Microsoft Word - NEF736BF

Osamu Hotta, MD, Department of Nephrology, Sendai Shakaihoken Hospital, 3-16-1 Tsutsumimachi, Aoba-ku, Sendai, Miyagi, 981 (Japan) Dear Sir, The endothelial leukocyte adhesion molecule (ELAM)-1 ‚ a member of the selectin family with a lectin-like N-terminal domain [1], binds granulocytes, monocytes and a subset of memory T cells [2-4]. ELAM-1 is expressed only on vascular endothelium, predominantly on postcapillary venules [5-7]. Expression of ELAM-1 on vascular endothelium can be observed in the proximity of cells producing inflammatory cytokines such as interleukin-1 and the tumor necrosis factor, stimuli which, in vitro, are known to induce an upregulation of adhesion [5]. Recently, a quantitative sandwich ELISA for ELAM-1 in the fluid phase (soluble ELAM-1, sELAM-1) has been developed [6]. The expression of ELAM-1 has been described only on activated endothelial cells, not on other cell types; therefore, levels of ELAM-1 in serum may provide a basis for the assessment of endothelial damage or activation [6, 7]. We examined the level of s-ELAM-1 in patients with IgA nephropathy (IgAN), and those with polycystic kidney disease (PCK), paying special attention to its correlation with the decline of renal function. A total of 38 patients were enrolled in the present study: 24 with IgAN, and 14 with PCK with varying degrees of renal function. Twenty-seven healthy adult volunteers served as normal controls for s-ELAM-1 assay. They were determined healthy by biochemical tests and urinalysis. All blood samples were obtained in the morning (07.00-09.00) at Sendai Shakaihoken Hospital. In 5 patients with IgAN, blood samples were obtained twice: before steroid therapy and 1