Browsing by Subject "Glomerulonephritis"

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    C4d immunohistochemical staining is a sensitive method to confirm immunoreactant deposition in formalin-fixed paraffin-embedded tissue in membranous glomerulonephritis
    (F. Hernández y J.F. Madrid. Murcia: Universidad de Murcia, Departamento de Biología Celular e Histología., 2011) Val-Bernal, J. Fernando; Garijo, M. Francisca; Val, Daniel; Rodrigo, Emilio; Arias, Manuel
    Although the diagnosis of membranous glomerulonephritis (MGN) may be suspected on routine histology of formalin-fixed paraffin-embedded tissue, fresh-frozen tissue must be used to show the immunologic nature of the process by direct immunofluorescence (IF). The efficiency of IF or immunoperoxidase (IP) detection of IgG and C3 using paraffin sections is controversial. This study was designed to evaluate whether glomerular C4d deposition using an IP method in formalin-fixed paraffin-embedded tissue may be a useful marker for MGN. We showed characteristic glomerular, granular basement membrane deposition of C4d in 31 (100%) cases of idiopathic MGN and in 5 cases (100%) of pure class V membranous lupus nephritis, in which we had a positive diagnosis of the lesions for conventional IF study. Control cases were negative. Nineteen cases of different glomerulopathies, including IgA nephropathy, primary type I membranoproliferative glomerulonephritis, focal segmental glomerulosclerosis and minimal change disease showed diverse reproducible patterns of C4d deposition, without intrinsic background. Our results indicate that staining of formalin-fixed paraffin-embedded tissue for C4d can be used for confirmation of granular basement membrane immunoreactant deposition in cases of MGN. This proved to be a reliable method that could potentially obviate the need for rebiopsy in cases with absence of glomeruli in renal frozen sections or when other adjunct IF or IP methods on paraffin sections are negative. C4d immunostaining, using an IP method, deserves a place as an adjunct method in the biopsy diagnosis of MGN.
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    Crescentic glomerulonephritis - a manifestation of a nephritogenic Thl response?
    (F. Hernández y Juan F. Madrid. Universidad de Murcia: Departamento de Biología Celular e Histología, 2000) Kitching, A.R.; Holdsworth, S. R.; Tipping, P. G.
    Crescentic glomerulonephritis (GN) is the histopathological correlate of the clinical syndrome of rapidly progressive glomerulonephritis. Glomerular crescent formation complicates proliferative forms of GN and indicates severe disease with a poor renal prognosis. In the past 10 years evidence from experimental models of GN and from human disease has accumulated suggesting that crescentic glomerulonephritis is a manifestation of a delayed type hypersensitivity (DTH)-like response to nephritogenic antigens. The elucidation of T helper 1 (Thl) and Th2 subsets in mice and in humans has led to the hypothesis that crescentic GN is a manifestation of a Thl predominant DTH mediated immune response. Recent experiments performed mainly in a murine model of crescentic glomerulonephritis have tested this hypothesis. Crescent formation in this model is substantially interleukin (IL)-12 and interferon-y (IFN-y) dependent. Administration of IL-12, deletion of endogenous IL-4 or IL-lO results in enhanced disease , while administration of exogenous IL-4 and/or IL-IO reduces crescentic injury. These findings, together with the available evidence from human studies (examining the pattern of immune effectors in glomeruli, data on cytokine production by peripheral blood mononuclear cells and case reports of the induction of proliferative and/or crescentic GN by administration of IFN-y or IL2) suggest that human crescentic GN is manifestation of a Thl mediated DTH-like nephritogenic immune response.
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    Immune complex-mediated glomerulopathy in Barbus graellsi infected with Myxobolus Spp
    (Murcia : F. Hernández, 1993) Peribañez, M.A.; Cacho, Emilio del; Castillo, J.A.; Arnal, M.C.
    Membranous glomerulonephritis caused in Barbus graellsi by myxosporidian infections have been studied by electron microscopy and immunoelectron microscopy techniques. This study indicates that Myxosporidian infection produces a chronic severe aggression. Spores reach the spleen, the kidney and the liver, where they are trapped and phagocyted by Melano Macrophage Centres. Consequently, the commencement of a immunological response to myxosporidian is evident. Our results show the presence of immunodeposits in the basement membrane of the glomeruli, suggesting that they might initiate glomerulonephritis. The lesion was markedly similar to immune complex-mediated glomerulonephritis disease in higher vertebrates.
