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Complement profiles in acute post-streptococcal glomerulonephritis.

R J Wyatt¹, J Forristal, C D West

¹Department of Pediatrics, University of Tennessee, Memphis.

Pediatric Nephrology (Berlin, Germany)

|April 1, 1988

Summary

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Acute post-streptococcal glomerulonephritis (APSGN) frequently activates the classical complement pathway early on. This study found evidence of C4 activation in most patients, indicating a common immune response.

Area of Science:

Immunology
Nephrology
Complement System Biology

Background:

Hypocomplementemia in APSGN is known, with reduced C3, C5, and properdin.
The role of the classical complement pathway and terminal components in APSGN is not fully understood.
Limited data exists on serum concentrations of terminal complement components beyond C5.

Purpose of the Study:

To investigate the activation of the classical complement pathway in acute post-streptococcal glomerulonephritis (APSGN).
To assess C4 activation and serum concentrations of other complement components in children with APSGN.
To clarify the involvement of terminal complement components in the early stages of APSGN.

Main Methods:

Analysis of serial serum specimens from 14 children diagnosed with APSGN.

Related Experiment Videos

Measurement of C4 activation using rocket immunoelectrophoresis to determine the C4d/C4 ratio.

Quantification of C2, C5, C6, C8, and 13 other complement and control proteins.

Main Results:

Elevated C4d/C4 ratios, indicating C4 activation, were observed in 8 out of 14 initial serum specimens.
C4 activation persisted for several weeks in some patients; serum C4 levels were low in only one instance.
Depressed C2 levels were noted in 5 patients, and occasional low C6 and C8 levels were found, particularly in those with the lowest C3.

Conclusions:

The classical complement pathway is frequently activated early in the course of APSGN.
Subtle abnormalities in C6 and C8 levels can occasionally be present in APSGN patients.
These findings highlight the significant role of complement system activation in the pathophysiology of APSGN.