Studies on pathogenesis of IgA nephropathy

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1) Affinitiy to goat IgG of serum IgA from patients with IgA nephritisELISA showed that serum IgA from patients with IgA nephritis bound to goat IgG. Mean absorbance of ELISA in 32 IgA nephritis patients was segnificantly highir than that in normal human sera, but not difficant from that in other types of glomerulonephritis. IgA rheumaloid factor in plasma is not specific to IgA nephritis.2) Tissue-type plasminogen activator and its inhibitor in human glomerulonephrtis 1)We carried out an immunohistochemical study of tissue-type plasminogen activator (PA) and urokinase-type PA, and their inhibitors, PA inhibitor-1 and PA inhibitor-2, using renal biopsy specimens obtained from 86 patients with various forms of glomerulonephritis. The control were four normal renal tissue specimens.On immunofluorescent observation, granular staining for tissue-type PA was found to be distributed along the glomerular capillary walls. The fluorescence was weak in the normal renal tissue and occasionally intense in the tissues of patients with IgA nephritis, minimal change nephrotic syndrome, and lupus nephritis. PA inhibitor-1 was abundant in the glomerular epithelial cells and scarce in the mesangial area and glomerular capillary lumens of the normal renal tissues. This was confirmed by immunoelectron microscopy using gold staining.3) Transforming growth factor-beta protein and mRNA in glomeruli in normal and diseased human kidneys 2)Expression of transforming growth factor-beta1 (TGF-beta1) in normal and diseased human kidneys was examined by immunohistochemical staining with two antibodies, and by in situ hybridization with an oligonucleotide probe.The results indicate that mature TGF-beta and TGF-beta-LAP are localized in association with the matrix components of GBM or mesangium, and with immune deposit in human glomeruli. Expression of TGF-beta, mainly synthesized by mesangial cells, is enhanced in human glomerular diseases, and may contribute to the mesangial matrix increase.