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    T cell subsets in immunologically-mediated glomerulonephritis
    (Murcia : F. Hernández, 1997) van Alderwegen, I.E.; Bruijn, J.A.; Heer, E.de
    Until recently, research on the pathogenesis of glomerulonephritis has been mainly focused on the characterization of humoral immune responses in the initiation of glomerular injury. However, there is a growing recognition that both cellular and humoral immune responses, in varying proportions, are involved in the pathogenesis of immunologically-mediated glomerulonephritis. T lymphocytes are essential cellular elements of cell-mediated immunity. Both in experimental models of immune-mediated renal disease and in histopathological analyses of human nephropathies, the involvement of T cells has been demonstrated in the immunoregulation of nephritogenic immune responses and in the immune injury in the kidney. T cell activation resulting in either delayed-type hypersensitivity, cytolytic reactions, abnormal expression of major histocompatibility complex (MHC) molecules, or B cell activation can result in glomerulonephritis. These different types of responses are exerted by distinct T cell subsets defined by cell surface markers and cytokine profiles. CD4+ T cells in vivo are functionally heterogeneous with respect to cytokine production and the CD45 isoforms that are found on their surface. Like CD4+ T cells, CD8+ T cells may also be heterogeneous at the leve1 of cytokine production. The roles of CD4+ and CD8+ cells and their cytokine profiles in glomerulonephritis have not been extensively investigated yet, but such studies might improve the understanding of the pathogenesis and possibly lead to new therapeutic approaches of human glomerulonephritis. In this review the role of distinct T lymphocyte subsets in experimental and human glomerulonephritis will be discussed.
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    The value of proliferating cell nuclear antigen (PCNA)-cyclin in the assessment of cell proliferation in glomerulonephritis
    (Murcia : F. Hernández, 1997) Nakopoulou, Lydia; Stefanaki, K.; Salpigidis, K.; Boletis, J.; Papadakis, J.; Zeis, P.M.; Vosnides, Gr.
    Proliferating cell nuclear antigen (PCNA)/ cyclin is an acidic nuclear protein increasing from the late G1 to S phases of the cell cycle and whose detection parallels other standard methods for assessing cell proliferation. The aim of this study was to investigate PCNA expression in normal and diseased human kidneys, in order to clarify cell proliferation in renal tissue and to define a possible correlation of its expression with various types of glomerulonephritis (GN). The immunohistochemical avidin-biotin complex (ABC) method was used for the demonstration of PCNA applying the monoclonal antibody PC-10 to paraffin sections from: 10 normal kidneys, 55 renal biopsies with various types of proliferative GN (PGN), 44 renal biopsies with various types of non proliferative GN (NPGN). In PCNA-positive renal biopsies with GN the antigen showed a heterogeneous nuclear expression in occasional or few mesangial and glomerular epithelial cells as well as in a greater number of tubular epithelial cells. PCNA was expressed in 20% of normal kidneys and in 38% of renal biopsies with GN. The frequency of PCNA expression was significantly increased in the cases of PGN (47%) compared to that observed in the cases of NPGN (27%) (p=0.03). PCNA was detected in 10124 cases of IgA nephropathy, in 314 cases of IgM nephropathy, in 5/14 of other types of primary PGN and in 8/13 of secondary PGN. PCNA expression was not correlated with the degree of mesangial cellularity in PGN. Moreover, there was no significant difference in PCNA expression between primary and secondary PGN. PCNA demonstrated an intense expression in the majority of epithelial cells forming cellular crescents in 811 1 cases of PGN. In conclusion, PCNA was observed more frequently in diseased than in normal kidneys. The significant increase in the frequency of PCNA intraglomerular expression in PGN suggests that PCNA has a certain value in the assessment of mesangial proliferation. Moreover, the increased PCNA expression in tubular epithelial cells especially in PGN, indicates their proliferative state and may be correlated with their proposed activation and role in the progression of renal injury