PubMed · 13006385
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1952. SUBACUTE glomerulonephritis.. https://pubmed.ncbi.nlm.nih.gov/13006385/
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A direct causal association between hepatitis B virus (HBV) infection and the development of nephropathy remains controversial. Epidemiological studies have shown that chronic carriage of HBV in some individuals (particularly children) leads to the development of nephrotic syndrome with a strong male predominance, the commonest histological type being membranous nephropathy (MN). Spontaneous clearance of HBV antigens (particularly the HBeAg) leads to abrogation of proteinuria. The isolation of immune complexes in the kidney suggests that the pathogenesis of the disease may have an immune-complex basis. Recent studies showing expression of HBV viral antigens in kidney tissue suggest direct viral-induced pathological alterations and chronic immunologic injury. Biosocial studies have detected no correlation between HBV carriage and proteinuria using both quantitative and qualitative urinary protein analysis. Genetic studies of HLA class I and II genes showed a predisposition to MN but no similar correlation in those with milder degrees of proteinuria. These findings suggest that milder proteinuria is unrelated to HBV carriage or genetic factors but the development of nephropathy, particularly MN, in patients with chronic HBV carriage (HBsAg and/or HBV DNA positive) is based on an interaction of virus and host factors. Although the natural history of the disease tends to remission with preservation of renal function, there is considerable morbidity and a small but significant mortality. Use of naturally occurring cytokines (such as interferon-alpha2b) and other candidate therapies accelerates clearance of the virus and proteinuria. The most effective tool in reducing the incidence of the disease is the use of HBV vaccines.
Hepatitis C virus (HCV) infection is the main cause of chronic liver disease after renal transplantation (RT). It is considered in some series to be a risk factor for graft loss and patient death. Also, HCV has been implicated in the pathogenesis of glomerular diseases in native and transplanted kidneys. The presence of membranoproliferative (MP) or membranous (M) glomerulonephritis (GN) in HCV-positive patients has been well documented after RT, but there is no clear data concerning the real prevalence of HCV-induced glomerulonephritis. MPGN with or without cryoglobulinemia and MGN have been described in HCV RNA-positive patients in general without severe liver disease. Also, there is a possible association between HCV infection and acute/chronic transplant glomerulopathy. Renal thrombotic microangiopathy has been described in HCV-positive patients with positive anti-cardolipin antibodies. The pathogenesis of MPGN and MGN in HCV patients after RT seems to be similar to that which occurs in native kidneys: the deposition of immune complexes containing HCV proteins in the glomeruli. Renal biopsy, using light microscopy, immunofluorescence techniques, and electron microscopy, is useful to achieve a correct diagnosis. Unfortunately, interferon is not recommended due to the significant risk of rejection. The possibility of pegylated interferon needs to be tested. Ribavirin can improve proteinuria but HCV RNA remains positive. Finally, recent data suggest that the use of interferon in HCV patients on dialysis can negate HCV RNA and prevent associated glomerulonephritis after RT.