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[HB viral infection in kidney diseases in children]
Insights
Hepatitis B virus (HBV) infection markers were analyzed in children with kidney diseases. Active HBV infection, indicated by HBsAg and anti-HBc IgM, correlated with more severe glomerulonephritis (GN), suggesting HBV
Area of Science:
- Pediatric Nephrology
- Hepatology
- Immunology
Background:
- Nephropathies are common in children.
- Hepatitis B virus (HBV) infection is a global health concern.
- The role of HBV in pediatric kidney diseases requires further elucidation.
Purpose of the Study:
- To investigate the prevalence and significance of HBV infection markers in children with various nephropathies.
- To explore the correlation between HBV infection activity and the severity of glomerulonephritis (GN).
Main Methods:
- Enzyme immunoassay was used to detect HBV markers (HBsAg, anti-HBs, anti-HBc total immunoglobulins, anti-HBc IgM) in 142 children (aged 2-15 years) with nephropathies.
- Histological confirmation of diagnosis was performed in 36 children.
- Specific GN subtypes, including mesangial proliferative GN and membrane proliferative GN, were identified.
Main Results:
- All patients exhibited HBV infection markers.
- The combination of HBsAg and anti-HBc IgM, indicative of active HBV infection, was most characteristic in patients with nephrotic syndrome.
- This combination occurred twice as frequently in patients with mixed GN.
- A higher detection rate of HBsAg and anti-HBc IgM was observed in patients with membrane proliferative GN.
Conclusions:
- Active HBV infection is associated with specific nephropathies and disease severity in children.
- The findings suggest a potential role of HBV in the pathogenesis of pediatric glomerulonephritis.
- Further research is warranted to confirm the direct pathogenic role of HBV in these kidney diseases.
Abstract:
A total of 142 children aged 2-15 years with different nephropathies, among them 94 children with glomerulonephritis (GN), 26 children with pyelonephritis and 22 children with oxalate nephropathy, were examined. The diagnosis was histologically confirmed in 36 children. Mesangial proliferative GN was detected in 22 patients and membrane proliferative GN, in 14 children. The presence of the markers of HBV infection (HBsAg, anti-HBs and anti-HBc total immunoglobulins, anti-HBc IgM) was detected in the sera of all patients by the enzyme immunoassay. As the result of this examination, essential changes in the distribution of different markers of HBV infection in children with nephropathies were detected. The combination of HBsAg with anti-HBc IgM proved to be the most characteristic feature of patients with the nephrotic syndrome; this was indicative of active HBV infection, and in patients with the mixed form of GN this combination occurred twice as frequently. The established correlation between the activity of HBV infection and the severity of the course of GN made it possible to suggest the participation of HBV in the pathogenesis of GN. This suggestion was indirectly confirmed by a higher detection rate of HBsAg and anti-HBc IgM in patients with the membrane proliferative form of GN.