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Glomerular Complement Factor H-Related Protein 5 (FHR5) Is Highly Prevalent in C3 Glomerulopathy and Associated With

Nicholas R Medjeral-Thomas1, Hilary Moffitt1, Hannah J Lomax-Browne1

  • 1Centre for Inflammatory Disease, Division of Immunology and Inflammation, Department of Medicine, Imperial College London, UK.

Kidney International Reports
|November 9, 2019
PubMed

Insights

Complement factor H-related protein 5 (FHR5) is common in C3 glomerulopathy (C3G) and linked to kidney damage. Targeting FHR5 may help treat C3G by reducing complement-mediated injury.

Area of Science:

  • Nephrology
  • Immunology
  • Complement System Biology

Background:

  • Therapeutic targeting of the complement system is advancing for glomerular diseases.
  • Mechanisms linking glomerular complement deposition to inflammation and damage remain unclear.
  • Complement factor H-related protein 5 (FHR5) interacts with C3 and may promote complement activation.

Purpose of the Study:

  • To characterize glomerular FHR5 staining in C3 glomerulopathy (C3G).
  • To assess the relationship between glomerular FHR5 and histological features of kidney injury.
  • To evaluate the association of glomerular FHR5 with clinical outcomes in C3G patients.

Main Methods:

  • Developed staining protocols for FHR5 in formalin-fixed paraffin-embedded renal tissue.
  • Applied FHR5 staining to biopsy sections from a C3G cohort.
  • Correlated FHR5 staining with complement components (C3, C5b-9) and clinical parameters (eGFR, histology).

Main Results:

  • Glomerular FHR5 was highly prevalent in native and transplant C3G, correlating with C3 and C5b-9 deposition.
  • FHR5 staining negatively correlated with estimated glomerular filtration rate (eGFR).
  • Increased FHR5 staining was associated with a membranoproliferative glomerulonephritis pattern and markers of complement activation (C3b/iC3b/C3c, C3dg, C5b9).

Conclusions:

  • Glomerular FHR5 is prevalent in C3G and interacts with glomerular C3, indicating a role in disease severity.
  • Glomerular FHR5 likely exacerbates complement-mediated kidney damage in C3G.
  • FHR5's interaction with glomerular complement presents a potential therapeutic target for C3G.
Abstract

Keywords:
C3 glomerulopathycomplementglomerulonephritis

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