Related Experiment Videos
Localization of decay accelerating factor in normal and diseased kidneys
F G Cosio1, D D Sedmak, J D Mahan
1Department of Internal Medicine, Ohio State University, Columbus.
Kidney International
|July 1, 1989
Summary
Decay accelerating factor (DAF) is found in normal kidneys, but is decreased in diseased kidneys. Its altered presence in kidney disease correlates with complement deposition, suggesting a protective role.
Area of Science:
- Nephrology
- Immunology
- Cell Biology
Background:
- Decay accelerating factor (DAF) is a glycoprotein inhibiting complement C3 activation.
- DAF is associated with cell membranes and plays a role in regulating complement pathways.
Purpose of the Study:
- To evaluate the presence and localization of DAF in normal and diseased human kidneys.
- To investigate the correlation between DAF distribution and kidney pathology, including complement deposition.
Main Methods:
- Immunoperoxidase staining of frozen kidney tissue sections from 15 normal and 76 diseased kidneys.
- Utilized three mouse monoclonal anti-DAF antibodies for DAF detection.
- Correlated DAF localization with pathological diagnoses and complement component (C1q, C3, IgM, fibrinogen) deposition.
Main Results:
- In normal kidneys, DAF was exclusively localized to the glomerular vascular pole (juxtaglomerular apparatus - JGA).
- In diseased kidneys, JGA-DAF was significantly decreased, correlating with complement deposition (C3, IgM, fibrinogen).
- DAF was aberrantly detected in the glomerular mesangium (67%), renal interstitium (68%), and blood vessels (38%) of diseased kidneys, correlating with C1q and C3 deposition.
Conclusions:
- DAF is present in the normal kidney exclusively at the glomerular vascular pole.
- Diseased kidneys show reduced DAF at the JGA and increased DAF in the mesangium, interstitium, and vasculature.
- Altered DAF distribution in kidney disease, particularly with complement deposition, suggests a potential role in kidney protection against complement-mediated damage.