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Thèses sur le sujet « Glomerulonephriti »

Auteur : Grafiati
Publié le 9 mars 2023
Mis à jour le 10 mars 2023

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1

IVANOVA, MARIIA. « Advanced proteomics MALDI-MSI imaging in chronic glomerulonephrites : from diagnostics to precision medicine ». Doctoral thesis, Università degli Studi di Milano-Bicocca, 2020. http://hdl.handle.net/10281/263391.

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Chronical kidney disease (CKD) is a worldwide health problem with increasing incidence, where the major part accounts for chronic glomerulonephrites (GN). It is a group of diseases of various aetiology and multiform clinical course, having various prognosis which is often hardly predictable as well as existing prognostic markers are not always certain. There is an urging need of new reliable and specific prognostic and therapeutic markers research. A modern proteomic technology - Matrix-assisted laser desorption/ionization mass spectrometry imaging (MALDI-MSI) has been employed in many GN studies showing promising results. We aimed to study several forms of primary and secondary glomerulonephrites (membranous nephropathy, IgA nephropathy, diabetic nephropathy) to enlighten possible molecular alterations significant of diseases’ progression. The studies were performed on renal tissue biopsies, analysing them with high spatial resolution MALDI-MSI to get better visualisation of signals’ co-localisation on tissue. We performed a comparison of molecular profiles of various forms of GN. As a result, we were able to generate and distinguish specific tryptic peptides profiles of different cell regions (tubules, glomeruli, interstitium, connective tissue) and detect proteins with an altered intensity, implicated in inflammatory and healing pathways. MALDI-MSI, being able to define renal structures, could provide additional diagnostic and prognostic information. Generation of collective diagnostic panels may fulfil our pathogenesis understanding and assist clinical prognostic assessment.
Chronical kidney disease (CKD) is a worldwide health problem with increasing incidence, where the major part accounts for chronic glomerulonephrites (GN). It is a group of diseases of various aetiology and multiform clinical course, having various prognosis which is often hardly predictable as well as existing prognostic markers are not always certain. There is an urging need of new reliable and specific prognostic and therapeutic markers research. A modern proteomic technology - Matrix-assisted laser desorption/ionization mass spectrometry imaging (MALDI-MSI) has been employed in many GN studies showing promising results. We aimed to study several forms of primary and secondary glomerulonephrites (membranous nephropathy, IgA nephropathy, diabetic nephropathy) to enlighten possible molecular alterations significant of diseases’ progression. The studies were performed on renal tissue biopsies, analysing them with high spatial resolution MALDI-MSI to get better visualisation of signals’ co-localisation on tissue. We performed a comparison of molecular profiles of various forms of GN. As a result, we were able to generate and distinguish specific tryptic peptides profiles of different cell regions (tubules, glomeruli, interstitium, connective tissue) and detect proteins with an altered intensity, implicated in inflammatory and healing pathways. MALDI-MSI, being able to define renal structures, could provide additional diagnostic and prognostic information. Generation of collective diagnostic panels may fulfil our pathogenesis understanding and assist clinical prognostic assessment.
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2

Segelmark, Mårten. « Pathogenic aspects of rapidly progressive glomerulonephritis ». Lund : Dept. of Nephrology, Lund University, 1995. http://catalog.hathitrust.org/api/volumes/oclc/39160027.html.

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3

Westman, Kerstin. « Autoimmuity in glomerulonephritis serological diagnosis and clinical outcome with special reference to Wegener's granulomatosis and microscopic polyangiitis / ». Lund : Dept. of Nephrology, University Hospital, 1997. http://catalog.hathitrust.org/api/volumes/oclc/39116623.html.

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4

Condon, Marie. « Improving outcomes in glomerulonephritis ». Thesis, Imperial College London, 2015. http://hdl.handle.net/10044/1/41079.

