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Verfasst von:Neumann, Irmgard [VerfasserIn]   i
 Birck, Rainer [VerfasserIn]   i
 Newman, Mark [VerfasserIn]   i
 Schnülle, Peter [VerfasserIn]   i
 Kriz, Wilhelm [VerfasserIn]   i
 Nemoto, Kyuichi [VerfasserIn]   i
 Yard, Benito A. [VerfasserIn]   i
 Waldherr, Rüdiger [VerfasserIn]   i
 Woude, Fokko J. van der [VerfasserIn]   i
Titel:SCG/Kinjoh mice
Titelzusatz:a model of ANCA-associated crescentic glomerulonephritis with immune deposits
Verf.angabe:Irmgard Neumann, Rainer Birck, Mark Newman, Peter Schnülle, Wilhelm Kriz, Kyuichi Nemoto, Benito Yard, Rüdiger Waldherr, and Fokko J. van der Woude
Jahr:2003
Umfang:9 S.
Fussnoten:Gesehen am 30.09.2022
Titel Quelle:Enthalten in: Kidney international
Ort Quelle:New York, NY : Elsevier, 1972
Jahr Quelle:2003
Band/Heft Quelle:64(2003), 1, Seite 140-148
ISSN Quelle:1523-1755
Abstract:BACKGROUND: Spontaneous crescentic glomerulonephritis-forming/Kinjoh (SCG/Kj) mice spontaneously develop crescentic glomerulonephritis (CGN), systemic vasculitis, and perinuclear ANCA (pANCA), and have been suggested as an animal model for human antineutrophil cytoplasmic antibody (ANCA)-associated vasculitis (AASV). Since no systematic serologic, immunohistologic, or structural evaluation had been performed thus far, we reinvestigated the development of ANCA and CGN in these mice. METHODS: SCG/Kj mice were subjected to serologic and urinary analysis, as well as histologic evaluation of the kidneys by standard light, immunofluorescence, and electron microscopy at regular intervals during the course of the disease. RESULTS: Perinuclear ANCA developed as early as the 6th week of life, increasing both in frequency and titer in up to 100% of animals at week 20. Crescent formation began at week 10 and peaked at week 16, maximally affecting 57% of glomeruli. Crescent formation was initiated by "activated" podocytes that formed cell bridges between tuft and Bowman's capsule. The typical picture of a diffuse immune complex nephritis was found in all animals as early as 8 weeks. Fluorescence intensity increased with age and became strongly positive for immunoglobulin (Ig)A, IgM, IgG, and C3 in the mesangium and along the peripheral capillary loops. CONCLUSION: Although ANCAs were found in the majority of animals, the massive presence of glomerular immune deposits differed from the pauci-immune pattern found in human AASV, making this model not completely representative for human ANCA-associated CGN. However, the spontaneous and concomitant development of pANCA, small vessel vasculitis, and CGN raises the opportunity to analyze pathogenetic links between these disease manifestations in vivo.
DOI:doi:10.1046/j.1523-1755.2003.00061.x
URL:Bitte beachten Sie: Dies ist ein Bibliographieeintrag. Ein Volltextzugriff für Mitglieder der Universität besteht hier nur, falls für die entsprechende Zeitschrift/den entsprechenden Sammelband ein Abonnement besteht oder es sich um einen OpenAccess-Titel handelt.

Volltext: http://dx.doi.org/10.1046/j.1523-1755.2003.00061.x
 Volltext: https://www.sciencedirect.com/science/article/pii/S0085253815493019
 DOI: https://doi.org/10.1046/j.1523-1755.2003.00061.x
Datenträger:Online-Ressource
Sprache:eng
Sach-SW:Animals
 Antibodies, Antineutrophil Cytoplasmic
 Capillaries
 Complement C3
 Disease Models, Animal
 Female
 Glomerulonephritis
 Immunoglobulins
 Mice
 Mice, Inbred Strains
 Necrosis
 Vasculitis
K10plus-PPN:181789594X
Verknüpfungen:→ Zeitschrift

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