What is the role of nephritis-associated plasmin receptor (NAPlr) in the pathogenesis of acute poststreptococcal glomerulonephritis (APSGN)?

Updated: Dec 05, 2018
  • Author: Rajendra Bhimma, MBChB, MD, PhD, DCH (SA), FCP(Paeds)(SA), MMed(Natal); Chief Editor: Craig B Langman, MD  more...
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Yoshizawa et all isolated a 43-kd protein called preabsorbing antigen (PA-Ag) that is putatively identical to endostreptosin. [14, 15] PA-Ag has the ability to “preabsorb” the antibody in convalescent sera from patients with APSGN and thus prevent its deposition in glomeruli. PA-Ag activates the alternative pathway. [15] This 43-kd protein was later identified by Yamakami et al as NAPlr. [16] These researchers noted that NAPlr was present in 100% of the early biopsy samples from in glomeruli of patients with APSGN. [17] The glomerular distribution of NAPlr deposition and plasmin activity determined by in situ zymography are identical.

The fact that NAPlr did not co-localize with C3 in glomerular deposits suggests that: (1) complement was activated by NAPlr in the circulation rather than in situ, and (2) NAPlr induced APSGN independently of complement activation by binding to the glomerular basement membrane (GBM) and mesangial matrix via its adhesive character, subsequently trapping and activating plasmin and causing in situ glomerular damage by degrading the GBM or activating latent matrix metalloproteases. [17, 18]

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