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Crescentic glomerulonephritis related to hepatitis B virus
1Department of Anatomical and Cellular Pathology, Chinese University of Hong Kong, Shatin.
Insights
Hepatitis B infection can cause severe kidney disease, including crescentic glomerulonephritis. Some patients recover, while others require intensive treatment for kidney failure.
Area of Science:
- Nephrology
- Hepatology
- Virology
Background:
- Chronic hepatitis B infection is a global health concern.
- Hepatitis B virus (HBV) can affect various organs, including the kidneys.
- Glomerulonephritis is a serious kidney disease that can lead to renal failure.
Observation:
- Two patients with chronic hepatitis B surface antigenemia developed crescentic glomerulonephritis.
- Hepatitis B e antigen was detected in glomerular capillary tufts in both patients.
- One patient presented with nephrotic syndrome and acute renal failure, recovering spontaneously.
- The second patient initially had membranous nephropathy, which progressed to crescentic glomerulonephritis after interferon treatment, requiring immunosuppression and plasma exchange.
Findings:
- Crescentic glomerulonephritis is a potential renal manifestation of chronic hepatitis B.
- The presence of hepatitis B e antigen in glomeruli suggests a direct role in kidney injury.
- Treatment responses varied, with spontaneous recovery in one case and a need for aggressive therapy in another.
Implications:
- Early diagnosis and monitoring of renal function in chronic hepatitis B carriers are crucial.
- Understanding the pathogenesis of HBV-related glomerulonephritis can guide treatment strategies.
- Further research is needed to elucidate the mechanisms of kidney damage in HBV infection.
Abstract:
Crescentic glomerulonephritis was diagnosed in two chronic hepatitis B surface antigen carriers. In all three biopsies performed, hepatitis B e antigen was found in glomerular capillary tufts. The first patient presented with nephrotic syndrome and acute renal failure. The glomerular pathology revealed crescentic glomerulonephritis with endocapillary proliferation, and she recovered spontaneously with normal renal function over the following 6 mo despite a persistent hepatitis B surface antigenemia. The other patient presented with nephrotic syndrome and normal renal function. Hepatitis B virus-related membranous nephropathy was diagnosed on the first biopsy, and he did well on symptomatic treatment for 20 mo. The nephrotic syndrome recurred and subsequently he developed acute renal failure a month following interferon treatment. The repeated biopsy revealed a crescentic glomerulonephritis that was associated with mixed membranous and membranoproliferative glomerulopathies. This patient responded to immunosuppression and plasma exchange with residual impairment of renal function. He has been stable after 18 mo follow-up.