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Pathogenetic mechanisms involved in mesangial interposition in IgA nephropathy
1Second Department of Internal Medicine, University of Occupational and Environmental Health Japan. School of Medicine, Kitakyushu.
Nephron
|January 1, 1994
Summary
Mesangial interposition in IgA nephropathy involves mesangial cell protrusions and lamina rara interna widening. Platelet-derived growth factor-BB (PDGF-BB) in glomerular endothelial cells may also contribute to this kidney disease mechanism.
Area of Science:
- Nephrology
- Pathology
- Cell Biology
Background:
- IgA nephropathy is a common glomerular disease.
- Mesangial interposition (MI) is a characteristic finding in IgA nephropathy, but its pathogenesis is not fully understood.
Purpose of the Study:
- To elucidate the pathogenetic mechanisms of mesangial interposition (MI) in IgA nephropathy.
- To identify cellular and molecular factors contributing to MI.
Main Methods:
- Examination of renal biopsy samples from 20 IgA nephropathy patients.
- Electron microscopic morphometric analysis.
- Immunoelectron microscopy using antibodies against human platelet-derived growth factor (PDGF) BB and fibronectin.
Main Results:
- Cytoplasmic protrusion of mesangial cells (MCs) into endothelial cells (ECs) or capillary lumina and widening of the lamina rara interna (LRI) were significantly increased in glomeruli with MI.
- Higher endothelial staining for PDGF-BB was observed in capillary loops with MI.
- No enhanced capillary staining for fibronectin related to MI was detected.
Conclusions:
- MI in IgA nephropathy is associated with enhanced MC cytoplasmic extensibility and LRI widening.
- Chemotactic influence of PDGF-BB in glomerular ECs appears to play a role in MI pathogenesis.
- These findings provide insights into the cellular mechanisms driving IgA nephropathy progression.