Vascular expression of adhesion molecules in acute and chronic rejection of kidney allografts.

Abstract

Aims: It has been shown that adhesion molecules are upregulated on different structures in kidney during allograft rejection. Although vascular endothelium is one of the major targets in rejection, little is known about the expression of adhesion molecules in kidney vasculature.

Methods: Expression of adhesion molecules ICAM-1, VCAM-1 and E-selectin, and activation markers HLA-DR and IL2R was investigated in different vascular segments of nephrectomy specimens in 8 kidney allografts with acute and 5 with chronic rejection.

Results: In acute rejection, ICAM-1, VCAM-1 and HLA-DR were strongly upregulated on the endothelium and IL2R on inflammatory cells of all vessels. In chronic rejection, ICAM-1, VCAM-1 and HLA-DR were less intensive and focal, with the exception of peritubular capillaries and small veins in which VCAM-1 and HLA-DR were significantly upregulated.

Conclusion: Upregulation of adhesion molecules in acute rejection is probably important in inflammatory infiltration of tubulointerstitium and vessels, as a part of cellular immune mechanisms. Cellular immunity is also supported by finding of IL2R positive activated lymphocytes. In chronic rejection, upregulation of VCAM-1 and HLA-DR on capillaries and small veins may be one of the important etiological factors, explaining the characteristic interstitial and perivascular inflammation. Inflammatory cell infiltration of fibrosed vessel walls in chronic rejection was, as well as the expression of adhesion molecules, low-grade and focal. These findings are in accordance with the general opinion that the pathogenesis of chronic rejection is more complex than in acute rejection, and that, in addition to cellular response, probably include other mechanisms.