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Mesangial immune complex glomerulonephritis due to complement factor D deficiency.

M A Abrera-Abeleda1, Y Xu, M C Pickering

  • 1Department of Otolaryngology, University of Iowa, Iowa City, Iowa, USA.

Kidney International
|April 6, 2007
PubMed
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Mice lacking complement factor D develop spontaneous kidney disease with immune deposits in the mesangium. This suggests factor D is crucial for preventing glomerulonephritis, offering a new disease model.

Area of Science:

  • Immunology
  • Nephrology
  • Complement System

Background:

  • Complement factor D (Factor D) is a serine protease vital for the alternative pathway.
  • Factor D is present in the kidney glomeruli, hinting at a role in renal pathophysiology.
  • The alternative pathway of complement activation plays a role in immune complex-mediated kidney diseases.

Purpose of the Study:

  • To investigate the role of complement factor D in spontaneous glomerulonephritis.
  • To characterize the renal pathology in mice lacking factor D.
  • To compare the kidney disease phenotype in factor D-deficient mice with factor H-deficient mice.

Main Methods:

  • Utilized gene-targeted knockout mice lacking the complement factor D gene.
  • Compared factor D-deficient mice with age-matched mice lacking the complement factor H gene.

Related Experiment Videos

  • Assessed renal function through measurements of albuminuria and creatinine clearance.

    • Main Results:

    • Factor D-deficient mice spontaneously developed albuminuria and reduced creatinine clearance at eight months of age.
    • Histopathological analysis revealed mesangial immune complex glomerulonephritis in factor D-deficient mice, with deposits of C3 and IgM.
    • Factor H-deficient mice exhibited immune deposits along the glomerular capillary wall, differing from the mesangial location in factor D-deficient mice.

    Conclusions:

    • Complement factor D, or alternative pathway activation, is essential for preventing spontaneous C3 and IgM deposition in the renal mesangium.
    • Factor D-deficient mice represent a novel genetic model for studying spontaneous mesangial immune complex glomerulonephritis.
    • The localization of immune deposits differs between factor D and factor H deficiency, highlighting distinct roles in complement regulation within the glomerulus.