PRECISE ULTRASTRUCTURAL-LOCALIZATION OF ENDOTHELIAL-LEUKOCYTE ADHESION MOLECULE-1, VASCULAR CELL-ADHESION MOLECULE-1, AND INTERCELLULAR-ADHESION MOLECULE-1 IN PATIENTS WITH IGA NEPHROPATHY

Using light and electron microscopy, we performed an immunohistochemic al study of endothelial leukocyte adhesion molecule-1 (ELAM-1), vascul ar cell adhesion molecule-1 (VCAM-1), and intercellular adhesion molec ule-1 (ICAM-1) in 15 patients with IgA nephropathy to clarify the loca lization of these adhesion molecules. The normal portions of 2 kidneys removed due to localized carcinoma and 3 biopsies from patients witho ut glomerular disease were used as a control. By light microscopy, ELA M-1, VCAM-1, and ICAM-1 all showed positive staining in IgA nephropath y, with the intensity of staining following the sequence ICAM-1 > VCAM -1 > ELAM-1. ELAM-1 and VCAM-1 showed a patchy distribution of moderat e staining in the tissues, including the mesangium, crescents, adhesio ns, 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 ass ociation with inflammatory cell infiltration, while ICAM-1 was found o n the brush border. ICAM-1 was positive in the glomerular capillary wa lls and interstitial vessels of the control kidney tissue, while ELAM- 1 and VCAM-1 were virtually absent. By electron microscopy, ELAM-1 pos itivity on the urinary surface of the parietal/visceral epithelial cel ls was often associated with adherent mononuclear cells in the urinary space. VCAM-1 positivity was increased in the perinuclear space and/o r cytoplasm of mesangial cells as well as at the mesangial cell-endoth elial cell interface. These findings suggest that ELAM-1 and VCAM-1 ma y be more closely related than ICAM-1 to the major histopathological c hanges occurring in IgA nephropathy, including mesangial expansion, fo rmation of crescents and adhesions, and tubulointerstitial injury.