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INTRODUCTION: Lupus Nephritis (LN) and Idiopathic Membranous Nephropathy (IMN) are immune mediated kidney diseases. The gold standard test for diagnosis and monitoring is kidney biopsy. Current treatment regimens for both diseases can be toxic with long-term effects. AIMS: Assess the outcomes of less toxic steroid sparing regimens in both diseases. To validate urinary biomarkers in LN. Assess the indirect immunofluorescence test (IIFT) for identification of anti-PLA2R antibodies in IMN. METHODS: Prospectively data was collected on 50 consecutive patients with Lupus Nephritis (LN) were treated with the steroid sparing RITUXILUP regimen. Retrospectively data was collected on 43 patients with Idiopathic Membranous Nephropathy (IMN) who received >12 months of treatment with Tacrolimus Monotherapy (Tac). Enrolment and data monitoring of the IMN induction trial 'MTac' is described. The urine biomarker MIF was measured in 586 urine samples from 59 patients; results were correlated with disease activity. A Multiplex cytokine array identified Angiogenin (ANG) as a novel cytokine. ANG was measured in 342 urine samples from 34 patients treated with RITUXILUP regimen. IIFT was used to identify anti-PLA2R antibodies in 59 plasma samples from 24 patients in the MTac trial. RESULTS: RITUXILUP and Tac regimens were safe and effective with 86% response rate at 1 year (52% CR and 34% PR) and 98% response rate respectively. Tac can be valuable in relapsing or resistant disease to maintain remission. uMIF reflected the change in disease activity, baseline uMIF did not predict time to CR. ANG was identified in urine from patients with active LN. Levels were significantly lower when in remission. An association between uANG and the degree of renal impairment but not with proteinuria was shown. IIFT is effective and reproducible for the qualitative assessment of anti-PLA2R antibodies, however it is laborious and can have subjective variability when used in a quantitative manner. CONCLUSIONS: Steroid sparing treatment may be possible in both LN and IMN; but this needs to be validated in RCTs. uMIF and uANG both reflect disease activity in LN, more work is needed to assess if they have a unique role as a biomarker in LN or as a therapeutic target. The clinical application of anti-PLA2R antibodies is being investigated widely. The IIFT is sufficient for current research use, however probably not for a high throughput use.
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5

Ringsted, S. « Pathogenic mechanisms in glomerulonephritis ». Thesis, University of Oxford, 1988. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.670361.

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6

Hägele, Holger. « Molekulare Mechanismen viral getriggerter Glomerulonephritis ». Diss., lmu, 2013. http://nbn-resolving.de/urn:nbn:de:bvb:19-155778.

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7

Pickering, Matthew Caleb. « Glomerulonephritis and factor H deficieny ». Thesis, Imperial College London, 2002. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.252096.

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8

Tam, Wai Keung. « Cytokine gene expression in glomerulonephritis ». Thesis, Imperial College London, 1996. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.363081.

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9

Owen, Elizabeth Louise. « Endothelin-1 antagonism in glomerulonephritis ». Thesis, University of Edinburgh, 2016. http://hdl.handle.net/1842/23564.

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A common feature of glomerular disease is a protein leak into the urine. Proteinuria occurs in kidney disease and is an important risk factor for cardiovascular disease (CVD). ET‐1 is a potent vasoconstrictor/pressor peptide that is up‐regulated in CVD and many forms of inflammatory renal diseases. The actions of ET‐1 are mediated via two G‐protein coupled receptors, the ETAR which serves primarily in the pro‐hypertensive actions of ET‐1 and is often considered as the main pathological receptor subtype, with the ETBR serving to clear circulating ET‐1. Antagonism of one or both of receptors has been shown to be of clinical benefit in the treatment of hypertension. This research demonstrated a beneficial effect of selective ETAR antagonism using Sitaxsentan in a rat model of GN. ETAR blockade reduced blood pressure and importantly reduced glomerular inflammation as assessed by glomerular macrophage (Mϕ) infiltration. Further, we aimed to demonstrate that Mϕ, key mediators of inflammation are activated by ET‐1 to adopt a pro‐inflammatoy phenotype. However, early studies demonstrated that ET‐1 does not activate Mϕ as hypothesised. Mϕ were more phagocytic, and ET‐1 was chemokinetic for macrophages, an ETBR medicated event. ET‐1 was also removed by Mϕ, suggesting a potential regulatory role of Mϕ in the ET system. This phenomenon led to inclusion of additional in vivo studies to investigate the role of Mϕ in the regulation of ET‐1 and its pressor effects. These effects were investigated in a murine model of Mϕ ablation using CD11b‐DTR mice. These experiments determined in vivo that Mϕ ablation augments pressor responses to ET‐1, suggesting that Mϕ are required to regulate ET‐1. In vitro, Mϕ remove ET‐1 by several mechanisms involving proteolytic degradation of the peptide and ETBR mediated clearance, demonstrating a potential mechanism for the in vivo observation. Furthermore, proteinuria is believed to be due to damage or effacement of specialized visceral glomerular epithelial cells or podocytes. We identified in vitro that the ETAR mediates ET‐1 induced human podocyte cell effacement by actin cytoskeleton aberrations and slit‐diaphragm protein down-regulation, ET‐1 and pro‐inflammatory cytokine production. This thesis provides evidence to support our initial hypotheses that selective ETAR antagonism ameliorates proteinuric renal disease via its effects on podocytes and macrophages. Continued studies both in vitro and in vivo will strengthen the body of evidence to promote the therapeutic use of ETR antagonists in inflammatory renal disease.
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10

