually but not always present at the time of onset of symp-aminotransferase (ALT) levels begin to increase and shortly thereafter, clinical symptoms appear. The severity of the toms. HCV RNA appears in the serum early during the incubation period, increases in titer and peaks at the time of symp-acute illness is variable; virtually all infected patients have a transient elevation in ALT, and peak levels are greater than toms, and then disappears in resolving disease. Importantly, 85% of patients with acute HCV infection develop chronic 10-fold elevated in more than 80% of patients. Yet, only a third of patients develop jaundice or symptoms; in the infection. In these patients, HCV RNA remains present and in approximately two thirds of patients, aminotransferases remainder, the disease is anicteric and subclinical. If clinically apparent, the illness generally lasts for 2 to 12 weeks. remain elevated in the range of 1.5-to 10-fold the upper limit of normal. The course of chronic hepatitis C is variable. Acute hepatitis C can result in fulminant hepatitis, but this is rare. 7 In cases of acute, self-limited disease, HCV RNA Probably fewer than 20% of patients have symptoms and they are usually intermittent, vague, and nonspecific, largely being becomes undetectable within a few weeks of onset of symptoms and aminotransferase levels return to normal. malaise and easy fatiguability. A small percentage of patients develop extrahepatic manifestations of hepatitis C, including CHRONIC HEPATITIS C cryoglobulinemia and glomerulonephritis. It is estimated that 20% to 30% of patients with chronic hepatitis C develop Unfortunately, acute, self-limited hepatitis is not the most cirrhosis, but the process is generally slow and insidious. common course of acute HCV infection. In the majority of Once cirrhosis develops, symptoms are more common and patients, symptoms of acute hepatitis resolve, but ALT levels the signs of end-stage liver disease can appear with jaundice, often remain elevated and HCV RNA persists (Fig. 2). [2][3][4][5][8][9][10] weakness, wasting, and gastrointestinal bleeding. Patie...

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“…Many patients with mild liver disease have more major systemic symptoms with chronic fatigue (Foster et al, 1998). Other extrahepatic diseases related to HCV infection include glomerulonephritis, cryoglobulinaemia and vasculitis (Johnson et al, 1993;Rollino et al, 1991;Agnello et al, 1992). Individual patients may be concerned regarding transmission of HCV to others and until effective vaccines are developed antiviral therapy is also important in controlling disease spread.…”

Section: Targeting Therapymentioning

confidence: 99%

Treatment of Chronic Viral Hepatitis

Main

McCarron

1998

Antivir Chem Chemother

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Interferon-α therapy has proved effective for up to 40% of patients with adult-acquired chronic hepatitis B virus (HBV) infection and for 20-25% of those with chronic hepatitis C virus (HCV) infection. Nucleoside analogues, such as lamivudine and famciclovir, are showing promise as antiviral agents for chronic HBV and the combination of interferon-α and ribavirin is proving to be successful therapy for 40-50% of patients with chronic HCV. In this article we review current therapy and discuss future strategies of the therapy of chronic viral hepatitis.

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Membranoproliferative glomerulonephritis associated with hepatitis C virus infection

Cited by 87 publications

References 0 publications

Extrahepatic Immunologic Features of Chronic Viral Hepatitis

Extrahepatic Immunologic Features of Chronic Viral Hepatitis

Hepatitis C: The clinical spectrum of disease

Treatment of Chronic Viral Hepatitis

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