Abstract
It is well known that glomerulonephritis can occur after streptococcal infection, which is classically referred to as acute poststreptococcal glomerulonephritis (APSGN). The pathogenic mechanism of APSGN has been described by so-called immune complex theory, which involves glomerular deposition of nephritogenic streptococcal antigen and subsequent formation of immune complexes in situ and/or the deposition of circulating antigen-antibody complexes. However, the exact entity of the causative antigen has remained a matter of debate. We isolated a nephritogenic antigen for APSGN from the cytoplasmic fractions of group A streptococcus (GAS) depending on the affinity for IgG of APSGN patients. The amino acid and the nucleotide sequences of the isolated protein revealed to be highly identical to those of reported plasmin(ogen) receptor of GAS. Thus, we termed this antigen nephritis-associated plasmin receptor (NAPlr). Immunofluorescence staining of the renal biopsy tissues with anti-NAPlr antibody revealed glomerular NAPlr deposition in essentially all patients with early-phase APSGN. Furthermore, glomerular plasmin activity was detected by in situ zymography in the distribution almost identical to NAPlr deposition in renal biopsy tissues of APSGN patients. These data suggest that NAPlr has a direct, nonimmunologic function as a plasmin receptor and may contribute to the pathogenesis of APSGN by maintaining plasmin activity.
Highlights
Acute poststreptococcal glomerulonephritis (APSGN) develops after streptococcal infection with the obvious latent period of around 10 days
As nephritis-associated plasmin receptor (NAPlr) was found to be localized mainly in neutrophils, we examined the plasmin activity of glomerular neutrophils and found that many were positive for plasmin activity in renal tissues from APSGN patients (Figures 5(a)– 5(c))
We believe that there is a subgroup of patients in these diseases (DDD, membranoproliferative glomerulonephritis (MPGN), and Henoch-Schonlein Purpura nephritis (HSPN)) in which glomerulonephritis is induced by streptococcal infection and subsequent glomerular deposition of NAPlr and related plasmin activity
Summary
Acute poststreptococcal glomerulonephritis (APSGN) develops after streptococcal infection with the obvious latent period of around 10 days It is mostly accompanied by decrement in serum complement titer and glomerular deposition of C3 and IgG. The amino acid and the nucleotide sequences of the antigen revealed to be highly identical to those of reported Plr, or glyceraldehyde-3-phosphate dehydrogenase (GAPDH) of GAS [7,8,9,10]. We termed this antigen NAPlr. Plr has been shown in vitro to bind plasmin and maintain its proteolytic activity by protecting it from physiologic inhibitors like α2-antiplasmin (α2-AP) [11]. Further analysis revealed the nephritogenic characteristics of the isolated antigen as described
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