GOBERT, REGIS. « Glomerulonephrite membranoproliferative et cancer bronchique ». Lille 2, 1988. http://www.theses.fr/1988LIL2M210.

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11

Leung, Chi-kam Joseph, et 梁志錦. « The pathogenesis of IgA nephropathy : the roleof IgA molecule and the nature of IgA receptors ». Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 2003. http://hub.hku.hk/bib/B29744908.

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12

Ye, Yisha. « Proteomics study of the effects of fish oil and corn oil enriched diet on membranous nephritis ». Click to view the E-thesis via HKUTO, 2008. http://sunzi.lib.hku.hk/hkuto/record/B40887753.

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13

Flür, Katharina. « Molekulare Mechanismen der viral-getriggerten Glomerulonephritis ». Diss., lmu, 2010. http://nbn-resolving.de/urn:nbn:de:bvb:19-115463.

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14

Cook, Paul Roger. « Genetic analysis of experimental autoimmune glomerulonephritis ». Thesis, Imperial College London, 2008. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.506108.

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15

Sharp, Phoebe. « Mechanisms of injury in experimental glomerulonephritis ». Thesis, Imperial College London, 2013. http://hdl.handle.net/10044/1/22183.

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Proliferative glomerulonephritis (GN), seen in patients with Goodpasture's disease or systemic lupus erythematosus (SLE), is characterised by glomerular infiltration of macrophages and T cells as well as proliferation of intrinsic renal cells. Significant insights into the pathogenesis of GN have been obtained through the use of experimental rodent models, such as nephrotoxic nephritis (NTN). In this thesis I have investigated the role of two important immunological molecules in NTN: Fas ligand (FasL) and Fc gamma receptor IIB (FcγRIIB). FasL is a well-known inducer of apoptosis in cells expressing its receptor Fas; however FasL also mediates non-apoptotic pro-inflammatory responses. FasL is widely expressed throughout the hematopoietic system but is also expressed within healthy and diseased kidney. I describe a novel role for FasL in the promotion of NTN independent from antibody and T cell responses. This pathological effect correlates with enhanced glomerular inflammation and appears to be dependent on FasL expression on both circulating leukocytes and intrinsic renal cells. Additionally, I have shown FasL-defective mesangial cells have impaired signalling through the IL-1R with a reduction in MCP-1 production. FcγRIIB is the sole inhibitory Fc receptor for IgG and is involved in the negative regulation of B cells and cellular activation. FcγRIIB is widely expressed throughout the hematopoietic system but is also expressed on mesangial cells within the kidney. FcγRIIB deficiency greatly exacerbates NTN. Here I use cell-specific deletion to demonstrate the critical importance of FcγRIIB expressed on myeloid cells rather than B cells in the protection from NTN. Further to this, I highlight a role for FcγRIIB on intrinsic renal cells, possibly mesangial cells, in the protection from NTN. Overall, these data widen our knowledge on the pathogenesis of GN and open up possibilities for finding future novel treatments.
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16

Rimediotti, Michel Jules. « Glomerulonephritis mit transitorischer C'3-Hypokomplementämie / ». Bern, 1992. http://www.ub.unibe.ch/content/bibliotheken_sammlungen/sondersammlungen/dissen_bestellformular/index_ger.html.

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17

MAZEROLLES, BUREL-DELACOUR-OLIVIER CATHERINE. « Glomerulonephrites chroniques primitives et dna plasmatique : a propos de 119 observations ». Toulouse 3, 1988. http://www.theses.fr/1988TOU31039.

