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Related Experiment Videos

Experimental immune complex-mediated glomerulonephritis in the nonhuman primate.

L A Hebert1, F G Cosio, D J Birmingham

  • 1Department of Internal Medicine, Ohio State University, Columbus.

Kidney International
|January 1, 1991
PubMed
Summary

A new nonhuman primate model effectively induces immune complex-mediated glomerulonephritis (GN). Erythrocyte complement receptor (E-CR) levels decrease during GN induction, suggesting E-CR may protect against this disease.

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Area of Science:

  • Immunology
  • Nephrology
  • Primate Models

Background:

  • Immune complex (IC)-mediated glomerulonephritis (GN) is a significant kidney disease.
  • The role of erythrocyte complement receptor (E-CR) in IC-mediated GN pathogenesis is not fully understood.

Purpose of the Study:

  • To develop a nonhuman primate model of IC-mediated GN.
  • To investigate the role of E-CR in the pathogenesis of IC-mediated GN.

Main Methods:

  • Cynomolgus monkeys with varying E-CR levels were immunized with bovine gamma globulin (BGG).
  • GN induction was achieved through daily BGG administration.
  • Glomerular deposits and E-CR levels were quantified using morphometric studies and assays.

Main Results:

Related Experiment Videos

  • All cynomolgus monkeys developed IC-mediated GN within eight weeks.
  • Higher initial E-CR levels showed a tendency towards fewer glomerular deposits per BGG dose.
  • E-CR levels and the ability of erythrocytes to bind IC significantly decreased during GN induction.

Conclusions:

  • A viable nonhuman primate model for IC-mediated GN was established.
  • Decreased E-CR function during GN induction suggests a potential protective role for E-CR.
  • Further research is warranted to confirm the protective role of E-CR in IC-mediated diseases.