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Background: The upregulated renal expression of intercellular adhesion molecule 1 (ICAM-1) is associated with glomerular and interstitial infiltration of leukocytes., Aim: To test the hypothesis that renal expression of ICAM-1 may be predictive in the highly variable IgA nephropathy (IgAN)., Methods: ICAM-1 (CD54) in tubular epithelium and interstitial leukocytes, macrophages (CD14), and T cells (CD3) were assessed using avidin-biotin-peroxidase in renal biopsy specimens from 45 patients with IgAN and from 29 patients with no glomerulonephritis., Results: In IgAN, tubular ICAM-1+ was seen in 25 of 45 (55%) biopsy specimens, associated with glomerular hypercellularity, glomerulosclerosis involving less than 50% of the glomerular area, interstitial cellular infiltration, tubular atrophy, and proteinuria (U = 44, p = 0.005). Interstitial ICAM-1+ leukocytes were correlated with glomerulosclerosis involving less and more than 50% of the glomerular area, tubular atrophy, interstitial fibrosis, and serum creatinine concentration (r = 0.6343, p < 0.001). In patients with an increase of 50% in the serum creatinine concentration, interstitial ICAM-1+ leukocytes and CD14+ and CD3+ cells were significantly more numerous than in patients with a stable creatinine concentration. In patients with no glomerulonephritis, tubular ICAM-1+ was seen in 7 of 29 (24%) biopsy specimens, inversely correlated with the number of normal glomeruli and associated with glomerulosclerosis covering more than 50% of the glomerular area, tubular atrophy, and creatinine., Conclusions: Tubular and interstitial expression of ICAM-1 can be a marker of tubulointerstitial disturbance in IgAN. Interstitial ICAM-1 may be an adverse predictor of disease progression., (Copyright 2003 S. Karger AG, Basel)

Background: The aim of this study was to determine the significance of the renal expression of ICAM-1 in IgA nephropathy (IgAN)., Patients and Method: First, we identified ICAM-1 (CD54) expression in tubular epithelial cells and interstitial leucocytes in renal biopsies from 45 patients with IgAN and 29 patients with non-glomerulonephritis nephropathy (non-GN). We then analysed the relationship between this expression and both histological and clinical data at the time of renal biopsy and after 2.4 (2) (X [SD]) years in IgAN, and 1.8 (1.5) years in non-GN., Results: In IgAN, tubular ICAM-1 positive staining was seen in 25 (55%) biopsies; it was associated with extracapillary proliferation, glomerulosclerosis involving less than 50% of glomerular area, interstitial cell infiltration and tubular atrophy. ICAM-1 positive interstitial leucocytes were 234 (307)/mm2; this expression correlated with glomerulosclerosis, tubular atrophy, interstitial fibrosis and serum creatinine (Cr) level. In patients with 50% increase in Cr level, ICAM-1 positive interstitial leucocytes were 516 (360)/mm2 as compared with 66 (87.8)/mm2 (U = 16; p < 0.005) in patients with stable Cr. In non-GN, tubular ICAM-1 expression was observed in 7 (24%) biopsies., Conclusions: Tubular and Interstitial expression of ICAM-1 can be a marker of tubulointerstitial damage in IgAN. Interstitial ICAM-1, rather than tubular ICAM-1, may predict the progression of this disease.