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18

EPICUREO, ALFONSO. « Glomerulonephrites chroniques primitives et grossesse : a propos de 22 observations ». Lille 2, 1990. http://www.theses.fr/1990LIL2M037.

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19

松尾, 清一, 信夫 坂本, 征郎 丸山, 由起夫 湯沢, 大裕 水谷, Seiichi Matsuo, Nobuo Sakamoto, Ikuro Maruyama, Yukio Yuzawa et Motohiro Mizutani. « Glomerular localization of thrombomodulin in human glomerulonephritis ». Thesis, the United States and Canadian Academy of Pathology, 1993. http://hdl.handle.net/2237/16374.

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20

Lai, Ping-Chin. « The inflammatory mechanisms of experimental crescentic glomerulonephritis ». Thesis, Imperial College London, 2004. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.408001.

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21

Zent, Roy. « Rapidly progressive glomerulonephritis at Groote Schuur hospital ». Master's thesis, University of Cape Town, 1992. http://hdl.handle.net/11427/25732.

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22

Ramcke, Torben [Verfasser]. « The function of RORγt+Foxp3+ biTregs in glomerulonephritis : Die Rolle von RORγt+Foxp3+ biTregs im Rahmen der Glomerulonephritis / Torben Ramcke ». Hamburg : Staats- und Universitätsbibliothek Hamburg Carl von Ossietzky, 2019. http://d-nb.info/1221721011/34.

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23

Peyronnel, Annie. « Les glomérulonéphrites extra-membraneuses : revue de la littérature, analyse des observations recueillies dans le Service de Médecine interne C - Néphrologie du CHU de Nîmes ». Montpellier 1, 1993. http://www.theses.fr/1993MON11014.

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24

Gervais-Bertrand, Laure. « Glomérulonéphrite aigue͏̈ post-streptococcique (revue de la littérature à propos d'un cas) ». Montpellier 1, 1994. http://www.theses.fr/1994MON11160.

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25

Torres, Joe͏̈lle. « Glomérulonéphrites extracapillaires : à propos de 17 observations ». Bordeaux 2, 1991. http://www.theses.fr/1991BOR2M035.

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26

LAPASSET, CATHERINE. « Les glomerulonephrites extra-membraneuses chez l'enfant : etude anatomoclinique sur seize cas ». Toulouse 3, 1989. http://www.theses.fr/1989TOU31017.

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27

FRITZ, OLIVIER. « Glomerulonephrites rapidement progressives : a propos de 60 cas ». Toulouse 3, 1992. http://www.theses.fr/1992TOU31533.

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28

MATHIEU, COUKROUN BRIGITTE. « Valeur predictive de l'histologie dans les nephropathies du purpura rhumatoide : a propos de 10 observations ». Nantes, 1990. http://www.theses.fr/1990NANT062M.

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29

WEINBERG, ISABELLE. « La nephropathie primitive a iga en 1994 (maladie de berger) ». Aix-Marseille 2, 1994. http://www.theses.fr/1994AIX20095.

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30

McAdoo, Stephen. « The role of spleen tyrosine kinase in glomerulonephritis ». Thesis, Imperial College London, 2014. http://hdl.handle.net/10044/1/40926.

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Spleen tyrosine kinase (SYK) is a non-receptor tyrosine kinase that has an important role in immunoreceptor signalling, including for the B cell receptor and activatory Fc receptors. SYK inhibition has shown efficacy in animal models of non-renal autoimmune disease. The role of SYK in experimental and clinical renal disease, however, is not well defined. I have studied the effects of SYK inhibition using a specific small molecule inhibitor (R788; fostamatinib) in two distinct experimental models of glomerulonephritis in the rat. In experimental autoimmune glomerulonephritis (EAG; a model of anti-glomerular basement membrane disease), I have shown that SYK inhibition with fostamatinib both prevents and treats established disease. Significant attenuation of humoral autoimmune responses was observed, and ELISpot and flow cytometric analysis suggests that this was due to a direct inhibitory effect on B cell activity, rather than overall B cell survival. In addition, SYK inhibition appeared to inhibit antibody-dependent, Fc receptor-mediated pro-inflammatory responses, particularly within glomerular macrophages, in EAG. In experimental autoimmune vasculitis (EAV; a model of anti-neutrophil cytoplasm antibody [ANCA] associated vasculitis), SYK inhibition was an effective treatment for life-threatening manifestations of disease, including glomerulonephritis and lung haemorrhage. I have also examined the pattern of SYK expression by immunohistochemistry in clinical renal biopsy specimens from approximately 100 patients with a spectrum of glomerular pathologies. I found that SYK is expressed and activated in proliferative types of glomerulonephritis, and that expression levels correlate with disease activity in anti-GBM disease, ANCA-associated vasculitis, lupus nephritis and IgA nephropathy. These data suggest that SYK is important in the pathogenesis of proliferative glomerulonephritis. SYK inhibition is an effective treatment strategy for the organ-threatening manifestations of disease in two experimental models, and SYK inhibition therefore warrants further investigation in human renal disease.
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31

