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IgM contributes to glomerular injury in FSGS
Derek Strassheim1, Brandon Renner, Sarah Panzer
1Department of Medicine, School of Medicine, University of Colorado Denver, Aurora, Colorado 80045, USA.
Journal of the American Society of Nephrology : JASN
|February 9, 2013
Summary
B cells and IgM antibodies contribute to kidney damage in glomerulosclerosis. Depleting B cells reduced kidney injury and albuminuria in a mouse model, suggesting new therapeutic targets for this disease.
Area of Science:
- Nephrology
- Immunology
- Pathology
Background:
- Glomerular IgM and C3 deposits are common in FSGS and secondary glomerulosclerosis.
- The role of IgM in complement activation and disease pathogenesis remains unclear.
Purpose of the Study:
- To investigate if IgM natural antibodies contribute to glomerulosclerosis pathogenesis by activating complement.
- To examine the therapeutic potential of B cell depletion in adriamycin-induced glomerulosclerosis.
Main Methods:
- Utilized three distinct B cell depletion strategies in wild-type and Jh mice before adriamycin administration.
- Assessed glomerular IgM and C3 deposition, and albuminuria levels.
- Examined kidney tissues from FSGS patients for IgM and C3 co-localization.
Main Results:
- All B cell depletion methods reduced glomerular IgM deposition and attenuated albuminuria in the mouse model.
- Glomerular IgM and C3 activation fragments were detected in a subset of FSGS patients, with IgM and C3 co-localizing.
- These findings suggest IgM activates the complement system in the glomerulus.
Conclusions:
- IgM natural antibodies may play a role in glomerulosclerosis pathogenesis by activating the complement cascade.
- Targeting IgM or complement activation presents a potential therapeutic strategy for slowing glomerulosclerosis progression.
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