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Glomerulonephritis 

HCV Associated Nephropathy

INTERNAL MEDICINE 1996 JUL;35(7):529-533 Authors: KOMATSUDA A, IMAI H, WAKUI H, HAMAI K, OHTANI H, KODAMA T, OYAMA Y, MIURA AB, NAKAMOTO Y

We analyzed the clinicopathological features and therapy in 19 patients with kidney disease accompanied by hepatitis C viral infection, including 12 patients with mesangial proliferative glomerulonephritis (including eight with IgA nephropathy), six with membranoproliferative glomerulonephritis (MPGN), and one with membranous nephropathy. Persistent hematuria and/or proteinuria (10 patients) was the most common finding, followed by nephrotic syndrome (8 patients). Cryoglobulinemia was detected in six of 19 patients examined (four of six patients with MPGN), Analysis of hepatitis C virus (HCV)-RNA genotype in 13 patients revealed that nine of them had type II genotype. All four patients with MPGN, who had serum positive for HCV-RNA, had type II genotype. Five patients were treated with interferon-alpha (IFN-alpha) without a demonstrable effect on renal impairment, whereas five of 11 patients treated with steroids showed improvement of the renal impairment. During the course of steroid therapy, the serum titer of HCV-RNA decreased in 5 of 7 patients. These observations suggest that HCV infection may be associated with several forms of glomerulonephritis. Type II HCV-RNA may have a strong association with MPGN in Japan. Steroid therapy is not contraindicated in patients with HCV-associated nephropathy if they are resistant to IFN-alpha treatment.

Leukocytoclastic Vasculitis Associated with HCV Antibodies

Author: MANNA R, POLICLIN A GEMELLI, IST CLIN MED, L A GEMELLI 8, I-00168 ROME, ITALY Source: BRITISH JOURNAL OF RHEUMATOLOGY 1997 JAN;36(1):124-125

The aetiopathogenesis of leucocytoclastic vasculitis is still unknown, but recently hepatitis C virus (HCV) has been suggested as trigger of autoimmunity. We report a case of a 26-yr-old patient with purpura due to leucocytoclastic vasculitis associated with hepatitis C virus infection. Laboratory findings showed AST, ALT: gamma GT within normal limits, positive antibodies to HCV (IIF and Riba II) and polymerase chain reaction for HCV RNA. Anti-nuclear antibodies, IgG and IgM anti-cardiolipin antibodies, anti-platelet antibodies and anti-neutrophil cytoplasmic antibodies with perinuclear pattern were also present. A skin biopsy specimen of a purpuric lesion showed leucocytoclastic vasculitis with small vessel thrombosis and perivascular deposition of IgM and fibrinogen on immunofluorescence study. This case shows a role of HCV in leucocytoclastic vasculitis; it is possible that this HCV can induce autoimmunity independently of cryoglobulins and liver involvement.

Infection with hepatitis C virus (HCV) may affect not only the liver but also various nonhepatic tissues and organs and may combine with many etiologically unrelated diseases and morbid conditions. Numerous nonhepatic manifestations in HCV infection have been previously reported. For some (eg, cryoglobulinemia), the association is well established. For others, such as sialadenitis and lichen planus, the association is probable (but not completely documented) and, for the remainder, the associations are weak. Extrahepatic manifestations may result from immunological mechanisms as well as virus invasion and replication in the affected extrahepatic tissues and organs. Thyroid abnormalities, primarily Hashimoto's disease, and isolated increases of anti-thyroid antibodies (ATPO) appear to be more frequent in chronic hepatitis C than B or D, with high ATPO titers clustering mainly among females. Interferon-alpha (IFN-alpha) therapy is associated with development of thyroid dysfunction in 5.5-12.9% of patients, usually exposing preexisting subclinical thyroid abnormalities. Mixed cryoglobulinemia (MC) is commonly found (36-45%) in patients with chronic HCV infection; however, only in a minority of cases does it become clinically manifested as systemic vasculitis with purpura, neuropathy, or Raynaud's phenomenon. In a number of patients, MC may terminate in non-Hodgkin's B-cell lymphoma. Treatment of these lymphoproliferative disorders with IFN-alpha is advocated. Idiopathic thrombocytopenia is now recognized more frequently in association with chronic HCV infection and is usually aggravated by IFN-alpha therapy. Patients with porphyria cutanea tarda (PCT) have demonstrated serological markers of HCV infection in 62-82% of cases. The usefulness of IFN-alpha in PCT remains to be demonstrated. Lichen planus has also been found in association with chronic HCV infection, particularly when severe or affecting the oral cavity. Other nonhepatic manifestations have also been reported in HCV infection such as diabetes, corneal ulceration, uveitis, and sialadenitis. These manifestations deserve further study and documentation. Finally, markers of autoimmunity occur with high frequency in chronic HCV infection; however, combination with the classical syndrome of autoimmune hepatitis is rare. In the presence of various autoantibodies, the clinical features of chronic hepatitis C do not appear to be modified and, contrary to general perception, IFN-alpha therapy within randomized controlled trials should not be withheld since the response rate to IFN-alpha does not appear to differ in the presence or absence of low titers of these markers.

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