Journal Article

Expression of cell adhesion molecules in primary renal disease and renal allograft rejection.

I A Hauser, R Riess, B Hausknecht, H Thüringer and R B Sterzel

in Nephrology Dialysis Transplantation

Volume 12, issue 6, pages 1122-1131
Published in print June 1997 | ISSN: 0931-0509
Published online June 1997 | e-ISSN: 1460-2385 | DOI:
Expression of cell adhesion molecules in primary renal disease and renal allograft rejection.

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BACKGROUND: In vitro studies have demonstrated that inflammatory mediators such as the cytokines TNF alpha and IL-1 upregulate or induce de novo expression of cell adhesion molecules on endothelial and epithelial cells. In the present study the expression of the cell adhesion molecules ICAM-1, VCAM-1, E-selectin and PECAM-1 was investigated in renal biopsies from patients with primary renal diseases (n = 66) and from renal allograft recipients (n = 42). METHODS: Expression of the cell adhesion molecules was determined by immunohistochemistry of frozen sections using monoclonal antibodies directed against PECAM-1, ICAM-1, VCAM-1, E-selectin and MHC class II molecules (APAAP method). RESULTS AND CONCLUSIONS: PECAM-1 and ICAM-1 were expressed in the renal vasculature and disappeared in obliterated glomeruli with endothelial cell destruction. ICAM-1 but not PECAM-1 was upregulated in renal endothelia in acute allograft rejection and inflammatory primary renal diseases. Tubular de novo expression of ICAM-1 and VCAM-1 correlated with severe structural damage of the renal parenchyma including interstitial fibrosis. Vascular and/or glomerular VCAM-1 and E-selectin expression was pronounced in severe acute allograft rejection and also reflected the intensity of inflammatory reactions in primary renal diseases with or without autoimmune disorders. De novo expression of VCAM-1 and E-selectin in renal vessels and/or glomeruli and overexpression of ICAM-1 are markers of acute and severe inflammatory processes in biopsies from allograft recipients and patients with primary renal diseases.

Journal Article.  0 words. 

Subjects: Nephrology

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