Heterogeneity of antibody response to glomerular basement membrane antigen in patients with different forms of glomerulonephritis.

Antibodies to collagenous and noncollagenous components of glomerular basement membrane (GBM) have been detected by immunoblotting in some sera from patients with various kinds of glomerulonephritis. A half proportion of patients with rapidly progressive glomerulonephritis (RPGN), chronic focal glomerulonephritis (CFGN), idiopathic membranous glomerulonephritis (MGN). IgA nephropathy and lupus nephritis (LE-GN) had IgG antibodies to heterogenous components in acid insoluble fraction of pepsin digested GBM. This acid insoluble fraction represented a complex of collagen and noncollagenous proteins of GBM. Following digestion of acid insoluble fraction with bacterial collagenase, the triple helical collagenous components of GBM were destroyed and released most likely of noncollagenous proteins. Antibodies to this noncollagenous proteins were found in only some patients with chronic glomerulonephritis (17.6%) and lupus nephritis (21.4%). Upon reaction with human placenta derived type IV collagen, different frequencies of antibody response were found in patients of different groups. However, all these reactive sera showed a similar immunoblotting pattern. The relationship between antibody response to antigenic components from human GBM or human placenta and pathogenesis of renal disease is unclear. However, the occurrence of spontaneous autoantibody response to some exposed GBM self antigens may mediate further renal destruction resulting in chronic ongoing stage of the disease.

Development of immune-complex glomerulonephritis and amyloidosis in Syrian golden hamsters infected with Opisthorchis viverrini.

Renal disease associated with Opisthorchis viverrini infection was investigated in Syrian golden hamsters. On the fourth week after infection with 100 viable metacercariae; anti-tegumental membrane antibodies were detected in the sera by immunofluorescence antibody technic and by enzyme-linked immunosorbent assay. Six weeks after infection tegumental and anti-tegumental membrane immune-complex and amyloid fibrils were found in the glomeruli. Amyloid was characterized to be AA protein. Acute proliferative glomerulonephritis associated with the brightest immune-complex deposits developed in week 8 after infection. Intensity of immune-complexes in all glomeruli were reduce gradually thereafter and replaced by amyloid. Progressive obsolescence of the glomeruli, tubular atrophy, interstitial inflammation and fibrosis associated with massive proteinuria and deterioration of renal function appeared in week 10 after infection toward the end of the experiment in week 38 after infection.