EXPRESSION OF BCL-2 ONCOPROTEIN IN VARIOUS TYPES OF GLOMERULONEPHRITIS AND RENAL-ALLOGRAFTS

Background. Bcl-2 oncogene was identified as a transcript associated w ith the t (14;18) and exhibits the unique functional role of blocking apoptosis. Apoptosis as a remodelling mechanism has been reported to e mbryonic and adult kidney. The aim of this study was to investigate th e expression of bcl-2 protein in normal and diseased renal tissue and to define any correlation with the type of renal injury. Materials and methods. Our material comprised of 10 normal adult kidneys, 31 renal allografts with acute (22) and chronic (9) rejection, and 70 renal bio psies with various types of primary (49) (31 proliferative and 18 non- proliferative) and secondary (21) glomerulonephritis. The immunohistoc hemical strept.ABC method was performed on paraffin sections for the d etection of bcl-2 protein with a monoclonal antibody after microwave p retreatment. Results. Bcl-2 protein was detected in all the cases of n ormal and diseased renal tissue, showing an analogous expression. The antigen was expressed in a few parietal epithelial cells, in scattered proximal tubular epithelial cells, and in the majority of distal and collecting tubular epithelial cells, but not in the glomerular capilla ry tuft. No difference was found in bcl-2 expression between cases of proliferative and nonproliferative glomerulonephritis as a whole, or b etween primary and secondary glomerulonephritis. Bcl-2 expression in a cute and chronic rejection demonstrated a similar cytoarchitectural ex pression to the one observed in normal kidneys and glomerulonephritis. Bcl-2 was detected in podocytes near intraglomerular fibrotic lesions and in epithelial cells of early adhesions and cellular crescents, wh erever observed in cases of glomerulonephritis. However, bcl-2 express ion in proximal tubular epithelial cells was significantly higher in c ases of proliferative glomerulonephritis than in nonproliferative glom erulonephritis (P<0.001), while bcl-2 expression in parietal epithelia l cells in cases of chronic rejection was higher than in cases of acut e rejection (P<0.08). Conclusions. The absence of bcl-2 expression in normal and diseased glomeruli suggests and supports the reported notio n that the mechanism of apoptosis may be available in the injured glom erulus. Moreover, bcl-2 expression in podocytes near intraglomerular f ibrotic lesions and in epithelial cells of early adhesions and cellula r crescents indicates the deregulation of apoptosis and its possible r ole in the progression of glomerular scarring.