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Letteratura scientifica selezionata sul tema "Glomerulonephritis Immunological aspects"

Autore: Grafiati

Pubblicato: 4 giugno 2021

Ultima modifica: 28 gennaio 2023

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Articoli di riviste sul tema "Glomerulonephritis Immunological aspects"

1

Sethi, D., and E. R. Maher. "Immunological Aspects of Glomerulonephritis." Journal of the Royal Society of Medicine 80, no. 3 (March 1987): 189–91. http://dx.doi.org/10.1177/014107688708000322.

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2

Bondareva, L., and L. Vykhristenko. "Pathogenetic and morphological features in certain types of primary glomerulonephritis." Immunopathology, Allergology, Infectology 2021, no. 2 (April 1, 2021): 69–79. http://dx.doi.org/10.14427/jipai.2021.2.69.

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Abstract (sommario):

The kidney, as an organ, quite often appears as the target of immune system dysregulation in the context of a primary or systemic disease. Glomerulonephritis (GL) is the most common clinical and pathological manifestation of this process. Currently, there is no unified view on the classification of GN. However, the study and recognition of the pathophysiological mechanisms of GN made it possible to determine the immunological features, biomarkers and genetic aspects of the disease. In the review, we update modern ideas about the genetic factors, etiology, immunopathogenesis of primary GN, and the variety of damage to each of the components of the glomerular filtration barrier, including the endothelium of glomerular capillaries, glomerular basement membrane and podocytes. Special attention is paid to the pathogenesis of various morphological forms of primary GN, diagnostic and prognostic biomarkers of the disease (markers of blood, urine, histopathological and genetic markers).

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3

Schena, F. P., L. Gesualdo, and V. Montinaro. "Immunopathological aspects of immunoglobulin A nephropathy and other mesangial proliferative glomerulonephritides." Journal of the American Society of Nephrology 2, no. 10 (April 1992): S167. http://dx.doi.org/10.1681/asn.v210s167.

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Immunoglobulin A nephropathy (IgAN) is an immune complex (IC) glomerulonephritis (GN) that represents one of the most common forms of primary glomerular disease. Proliferation of mesangial cells and the increase of mesangial matrix are histological hallmarks of mesangioproliferative GN. Increased serum levels of IgA, polymeric IgA, IgA rheumatoid factor, IgA-IC, and spontaneous or pokeweed mitogen-induced production of IgA by peripheral blood mononuclear cells are major humoral immune alterations reported in IgAN. Recently, we focused on the role of cytokines and growth factors in the mediation of glomerular injury. Platelet-derived growth factor, transforming growth factor beta, interleukin (IL)-1 and IL-6 are expressed by and act on mesangial cells. Increased expression of platelet-derived growth factor was found in both an active model of IgAN and in renal biopsies of patients with proliferative GN. A strict correlation between increased expression of B-chain mRNA and mesangial proliferation was found. Cytokines such as IL-1, interferon gamma, and IL-6, released by infiltrating mononuclear cells or produced locally by mesangial cells, affect the glomerular response to IgA-IC. In a passive murine experimental model of IgAN, IL-1 and interferon gamma increased mesangial hypercellularity, whereas IL-6 was highly pathogenic when associated to IL-1. In conclusion, classical immunological mechanisms in mesangial GN could interact with other pathways involving cytokines and growth factors in the progression of glomerular injury.

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4

Maixnerova, Dita, Delphine El Mehdi, Dana V. Rizk, Hong Zhang, and Vladimir Tesar. "New Treatment Strategies for IgA Nephropathy: Targeting Plasma Cells as the Main Source of Pathogenic Antibodies." Journal of Clinical Medicine 11, no. 10 (May 16, 2022): 2810. http://dx.doi.org/10.3390/jcm11102810.

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Abstract (sommario):

Immunoglobulin A nephropathy (IgAN) is a rare autoimmune disorder and the leading cause of biopsy-reported glomerulonephritis (GN) worldwide. Disease progression is driven by the formation and deposition of immune complexes composed of galactose-deficient IgA1 (Gd-IgA1) and Gd-IgA1 autoantibodies (anti-Gd-IgA1 antibodies) in the glomeruli, where they trigger complement-mediated inflammation that can result in loss of kidney function and end-stage kidney disease (ESKD). With the risk of progression and limited treatment options, there is an unmet need for therapies that address the formation of pathogenic Gd-IgA1 antibody and anti-Gd-IgA1 antibody-containing immune complexes. New therapeutic approaches target immunological aspects of IgAN, including complement-mediated inflammation and pathogenic antibody production by inhibiting activation or promoting depletion of B cells and CD38-positive plasma cells. This article will review therapies, both approved and in development, that support the depletion of Gd-IgA1-producing cells in IgAN and have the potential to modify the course of this disease. Ultimately, we propose here a novel therapeutic approach by depleting CD38-positive plasma cells, as the source of the autoimmunity, to treat patients with IgAN.

