IMMUNOLOCALIZATION OF TENASCIN AND CELLULAR FIBRONECTINS IN DIVERSE GLOMERULOPATHIES

Frozen samples of minimal change glomerulopathy (MCG), and of membrano us, segmental and diffuse lupus glomerulonephritis (MGN, SGN, DLGN) we re studied to assess the distribution of tenascin (Ten), and the extra domains A and B (EDA- and EDB-) and oncofetal (Onc-) isoforms of cellu lar fibronectin (cFn). Cryosections were immunostained by the ABC meth od with specific monoclonal antibodies. In MCG, mesangial Ten and EDA- cFn reactions were increased. In MGN, mesangial Ten and EDA-cFn staini ng was enhanced except in segmental scars; convincing reactions were s een in cases with membranous transformation; spikes stained strongly. In SGN, variably intense staining for Ten and all cFn isoforms was see n in glomerular necrosis, proliferation and crescents; parietal epithe lium EDA-cFn staining was noted. In DLGN, strong and extensive mesangi al Ten and EDA-cFn staining was seen as were focal EDB- and Onc-cFn re actions. Parietal cells with and without crescents stained variably wi th all Mabs. Obsolete glomeruli were unreactive save for rare periglom erular Ten rims. Interstitial inflammation and fibrosis in MGN, SGN an d DLGN had moderate to strong Ten and EDA-cFn staining with rare trace s of EDB- and Onc-cFn. We conclude that enhanced Ten and EDA-cFn is a potentially reversible response to glomerular injury whereas the expre ssion of EDB- and Onc-cFn apparently result from necrosis and/or cellu lar proliferation which lead to scarring. And, while mesangial cells a re the major source of these molecules, epithelial cells might also pa rtake in their synthesis.