Pressler, Barrak. « The Role of Complementary Proteins in Autoimmune Glomerulonephritis ». NCSU, 2008. http://www.lib.ncsu.edu/theses/available/etd-05062008-155750/.

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Although numerous theories exist proposing mechanisms whereby autoimmune diseases may be initiated, as of yet none of these have been definitively shown to be responsible for the induction of any naturally-occurring disease. One of these theories, known as autoantigen complementarity, states that the initiator of an autoimmune response may not be the target autoantigen itself or an exogenous mimic, but instead is a peptide or protein that is âantisenseâ or âcomplementaryâ in shape and/or charge to the autoantigen. The first immune response is therefore production of an antibody specific for this complementary protein, followed by an anti-antibody (i.e. anti-idiotypic antibody) that reacts with the paratope of the first antibody and also recognizes the âsenseâ or self-protein due to surface contour, charge, and/or hydropathy complementarity. Our laboratory group has published evidence for autoantigen complementarity in one autoimmune glomerular disease, proteinase-3 specific antineutrophil cytoplasmic autoantibody glomerulonephritis. The overall objective of the work described here was to provide further evidence for complementary proteins as inciting antigens in autoimmune glomerulonephritis using anti-GBM disease as the classic antibody-mediated autoimmune glomerulopathy; our central hypothesis was that anti-GBM disease is caused by a protein or peptide complementary to the anti-GBM autoantigen. The design of synthetic peptides complementary in sequence to portions of the human and rat α3(IV)NC1 collagen domains, and the design and production of a recombinant complementary α3(IV)NC1 protein more likely to possess appropriate tertiary structure to be complementary in sequence and in structure to the full-length anti-GBM epitope are described. These antigens were used to demonstrate that a subset of patients with anti-GBM disease have anti-idiotypic antibodies specific for α3(IV)NC1-complementary peptides and proteins, that these antibodies are distinct from their pathogenic idiotypic partners, and that the anti-GBM antibodies bind to these anti-complementary protein antibodies as expected by idiotypic:anti-idiotypic partners. Finally, we describe the immunologic and clinicopathologic consequences of immunization of two rodent models with anti-GBM-complementary peptides, thus providing provisional evidence for autoantigen complementarity-induced anti-GBM disease.
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32

Walters, Giles. « T cell repertoires in animal and human glomerulonephritis ». Thesis, University of Leicester, 2005. http://hdl.handle.net/2381/29506.

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This thesis aims to study the role of T cells in glomerulonephritis and to take a first step towards design of novel T cell based treatments of these conditions. Two animal models, Heymann nephritis (HN) and experimental autoimmune glomerulonephritis (EAG), are studied. Glomerular T cell receptor (TCR) repertoires from each of these models are analysed using polymerase chain reaction, CDR3 spectratyping and DNA sequencing of their CDR3 regions. In HN, a restricted set of T cells defined by their Vbeta J beta and CDR3 regions are identified as potentially pathogenic cells. In EAG, infiltrating T cells are shown to be clearly oligoclonal with restricted TCR repertoires in each animal. The repertoire restriction differs in each animal studied but the entire population carries multiple TCR CDR3 motifs which are absent in control cells.;The data from HN is utilised to design a DNA vaccination based upon the identified PCR products of infiltrating T cells. Vaccinated rats have significantly improved disease with reduced proteinuria. CD8 + and macrophage infiltration and IFN-gamma. The mechanism of action of DNA vaccination is explored, demonstrating specific anti-TCR antibodies in vaccination rats. The antibodies appear to reduce specific T cell infiltration to the kidneys and to reduce IFN-gamma expression.;Oligoclonal T cells are also identified in archival human renal biopsy tissue. Restricted TCR repertoires are variable but CDR3 spectratypes clearly show oligoclonality within multiple TCR Vbeta families. The data suggest that the most frequently represented T cell mRNA species may account for a large proportion of total T cell receptor mRNA signal.
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33

