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Distinct patterns of expression of intercellular adhesion molecule-1, vascular cell adhesion molecule-1, and
1Department of Pathology, University of Leiden, The Netherlands.
Insights
Cellular adhesion molecules like ICAM-1 and VCAM-1 are upregulated in diseased kidneys, indicating their role in immune-mediated renal diseases. This study highlights their distinct functions in kidney pathology.
Area of Science:
- Nephrology
- Immunology
- Pathology
Background:
- Investigates cellular adhesion molecules in normal and diseased human kidneys using immunohistochemistry.
- Analyzes 44 renal biopsies across eight pathological groups.
Purpose of the Study:
- To analyze the expression of intercellular adhesion molecule-1 (ICAM-1), vascular cell adhesion molecule-1 (VCAM-1), and endothelial-leukocyte adhesion molecule-1 (ELAM-1) in diseased versus normal kidneys.
- To determine the role of these adhesion molecules in the pathogenesis of immune-mediated renal diseases.
Main Methods:
- Immunohistochemical analysis of 44 renal biopsies.
- Blinded microscopical evaluation by two observers.
- Statistical analysis with p < 0.01.
Main Results:
- VCAM-1 showed decreased expression in small vessels but upregulation on interstitial arterioles/venules in diseased kidneys.
- ICAM-1 expression was significantly increased in various glomerulonephritides, including membranous nephropathy, Henoch-Schönlein purpura, IgA nephropathy, and lupus nephritis.
- ELAM-1 was increased on glomerular parietal epithelium and tubular epithelium in lupus nephritis and Henoch-Schönlein purpura.
Conclusions:
- First-time demonstration of endothelial VCAM-1 and ELAM-1 induction in the kidney.
- Findings suggest distinct roles for these adhesion molecules in the pathogenesis of immune-mediated renal diseases.
- Supports in vitro findings regarding the functions of ICAM-1, VCAM-1, and ELAM-1 in renal pathology.
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.
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