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[A case of hepatitis C virus associated membranous glomerulonephritis ameliorated by corticosteroid therapy]
I Kurihara1, T Saito, K Nakayama
1Internal Medicine, Iwate Prefectural Tono Hospital, Japan.
Insights
Corticosteroid therapy may be a viable treatment for membranous glomerulonephritis (MGN) associated with hepatitis C virus (HCV). This case study shows potential benefits despite HCV presence.
Area of Science:
- Nephrology
- Hepatology
- Immunology
Background:
- Hepatitis C virus (HCV) infection can lead to various extrahepatic manifestations, including glomerulonephritis.
- Membranous glomerulonephritis (MGN) is a potential renal complication of HCV, often presenting with nephrotic syndrome.
Observation:
- A 50-year-old male with a history of blood transfusion developed liver dysfunction, followed by proteinuria and microhematuria.
- Renal biopsy confirmed membranous glomerulonephritis with focal fibrocellular crescents. Serological tests for hepatitis B, cryoglobulin, and rheumatoid factor were negative.
- Initial treatment with prednisolone significantly reduced proteinuria and improved serum albumin levels.
Findings:
- Despite initial steroid effectiveness, the patient later tested positive for HCV antibodies.
- Proteinuria recurred after corticosteroid discontinuation, though liver disease markers remained mild.
- The patient's clinical course suggests a complex interplay between HCV, MGN, and corticosteroid treatment.
Implications:
- Corticosteroid therapy may be considered safe and potentially effective for managing HCV-associated MGN.
- Further research is warranted to elucidate the long-term efficacy and safety of immunosuppressants in HCV-related kidney diseases.
- This case highlights the importance of considering HCV in patients presenting with glomerulonephritis, even with initial negative serology.
Abstract:
We report a 50-year-old male patient with hepatitis C virus (HCV)-associated membranous glomerulonephritis (MN), for which he had been treated with corticosteroid therapy for one and a half years. This patient received blood infusion at 38 years of age. He visited our hospital because of liver dysfunction at 42 years. One year later, proteinuria and microhematuria were pointed out (43 years). Renal biopsy revealed MN with focal fibrocellular crescents. HBsAg, cryoglobulin, rheumatoid factor were all negative. Prednisolone was administered at the dose of 30 mg/day for 4 weeks and tapered subsequently. The steroid treatment was effective (urinary protein excretion: 4.2-->0.3 g/day, serum albumin: 2.4-->4.0 g/dl, 3 months later), and transaminase slightly elevated (GPT 50-->60-80 IU/l). One and a half years later he proved to be positive for HCV antibody, and corticosteroid administration was terminated. Subsequently proteinuria increased, and reached 3.0 g/day 6 years later. However, serological markers and ultrasonographic study for chronic hepatitis revealed mild changes of the liver. These findings suggest that corticosteroid therapy is not contraindicated against HCV-associated MN, and may possibly be used as the treatment for this condition.