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Tesi sul tema "Glomerulonephritis Immunological aspects"

1

Wootton, Andrew. "The glomerular basement membrane and nephritis /." Title page, contents and abstract only, 1985. http://web4.library.adelaide.edu.au/theses/09PH/09phw918.pdf.

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2

"Prognostic and immunogenetic factors of IgA nephropathy." 2003. http://library.cuhk.edu.hk/record=b6073641.

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Abstract (sommario):

Li Kam-tao, Philip.<br>"January 2003."<br>Thesis (M.D.)--Chinese University of Hong Kong, 2003.<br>Includes bibliographical references (p. 252-281).<br>Electronic reproduction. Hong Kong : Chinese University of Hong Kong, [2012] System requirements: Adobe Acrobat Reader. Available via World Wide Web.<br>Mode of access: World Wide Web.

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3

Wootton, Andrew. "The glomerular basement membrane and nephritis." 1986. http://web4.library.adelaide.edu.au/theses/09PH/09phw918.pdf.

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4

"The association of various HLA-A, -B and -DR loci with membranous glomerulonephritis, IgA nephropathy, and focal segmental glomerulosclerosis in KwaZulu-Natal renal patients." Thesis, 2007. http://hdl.handle.net/10413/1789.

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This KwaZulu-Natal (KZN) based study investigates hypertension, glomerulonephritides and the rarity of IgA Nephropathy (IgAN) in Africans in association with the Human Leukocyte Antigen (HLA). A retrospective hypertensive study found a positive association with HLA-B40 (P c<0.05) and HLA-B15 (Pc<0.02) in Indians and Africans respectively. No association was found in Whites. A prospective study showed glomerulonephritides to be positively associated with HLA-A33 in Indians (Pc 0.049). No associations were found with glomerulonephritides in Africans and Whites. Combined Race groups show no HLA associations. HLA-A30; HLA-A34; HLA-A29; HLA-B42; HLA-B58; HLA-B70 and HLA-DR11 were extremely significantly higher in Africans compared to Indians and Whites (all P<0.0001). In conclusion, HLA-B40 and I 1LA-B15 are possible disease susceptibility markers in Indian and African hypertensives; HLA-A33 is a possible disease susceptibility marker for glomerulonephritides in Indians and alleles in linkage might be responsible for the rarity of IgAN in Africans but further studies need to be employed.<br>Thesis (M.Med)-University of KwaZulu-Natal, 2007.

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Libri sul tema "Glomerulonephritis Immunological aspects"

1

A, Rakiti͡anskai͡a I., and Shutko A. N, eds. Pochki i sistema immuniteta. Leningrad: "Nauka," Leningradskoe otd-nie, 1989.

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2

D, Pusey C., ed. The treatment of glomerulonephritis. Dordrecht: Kluwer Academic, 1999.

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3

Claudio, Ponticelli, Minetti L, and D'Amico G. 1929-, eds. Antiglobulins, cryoglobulins, and glomerulonephritis: Second International Milano Meeting of Nephrology, 30 September-1 October 1985. Dordrecht: M. Nijhoff, 1986.

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4

Glomerulopathies: Cell biology and immunology. Australia: Harwood Academic Press, 1996.

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5

Pusey, C. D. The Treatment of Glomerulonephritis. Springer, 2014.

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6

Pusey, C. D. The Treatment of Glomerulonephritis. Springer, 1999.

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7

Pusey, Charles. Treatment of Glomerulonephritis. Springer London, Limited, 2007.

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8

1947-, Ballardie Francis W., ed. Autoimmunity in nephritis. Chur: Harwood Academic Publishers, 1992.

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9

B, Wilson Curtis, ed. Immunopathology of renal disease. New York: Churchill Livingstone, 1988.

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10

Berden, Jo H. M., and Jack F. M. Wetzels. Immunological investigation of the patient with renal disease. Edited by Christopher G. Winearls. Oxford University Press, 2015. http://dx.doi.org/10.1093/med/9780199592548.003.0017.

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Abstract (sommario):

Laboratory techniques (electrophoresis, indirect immunofluorescence, ELISA, and immunoblotting) required for immunological investigation of the patient with renal disease are described. Renal disease-related aspects of immunoglobulins (immunoglobulin A, paraproteins, cryoglobulins), complement, antinuclear antibodies, anti-C1q antibodies, antineutrophil cytoplasmic antibodies, anti-glomerular basement membrane antibodies, antipodocyte antibodies, antiphospholipid antibodies, and antimicrobial responses (streptococci, hepatitis C, hepatitis B) are reviewed. Laboratory assays which evaluate the immune response, in particular the identification of (auto)-antibodies are valuable tools in establishing a diagnosis and/or monitoring of the activity of the disease. Guidelines are given for immunological studies in patients with specific renal syndromes including nephrotic syndrome, rapidly progressive glomerulonephritis, systemic lupus erythematosus, and thrombotic microangiopathy.

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