Bruijn J A, Dinklo N J
Department of Pathology, University of Leiden, The Netherlands.
Lab Invest. 1993 Sep;69(3):329-35.
We have conducted an immunohistochemical analysis to investigate the presence of cellular adhesion molecules in normal and diseased human kidneys.
A total of 44 renal biopsies were classified in eight groups according to pathologic diagnosis. Using immunohistochemistry, microscopical evaluation by two observers in a blinded fashion, and statistical analysis (p < 0.01), significant changes in the expression of intercellular adhesion molecule-1, vascular cell adhesion molecule-1, and endothelial-leukocyte adhesion molecule-1 were evaluated in diseased versus normal kidneys.
Small caliber vessels, such as peritubular and interstitial capillaries remained negative or showed decreased expression of vascular cell adhesion molecule-1. Upregulation of this molecule was seen only on the endothelium of interstitial arterioles and venules of diseased kidneys. Expression of intercellular adhesion molecule-1 was significantly increased on parietal epithelium of glomeruli in membranous nephropathy and Henoch-Schönlein purpura, on mesangium in Henoch-Schönlein purpura, membranoproliferative glomerulonephritis and IgA nephropathy, and in small interstitial vessels in membranous nephropathy and membranoproliferative glomerulonephritis. Interstitial infiltrates contained only few intercellular adhesion molecule-1-positive cells in Henoch-Schönlein purpura and IgA nephropathy. Kidneys with lupus nephritis and Henoch-Schönlein purpura demonstrated an increase of endothelial-leukocyte adhesion molecule-1 on parietal epithelium of glomeruli and on tubular epithelium. In membranoproliferative glomerulonephritis, this increase was seen only on parietal epithelium of glomeruli.
These results show for the first time (a) endothelial vascular cell adhesion molecule-1 induction in various glomerulonephritides and (b) endothelial-leukocyte adhesion molecule-1 induction in the kidney. Complementary to earlier in vitro work, our findings indicate that these molecules play distinct roles in the pathogenesis of immune-mediated renal disease.
我们进行了一项免疫组织化学分析，以研究正常和患病人类肾脏中细胞黏附分子的存在情况。
根据病理诊断，将44份肾活检标本分为八组。采用免疫组织化学方法，由两名观察者以盲法进行显微镜评估，并进行统计学分析（p < 0.01），评估患病肾脏与正常肾脏中细胞间黏附分子-1、血管细胞黏附分子-1和内皮细胞-白细胞黏附分子-1表达的显著变化。
小口径血管，如肾小管周围和间质毛细血管，血管细胞黏附分子-1保持阴性或表达降低。仅在患病肾脏的间质小动脉和小静脉内皮上可见该分子上调。细胞间黏附分子-1在膜性肾病和过敏性紫癜的肾小球壁层上皮、过敏性紫癜的系膜、膜增生性肾小球肾炎和IgA肾病的系膜以及膜性肾病和膜增生性肾小球肾炎的小间质血管中表达显著增加。在过敏性紫癜和IgA肾病中，间质浸润仅含有少量细胞间黏附分子-1阳性细胞。狼疮性肾炎和过敏性紫癜的肾脏在肾小球壁层上皮和肾小管上皮上内皮细胞-白细胞黏附分子-1增加。在膜增生性肾小球肾炎中，这种增加仅见于肾小球壁层上皮。
这些结果首次表明（a）各种肾小球肾炎中内皮血管细胞黏附分子-1的诱导以及（b）肾脏中内皮细胞-白细胞黏附分子-1的诱导。与早期的体外研究互补，我们的发现表明这些分子在免疫介导的肾脏疾病发病机制中发挥不同作用。
