Korean Journal of Nephrology 1994;13(4):853-869.

정상 및 사구체신염 환자 신조직에서 조직인자 (Tissue Factor ) 의 발현

안규리 , 이정상

Abstract

Tissue factor(TF), a primary inhibitor of coagula- tion protease cascade, was demonstrated by imm- unohistochemistry using mouse monoclonal antibody to human TF in normal and diseased kidneys. In nor- mal kidneys, TF was localized at glomerular capil- lary walls. Further localization was perfornmed in serial sections using monoclonal antibodies specific for glomerular epithelial cells. TF positive cells were distributed in the same patterns as those positive to anti human cytokeratin and PHM 5, suggesting its presence in the glomerular in glomerular epithelial cells, In glomerular epithelial cells, most of the TF were found in intracytoplasmic vesicles, and only very small portion of TF were found in peri Golgi ar- eas or in pinocytic pits. Mesangial cells, endothelial cells, tubular epithelium or interstital cells were negative fot TF. I@mmunodouble staing with anti cyto- keratin and anti TF antibody confirmed above findings by showing double positivity. In diseased kidneys, the glomerular TF was stained in different patterns,l) proliferative, 2) lobular, 3) capillary. Most of the GNs such as minor change le- sions, membranous nephropathy, membranoproliferative GN, diffuse membranoproliferative GN, focal glomerulosclerosis and IgA nephropathy cases showed capillary staining like in normal glomeruli. Some secondary GNs, such as lupus nephritis(2/9), Henoch Schonlein nephritis(1/1) and transplantation rejec- tion(1/4) also showed cxapillary patterns. Among these, proliferative GNs showed some TF stainings in the mesangium. Lobular patterns were observed in cases with renal lesions combined with metabolic diseases(2/3), or lupus nephritis(6/9), in which TF negative materials or cells were accumulated the mesangium, displacing the TF positive epithelial cells to the periphery. Pro- liferative types were found in the glomerular tuft in a case with mesangioendothelial proliferative GN, a lupus nephritis, and 3 transplantation rejection cas es, and in crescerts in dne crescentic GN. This type was characterized by TF positive cell proliferation in a glomeruli or in crescent. Fibrin formation within glomeruli is an important pathophysiologic event seen in variety of clinical and experimental conditions associated with renal injury. In this study, TF was demonstrated in vivo in normal kidney tissue, showing TF produced exclusively in glomerular epithelial cells. Reforring from the histologic locations, TF in normal glomeruli could form an hemostatic envelope for the possible capillary injury. In glomerulonephritis, TF showed different patterns, which seemed to reflect its participation not only in coagulation but also in immune mediated renal injury.