TENASCIN IS AN IMPORTANT COMPONENT OF THE GLOMERULAR EXTRACELLULAR-MATRIX IN NORMAL AND PATHOLOGICAL CONDITIONS

Tenascin (TN), a large oligomeric glycoprotein, is a recently describe d component of the extracellular matrix (ECM). Previous reports focusi ng largely on the role of TN in nephrogenesis have documented the stro ng expression of TN in embryonic kidney tissue and implied an importan t role for TN in nephrogenesis. However, the expression of TN in norma l and pathologic kidneys in adults has not been systematically evaluat ed. In this study immunohistochemical staining for TN was applied to 1 84 renal specimens diagnosed as: normal kidney (23 cases); minimal cha nge disease and its variants (8); mesangial proliferative glomerulonep hritis (GN) including IgA nephropathy and mesangial proliferative lupu s nephritis (9); endocapillary proliferative GN including membranoprol iferative GN, lupus nephritis, and post-infectious GN (25); crescentic GN (11); membranous GN (19); focal segmental sclerosis (15); thrombot ic microangiopathy (8); amyloidosis (5); diabetic nephropathy (9); pri mary tubulointerstitial nephritis (14); transplant rejection (14); and ischemia (24). It was found that: (a) there was unequivocal global di ffuse staining limited to the mesangium in normal kidney; (b) regardle ss of the etiologies and the morphologic types of glomerular disease, whenever there was expansion of the ECM, whether in the mesangial, end ocapillary, or extracapillary spaces, there was a concomitant and prop ortional in situ increase in the TN staining; (c) globally sclerotic g lomeruli, regardless of causes, showed diffuse, strong staining, espec ially in the subcapsular fibrous deposition seen in ischemic sclerosis ; (d) non-sclerotic glomeruli showing early ischemic change uniformly displayed a marked decrease or complete loss of staining, (e) in cases of thrombotic microangiopathy, there was segmental or global staining of the capillary wall, probably corresponding to the enlarged lamina rara interna; (f) all nodular lesions in diabetic glomerulosclerosis s howed strong staining, but in several of them this staining was much m ore pronounced in the periphery than in the center of the lesion. Our study proves that TN is probably a component of the normal mesangial m atrix, that TN is an ubiquitous component of the expanded glomerular E CM in pathologic conditions regardless of morphologic subtypes, and th at further studies on the cell types and mechanisms responsible for TN synthesis may provide a new venue for the understanding of the proces s of glomerular sclerosis.