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Complement Activation Is Associated With Crescents in IgA Nephropathy.

Zi Wang1,2,3, Xinfang Xie1,2,3, Jingyi Li1,2,3

  • 1Renal Division, Peking University First Hospital, Peking University Institute of Nephrology, Beijing, China.

Frontiers in Immunology
|October 1, 2021
PubMed
Summary

Excess complement activation, particularly involving mannose-binding lectin (MBL) and C4d, is linked to crescent formation in IgA nephropathy (IgAN). Urinary C4d levels correlate with crescent proportion, serving as a potential biomarker for monitoring kidney disease progression.

Keywords:
complementcrescentimmunoglobulin A nephropathy (IgAN)lectin pathwayurinary C4d

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Area of Science:

  • Nephrology
  • Immunology
  • Molecular Biology

Background:

  • Crescents in IgA nephropathy (IgAN) are associated with rapid kidney disease progression.
  • The precise mechanisms driving crescent formation in IgAN remain incompletely understood.
  • Investigating the role of complement system overactivation is crucial for understanding IgAN pathogenesis.

Purpose of the Study:

  • To determine if excessive complement activation contributes to crescent formation in IgAN patients.
  • To evaluate the association between urinary complement markers and the proportion of crescents.
  • To assess the predictive value of complement activation markers for renal survival in IgAN.

Main Methods:

  • One hundred IgAN patients were categorized based on crescent percentage (0% to >75%).
  • Urinary levels of mannose-binding lectin (MBL), Bb, C4d, C3a, C5a, and soluble C5b-9 (sC5b-9) were quantified.
  • Immunohistochemistry was used to assess glomerular C4d, C5b-9, and C3d deposition; ROC curves analyzed predictive abilities.

Main Results:

  • Patients with >50% crescents exhibited significantly higher urinary C3a/Cr, C5a/Cr, and sC5b-9/Cr levels (p<0.001).
  • Urinary MBL and C4d levels showed a linear correlation with the proportion of crescents (r=0.457 and r=0.562, respectively; p<0.001).
  • Glomerular C4d deposition increased proportionally with crescent formation; combined urinary complement markers showed borderline improved prediction of renal survival.

Conclusions:

  • Excessive complement activation, particularly the lectin pathway, is implicated in crescent formation in IgAN.
  • Urinary C4d levels correlate with crescent proportion and may serve as a biomarker for monitoring disease activity.
  • These findings highlight complement activation as a key factor in the pathogenesis of crescentic IgAN.