Distinct patterns of expression of intercellular adhesion molecule-1, vascular cell adhesion molecule-1, and...

We have conducted an immunohistochemical analysis to investigate the presence of cellular adhesion molecules in normal and diseased human kidneys.

A total of 44 renal biopsies were classified in eight groups according to pathologic diagnosis. Using immunohistochemistry, microscopical evaluation by two observers in a blinded fashion, and statistical analysis (p < 0.01), significant changes in the expression of intercellular adhesion molecule-1, vascular cell adhesion molecule-1, and endothelial-leukocyte adhesion molecule-1 were evaluated in diseased versus normal kidneys.

Small caliber vessels, such as peritubular and interstitial capillaries remained negative or showed decreased expression of vascular cell adhesion molecule-1. Upregulation of this molecule was seen only on the endothelium of interstitial arterioles and venules of diseased kidneys. Expression of intercellular adhesion molecule-1 was significantly increased on parietal epithelium of glomeruli in membranous nephropathy and Henoch-Schönlein purpura, on mesangium in Henoch-Schönlein purpura, membranoproliferative glomerulonephritis and IgA nephropathy, and in small interstitial vessels in membranous nephropathy and membranoproliferative glomerulonephritis. Interstitial infiltrates contained only few intercellular adhesion molecule-1-positive cells in Henoch-Schönlein purpura and IgA nephropathy. Kidneys with lupus nephritis and Henoch-Schönlein purpura demonstrated an increase of endothelial-leukocyte adhesion molecule-1 on parietal epithelium of glomeruli and on tubular epithelium. In membranoproliferative glomerulonephritis, this increase was seen only on parietal epithelium of glomeruli.

These results show for the first time (a) endothelial vascular cell adhesion molecule-1 induction in various glomerulonephritides and (b) endothelial-leukocyte adhesion molecule-1 induction in the kidney. Complementary to earlier in vitro work, our findings indicate that these molecules play distinct roles in the pathogenesis of immune-mediated renal disease.