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Histopathology |
1 Department of Pediatric Cardiology and Nephrology, University of Medical Sciences in Poznan, Poland
2 Department of Histology and Embryology, University of Medical Sciences in Poznan, Poland
3 Department of Clinical Pathomorphology, University of Medical Sciences in Poznan, Poland
4 Department of Pediatric Cardiology and Nephrology, Univeristy of Medical Sciences in Poznan
5 Department of Anatomy, Technical University in Dresden, Germany
* To whom correspondence should be addressed. E-mail: dostalska{at}interia.pl.
Accepted 3 October 2005
| Abstract |
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Introduction: Minimal change disease (MCD) and diffuse mesangial proliferation (DMP) are the most common pathomorphological forms of nephrotic syndrome glomerulopathies in children. The clinical course of DMP can be characterized by sensitivity (DMP-S) or resistance (DMP-R) to steroids (the unfavourable course of the glomerulopathy). Although the clinical process of DMP-S and DMP-R are intially identical, the resistance to steroids may be foreseen by the immunohistochemical expression of cytoskeleton - associated proteins.
Aim: To estimate the immunohistochemical expression of ezrin in children with MCD, DMP and focal segmental glomerulosclerosis (FSGS) and to evaluate its usefullness in prognosis of the resistance to steroids.
Methods: Material included renal biopsies of MCD (n = 15), DMP (n = 16) and FSGS (n = 6). The control tissue consisted of normal appearing cortex taken from kidneys resected for localized neoplasms (n=6). The indirect immunohistochemical protocol with the use of a monoclonal antibody directed against ezrin was employed.
Results: Immunohistochemical expression of ezrin decreased from MCD, DMP-S, DMP-R to FSGS cases. Except of DMP-R and FSGS (p>0.05) the difference in the ezrin expression within podocytes was statistically significant.
Conclusions: Ezrin can be a potent marker of podocyte injury (podocytopathy) and may help in the histological qualification of MCD, DMP and FSGS. The increased permeability of the filtration barrier in steroid-resistant and proteinuric glomerulopathies may be a consequence of subcellular alterations of podocyte-associated proteins following decreased expression of ezrin.
Key Words: ezrin, immunohistochemistry, nephrotic syndrome, podocyte
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