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Glomerular C3 receptors in human renal disease
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Glomerular C3 receptor activity significantly decreases with C3 deposition along the glomerular basement membrane in kidney disease. Podocyte interaction with C3 appears crucial for this loss of receptor activity.
Area of Science:
- Nephrology
- Immunology
- Pathology
Background:
- Glomerular C3 deposition is a hallmark of various kidney diseases.
- The role of C3 receptor activity in the pathogenesis of these conditions is not fully understood.
Purpose of the Study:
- To investigate the correlation between glomerular C3 receptor activity and intraglomerular C3 deposition in diverse renal diseases.
- To elucidate the cellular interactions influencing C3 receptor function in glomerular pathology.
Main Methods:
- Studied 73 cases of renal disease.
- Measured C3 receptor activity by quantifying complement-coated sheep red blood cell (IgM EAC) adherence to glomeruli.
- Assessed C3 deposition in adjacent kidney sections using light and electron microscopy.
Main Results:
- Marked reduction in C3 receptor activity observed when C3 deposits accumulated along the glomerular basement membrane (subepithelial, intramembranous, or subendothelial locations).
- Moderate or no impact on C3 receptor activity when C3 was undetectable or confined to the mesangium.
- Data suggest podocyte interaction with C3 is a primary factor in C3 receptor activity loss.
Conclusions:
- Podocyte interaction with C3 is a significant determinant of C3 receptor activity loss in glomerular disease.
- Mesangial or endothelial cell interactions with C3 may also contribute to altered C3 receptor activity.
Abstract:
The relationship between glomerular C3 receptor activity and intraglomerular C3 deposition was studied in 73 cases of various forms of renal disease. C3 receptor activity was measured by enumeration of complement-coated sheep red blood cells (IgM EAC) that adhered to glomeruli in frozen sections and expressed as a percentage of the mean number present in control kidneys. Adjacent sections were studied for the presence and distribution of C3 deposits. The precise location of corresponding dense deposits was determined through 1-mu sections or electron micrographs. Marked depression of C3 receptor activity was found in most cases in which there was accumulation of C3 along the glomerular basement membrane, irrespective of whether the deposits were in a subepithelial, intramembranous, or subendothelial location. In contrast, when C3 was not detectable or was found exclusively in the mesangium, C3 receptor activity was affected only moderately, if at all. These data are consistent with the hypothesis that the interaction of C3 with podocytes is a major determinant in the loss of C3 receptor activity in glomerular disease, but do not exclude the possibility that interaction with mesangial or endothelial cells may also influence C3 receptor activity.