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      Spontaneous early-onset glomerulonephritis in a 8-week-old male Crj:CD1 (ICR) mouse

      case-report

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          Abstract

          Glomerular lesions including membranoproliferative glomerulonephritis occur spontaneously in aged mice, but they are rare in young animals. In our laboratory, spontaneous glomerulonephritis was observed in an 8-week-old male Crj:CD1 (ICR) mouse. Macroscopically, the bilateral kidneys were discolored, but no edema or ascites was observed. Glomerular lesions were characterized by a thickening of capillary walls, a double-contoured basement membrane and mesangial expansion due to increased amounts of matrix. Ultrastructurally, mesangial interposition in the capillary wall and subendothelial deposition of basement membrane-like material were observed. No evidence of immune complex deposition or amyloid was found. On the basis of the observed clinical pathology and histopathology, a secondary form of glomerular lesion was excluded. The glomerular lesion was compatible with glomerulonephritis in a young Crj:CD1 (ICR) mouse.

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          Uncontrolled C3 activation causes membranoproliferative glomerulonephritis in mice deficient in complement factor H.

          Joanna Warren, Anne Bygrave, M Walport … (2002)
          The alternative pathway of complement is activated continuously in vivo through the C3 'tick-over' pathway. This pathway is triggered by the hydrolysis of C3, resulting in the formation of C3 convertase. This, in turn, generates C3b, which mediates many of the biological functions of complement. Factor H, the main regulator of this activation, prevents formation and promotes dissociation of the C3 convertase enzyme, and, together with factor I, mediates the proteolytic inactivation of C3b. Factor H deficiency, described in 29 individuals from 12 families and in pigs, allows unhindered activation of fluid-phase C3 and severe depletion of plasma C3 (ref. 11). Membranoproliferative glomerulonephritis (MPGN) occurs in factor H-deficient humans and pigs. Although MPGN has been reported in other conditions in which uncontrolled activation of C3 occurs, the role of C3 dysregulation in the pathogenesis of MPGN is not understood. Here we show that mice deficient in factor H (Cfh(-/-) mice) develop MPGN spontaneously and are hypersensitive to developing renal injury caused by immune complexes. Introducing a second mutation in the gene encoding complement factor B, which prevents C3 turnover in vivo, obviates the phenotype of Cfh(-/-) mice. Thus, uncontrolled C3 activation in vivo is essential for the development of MPGN associated with deficiency of factor H.
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            Proliferative and nonproliferative lesions of the rat and mouse urinary system.

            Roger Burnett, K Frazier, Akiyoshi Nishikawa … (2012)
            The INHAND Project (International Harmonization of Nomenclature and Diagnostic Criteria for Lesions in Rats and Mice) is a joint initiative of the Societies of Toxicologic Pathology from Europe (ESTP), Great Britain (BSTP), Japan (JSTP), and North America (STP) to develop an internationally accepted nomenclature for proliferative and nonproliferative lesions in laboratory animals. The purpose of this publication is to provide a standardized nomenclature for classifying lesions observed in the urinary tract of rats and mice. The standardized nomenclature of urinary tract lesions presented in this document is also available electronically on the Internet (http://www.goreni.org/). Sources of material included histopathology databases from government, academia, and industrial laboratories throughout the world. Content includes spontaneous developmental and aging lesions as well as those induced by exposure to test materials. A widely accepted and utilized international harmonization of nomenclature for urinary tract lesions in laboratory animals will decrease confusion among regulatory and scientific research organizations in different countries and provide a common language to increase and enrich international exchanges of information among toxicologists and pathologists.
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              Experimental membranous nephropathy redux.

              R J Quigg, David Salant, Andrey V Cybulsky (2005)
              Membranous nephropathy (MN) is a common cause of nephrotic syndrome in adults. Active and passive Heymann nephritis (HN) in rats are valuable experimental models because their features so closely resemble human MN. In HN, subepithelial immune deposits form in situ as a result of circulating antibodies. Complement activation leads to assembly of C5b-9 on glomerular epithelial cell (GEC) plasma membranes and is essential for sublethal GEC injury and the onset of proteinuria. This review revisits HN and focuses on areas of substantial progress in recent years. The response of the GEC to sublethal C5b-9 attack is not simply due to disruption of the plasma membrane but is due to the activation of specific signaling pathways. These include activation of protein kinases, phospholipases, cyclooxygenases, transcription factors, growth factors, NADPH oxidase, stress proteins, proteinases, and others. Ultimately, these signals impact on cell metabolic pathways and the structure/function of lipids and key proteins in the cytoskeleton and slit-diaphragm. Some signals affect GEC adversely. Thus C5b-9 induces partial dissolution of the actin cytoskeleton. There is a decline in nephrin expression, reduction in F-actin-bound nephrin, and loss of slit-diaphragm integrity. Other signals, such as endoplasmic reticulum stress, may limit complement-induced injury, or promote recovery. The extent of complement activation and GEC injury is dependent, in part, on complement-regulatory proteins, which act at early or late steps within the complement cascade. Identification of key steps in complement activation, the cellular signaling pathways, and the targets will facilitate therapeutic intervention in reversing GEC injury in human MN.
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                Author and article information

                Journal
                Journal ID (nlm-ta): J Toxicol Pathol
                Journal ID (iso-abbrev): J Toxicol Pathol
                Journal ID (publisher-id): TOX
                Title: Journal of Toxicologic Pathology
                Publisher: Japanese Society of Toxicologic Pathology
                ISSN (Print): 0914-9198
                ISSN (Electronic): 1881-915X
                Publication date (Electronic): 04 September 2015
                Publication date (Print): October 2015
                Volume: 28
                Issue: 4
                Pages: 237-241
                Affiliations
                [1 ]Toxicology Laboratory, Pharmaceutical Research Center, Meiji Seika Pharma Co., Ltd., 760 Morooka-cho, Kohoku-ku, Yokohama, Kanagawa 222-8567, Japan
                [2 ]Research Institute of Biosciences, Azabu University, 1-17-71 Fuchinobe, Sagamihara, Kanagawa 229-8501, Japan
                [3 ]Laboratory of Veterinary Pathology, Azabu University, 1-17-71 Fuchinobe, Sagamihara, Kanagawa 229-8501, Japan
                Author notes
                *Corresponding author: K Ago (e-mail: kyouhei.agou@ 123456meiji.com )
                Article
                Publisher ID: 2015-0015
                DOI: 10.1293/tox.2015-0015
                PMC ID: 4604135
                SO-VID: 333f56e7-e763-4ecd-bcd4-7aed14cbb3d0
                Copyright © ©2015 The Japanese Society of Toxicologic Pathology
                License:

                This is an open-access article distributed under the terms of the Creative Commons Attribution Non-Commercial No Derivatives (by-nc-nd) License.

                History
                Date received : 11 March 2015
                Date accepted : 03 August 2015
                Categories
                Subject: Case Report

                ScienceOpen disciplines: Pathology
                Keywords: glomerulonephritis,spontaneous,kidney,mouse,cd-1
                Data availability:
                ScienceOpen disciplines: Pathology
                Keywords: glomerulonephritis, spontaneous, kidney, mouse, cd-1

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