Distinct patterns of expression of intercellular adhesion molecule-1, vascular cell adhesion molecule-1, and endothelial-leukocyte adhesion molecule-1 in renal disease

Lab Invest. 1993 Sep;69(3):329-35.

Abstract

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

Experimental design: 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.

Results: 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.

Conclusions: 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.

MeSH terms

  • Antibodies, Monoclonal
  • Biopsy
  • Cell Adhesion Molecules / analysis
  • Cell Adhesion Molecules / biosynthesis*
  • E-Selectin
  • Epithelium / pathology
  • Humans
  • Immunoenzyme Techniques
  • Intercellular Adhesion Molecule-1
  • Kidney / metabolism*
  • Kidney / pathology*
  • Kidney Diseases / metabolism*
  • Kidney Diseases / pathology*
  • Muscle, Smooth, Vascular / metabolism
  • Muscle, Smooth, Vascular / pathology
  • Organ Specificity
  • Reference Values
  • Renal Circulation
  • Vascular Cell Adhesion Molecule-1

Substances

  • Antibodies, Monoclonal
  • Cell Adhesion Molecules
  • E-Selectin
  • Vascular Cell Adhesion Molecule-1
  • Intercellular Adhesion Molecule-1