29 April 1998
Mononuclear cells, primarily macrophages and lymphocytes, infiltrate the renal glomeruli and are involved in the progression of various glomerular diseases. Intercellular adhesion molecule 1 (ICAM-1) is expressed on the vascular endothelium and mediates the infiltration of leukocytes into the site of inflammation. Although the expression of ICAM-1 can be induced by the stimulation of inflammatory cytokine, ICAM-1 expression can also be induced by such nonimmune mechanisms as shear stress. Glomerular hyperfiltration is a major mechanism that contributes to the progression of the glomerular sclerosis that results from the loss of functioning nephrons. In the present study, we examined the role of ICAM-1 for mononuclear cell infiltration in the glomeruli of the five-sixth nephrectomized rat as a model of glomerular hyperfiltration. The fluorescence intensity score of the staining for ICAM-1 in the glomeruli of the five-sixth nephrectomized rats was significantly increased as compared with that in the control (sham-operated) rats at 1 week (1.51 ± 0.15 vs. 0.61 ± 0.13; p < 0.01) and 2 weeks (1.31 ± 0.17 vs. 0.51 ± 0.09; p < 0.01). The number of leukocytes present in the glomeruli was significantly increased in the five-sixth nephrectomized rats compared with control (sham-operated) rats at 1 week (3.44 ± 0.16 vs. 0.99 ± 0.08; p < 0.01) and 2 weeks (3.14 ± 0.14 vs. 0.89 ± 0.07; p < 0.01). Leukocytes mainly consisted of macrophages in the five-sixth nephrectomized rats at 1 week (2.39 ± 0.19) and 2 weeks (1.46 ± 0.11). Anti-ICAM-1 monoclonal antibody effectively prevented the infiltration of macrophages into the glomeruli following nephrectomy. These results indicate that glomerular hyperfiltration may be involved in the induction of the expression of ICAM-1 and the infiltration of macrophages into the renal glomeruli following glomerular injury.