THE GLOMERULAR DISTRIBUTION OF LAMININ AND FIBRONECTIN IN GLOMERULONEPHRITIS

Laminin (LAM) and fibronectin (FI) are regarded as major components of the glomerular extracellular matrix The aim of this study was to defi ne the distribution of LAM and FI in primary glomerulonephritis (GN) a nd GN of systemic lupus erythematosus (SLE) and to correlate the type of glomerular disorders with possible changes in the expression of the se components. Normal portions of kidney tissue from 10 patients with renal tumors and sixty-six renal biopsies obtained from patients with GN were studied by the immunoperoxidase-antiperoxidase (PAP) method fo r the detection of LAM and FI. Twelve patients had membranous GN (MGN) , 8 mesangiocapillary GN (MCGN), 21 mesangioproliferative GN (MPGN), i ncluding 11 cases of IgA nephropathy, 11 focal segmental glomeruloscle rosis (FSGS) and 14 had SLE. In MGN, LAM was detected more intensely t han FI along the glomerular basement membranes (GBM), in subepithelial GBM protrusions and in the newly-formed GBM. On the contrary, FI was intensely expressed in the mesangium. LAM and FI expression was pronou nced in stages II and III of MGN. In MCGN, LAM and FI were diffusely e xpressed along the GBM and in the mesangium. The distribution of the t wo antigens in MPGN and FSGS was similar to that seen in normal glomer uli. However, the FI staining reaction was more intense in severe mesa ngioproliferative lesions, mainly observed in the cases of IgA-nephrop athy. There were no differences in the distribution of LAM and FI betw een primary and SLE GN. The antigen staining pattern was pronounced in the membranous and mesangiocapillary lesions of SLE GN. The crescents observed in 7 cases contained increased amounts of both LAM and FI, w hile the adhesions with Bowman's capsule seen in 9 cases demonstrated increased amounts of LAM. In contrast, the large adhesions observed in 2 cases and the sclerotic lesions in 4 cases contained only small amo unts of LAM. In conclusion, the increased LAM and FI glomerular expres sion mainly in MGN and MCGN, and the FI overexpression in severe mesan gioproliferative lesions of IgA nephropathy suggest that the disturban ce of extracellular glomerular matrix is probably due to the damage of glomerular cells or the involvement of the above components in immune -complex formation.