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Pattern of renal beta 1(alpha 1-alpha 6) integrins distribution in IgA nephropathy and Henoch-Schoenlein nephritis
Małgorzata Wagrowska-Danilewicz1, Marian Danilewicz
1Department of Pathomorphology, Nephropathology Division, Medical University, Łódź. emwude@poczta.onet.pl
Immunoperoxidase staining was carried out using monoclonal antibodies against integrins alpha 1 beta 1, alpha 2 beta 1, alpha 3 beta 1, alpha 4 beta 1, alpha 5 beta 1 and alpha 6 beta 1 on renal biopsy specimens from patients with IgA nephropathy (IgAN, n = 15) and Henoch-Schoenlein nephritis (HSN, n = 10). The basic pattern of glomerular and tubulointerstitial (alpha 1-beta 6)beta 1 integrin distribution was similar in both studied groups, however increase in mesangial alpha 1 beta 1 integrin immunoexpression in biopsies from HSN patients as compared to biopsies from IgAN patients was observed. There were no statistical differences in the intensity of tubulointerstitial (alpha 1-alpha 6)beta 1 integrins immunolabelling in renal tissue between IgAN and HSN patients. The similar pattern of distribution of beta 1 integrins in renal tissue in IgAN and HSN patients may support the hypothesis of common pathogenesis of IgAN and HSN. Upregulation of alpha 1 beta 1 integrin on mesangial regions in biopsy specimens in patients with HSN may be connected to the much more florid glomerular changes in renal tissue in this type of glomerulonephritis than in IgAN.
Immunoperoxidase staining was carried out using monoclonal antibodies against integrins alpha 1 beta 1, alpha 2 beta 1, alpha 3 beta 1, alpha 4 beta 1, alpha 5 beta 1 and alpha 6 beta 1 on renal biopsy specimens from patients with IgA nephropathy (IgAN, n = 15) and Henoch-Schoenlein nephritis (HSN, n = 10). The basic pattern of glomerular and tubulointerstitial (alpha 1-beta 6)beta 1 integrin distribution was similar in both studied groups, however increase in mesangial alpha 1 beta 1 integrin immunoexpression in biopsies from HSN patients as compared to biopsies from IgAN patients was observed. There were no statistical differences in the intensity of tubulointerstitial (alpha 1-alpha 6)beta 1 integrins immunolabelling in renal tissue between IgAN and HSN patients. The similar pattern of distribution of beta 1 integrins in renal tissue in IgAN and HSN patients may support the hypothesis of common pathogenesis of IgAN and HSN. Upregulation of alpha 1 beta 1 integrin on mesangial regions in biopsy specimens in patients with HSN may be connected to the much more florid glomerular changes in renal tissue in this type of glomerulonephritis than in IgAN.
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