Renal expression of intercellular adhesion molecule-1 in immunoglobulin A nephropathy: tubulointerstitial injury and prognosis

In immunoglobulin A nephropathy (IgAN), the abnormal expression of intercel lular adhesion molecule-1 (ICAM-1) on proximal tubule epithelium is associa ted with the glomerular and interstitial infiltration of leucocytes, but it s clinical significance remains uncertain. We analysed the relationship bet ween the ICAM-1 (CD54) expression in tubular epithelial cells and interstit ial leucocytes, macrophages (CD14) and T lymphocytes (CD3) with the histolo gic features, proteinuria and serum creatinine at the time of renal biopsy and after 2.42 years in 45 patients with IgAN and after 1.8 +/-1.5 years in 29 patients with non-glomerulonephritis (non-GN). In IgAN, ICAM-1(+) tubul e epithelium was 0.1 +/-0.18 ((x) over bar +/- SD), and this was associated with extracapillary proliferation (up to 20% of Bowman's space), glomerula r sclerosis involving less than 50% of glomerular area, interstitial cellul ar infiltration, tubular atrophy and proteinuria level. ICAM-1(+) interstit ial leucocytes were correlated with glomerular sclerosis involving less tha n 50% of glomerular area, glomerular sclerosis involving more than 50% of g lomerular area, tubular atrophy, interstitial fibrosis and serum creatinine level. In patients with an increase of 50% in serum creatinine, ICAM-1(+), CD14(+) and CD3(+), interstitial leucocytes were significantly outnumbered than in patients with stable serum creatinine. In non-GN, ICAM-1(+) tubule epithelium was 0.02 +/-0.04 (U=344, P <0.05, vs IgAN), and this was invers ely correlated with the percentage of the normal glomeruli and associated w ith glomerular sclerosis covering more than 50% of glomerular area, tubular atrophy and serum creatinine level. The association between tubular ICAM-1 and proteinuria and the association between interstitial ICAM-1(+), CD14() and CD3(+), leucocytes and renal failure at presentation and the deterior ation in IgAN in contrast with non-GN suggest that tubular and interstitial expression of ICAM-1 may be a marker of tubulointerstitial disturbance in IgAN.