title: Precise ultrastructural localization of endothelial leukocyte adhesion molecule-1, vascular cell adhesion molecule-1, and intercellular adhesion molecule-1 in patients with IgA nephropathy.
abstract: Using light and electron microscopy, we performed an immunohistochemical study of endothelial leukocyte adhesion molecule-1 (ELAM-1), vascular cell adhesion molecule-1 (VCAM-1), and intercellular adhesion molecule-1 (ICAM-1) in 15 patients with IgA nephropathy to clarify the localization of these adhesion molecules. The normal portions of 2 kidneys removed due to localized carcinoma and 3 biopsies from patients without glomerular disease were used as a control. By light microscopy, ELAM-1, VCAM-1, and ICAM-1 all showed positive staining in IgA nephropathy, with the intensity of staining following the sequence ICAM-1 > VCAM-1 > ELAM-1. ELAM-1 and VCAM-1 showed a patchy distribution of moderate staining in the tissues, including the mesangium, crescents, adhesions, and tubules. In contrast, there was marked linear ICAM-1 staining throughout the vascular walls. ELAM-1 and VCAM-1 were positive on the basolateral surfaces of a few proximal tubular epithelial cells in association with inflammatory cell infiltration, while ICAM-1 was found on the brush border. ICAM-1 was positive in the glomerular capillary walls and interstitial vessels of the control kidney tissue, while ELAM-1 and VCAM-1 were virtually absent. By electron microscopy, ELAM-1 positivity on the urinary surface of the parietal/visceral epithelial cells was often associated with adherent mononuclear cells in the urinary space. VCAM-1 positivity was increased in the perinuclear space and/or cytoplasm of mesangial cells as well as at the mesangial cell-endothelial cell interface. These findings suggest that ELAM-1 and VCAM-1 may be more closely related than ICAM-1 to the major histopathological changes occurring in IgA nephropathy, including mesangial expansion, formation of crescents and adhesions, and tubulointerstitial injury.
authors.affiliation: 2nd Department of Internal Medicine, Hiroshima University School of Medicine, Japan.
authors.forename: T
authors.initials: T
authors.lastname: Ogawa
authors.forename: N
authors.initials: N
authors.lastname: Yorioka
authors.forename: T
authors.initials: T
authors.lastname: Ito
authors.forename: S
authors.initials: S
authors.lastname: Ogata
authors.forename: J
authors.initials: J
authors.lastname: Kumagai
authors.forename: H
authors.initials: H
authors.lastname: Kawanishi
authors.forename: M
authors.initials: M
authors.lastname: Yamakido
mesh_terms: D000293:Adolescent; D000328:Adult; D000368:Aged; D000911:Antibodies, Monoclonal; D015415:Biomarkers; D001706:Biopsy; D019040:E-Selectin / Q000276:immunology / Q000648:ultrastructure*; D005260:Female; D005922:Glomerulonephritis, IGA / Q000473:pathology*; D006801:Humans; D007150:Immunohistochemistry; D018799:Intercellular Adhesion Molecule-1 / Q000276:immunology / Q000648:ultrastructure*; D008297:Male; D016253:Microscopy, Immunoelectron; D008875:Middle Aged; D009399:Nephrons / Q000648:ultrastructure*; D019010:Vascular Cell Adhesion Molecule-1 / Q000276:immunology / Q000648:ultrastructure*
chemical_list: D000911:Antibodies, Monoclonal; D015415:Biomarkers; D019040:E-Selectin; D019010:Vascular Cell Adhesion Molecule-1; D018799:Intercellular Adhesion Molecule-1