Wong, Edwin Kwan Soon. « Complement abnormalities in membranoproliferative glomerulonephritis and C3 glomerulopathy ». Thesis, University of Newcastle upon Tyne, 2016. http://hdl.handle.net/10443/3307.

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Membranoproliferative glomerulonephritis (MPGN) and C3 glomerulopathy (C3G) are rare diseases that associate with dysregulation of the alternative pathway (AP). The earliest abnormalities associated with these diseases were C3 nephritic factor and also rare genetic variants in the gene CFH that caused factor H (FH) deficiency. Since then, other acquired and genetic abnormalities in AP have been reported in MPGN and C3G. The aim of this project was to screen cohorts of MPGN and C3G for such abnormalities. Screening for rare sequence variants in genes encoding proteins involved in AP activity in two cohorts revealed a low prevalence of genetic abnormalities. Compared to the prevalence of C3 nephritic factor and autoantibodies to complement proteins, it was clear that the predominant abnormalities in these cohorts were acquired. Though few, rare genetic variants identified in CFH were studied in functional studies. The first was identified in a case of familial MPGN in the N-terminal domain of CFH. Functional studies included surface plasmon resonance and haemolytic assays to study a mutant protein in the setting of a short fragment comprising the N-terminal domain of FH. This initial study confirmed loss of function in a familial variant and formed the basis for further studies. In studies of eight other variants identified in MPGN and C3G and two other diseases that share complement risk factors, only two variants were likely to be functionally significant as demonstrated by complete loss of function. This highlights the need for such studies to correctly identify important variants. The significant functional effects initially identified in studies using short fragments were then confirmed in studies using full length protein. The significance of rare genetic variants in CFH needs to be considered even though MPGN and C3G are largely an autoimmune phenomenon.
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34

Deplano, Simona. « Role of P2X7-mediated inflammasome activation in glomerulonephritis ». Thesis, Imperial College London, 2012. http://hdl.handle.net/10044/1/17794.

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Glomerulonephritis is a major cause of kidney failure and current treatment is based on nonspecific immunosuppressive therapies. The purinergic P2X7 receptor (P2X7R) is usually not detectable in renal tissue. However, previous studies have demonstrated an increased glomerular P2X7R expression in animal models of glomerulonephritis. Furthermore, P2X7R knock-out mice have been shown to be significantly protected from antibody-mediated glomerulonephritis. P2X7R activation represents a fundamental step for the activation of the NLRP3 inflammasome which leads to the processing and release of IL-1β and IL-18. The role of the inflammasome activation in glomerulonephritis is not clear yet. The work presented in this thesis describes three aspects of P2X7R activation: cytokine production, signalling cascade following ATP stimulation and inflammasome activation. My data show that macrophages from wild type mice produce higher levels of IL-1β and IL-18 compared to macrophages from P2X7 deficient mice. ATP stimulation activates several signalling pathways in macrophages. Among them, the ribosomal pathway appears to be strictly regulated by P2X7R. To investigate the role of the inflammasome activation in glomerulonephritis I have compared macrophages from the susceptible rat strain Wistar-Kyoto with macrophages from the resistant strain Lewis. WKY macrophages express higher P2X7 mRNA and protein levels, release higher levels of IL-1β and IL-18 and exhibit a greater caspase-1 activity. Similarly, WKY nephritic glomeruli show higher P2X7, IL-1β, IL-18 and caspase-1 levels compared to Lewis glomeruli. Finally, in the attempt to identify genes responsible for the inflammasome regulation, I have examined macrophages and nephritic glomeruli from congenic rats. My data seem to indicate that the susceptibility locus Crgn2 contains one or more genes that control IL-1β and IL-18 release in macrophages. Further studies are certainly required to verify the relevance of these data. The results are important in understanding the pathogenesis of glomerulonephritis and identification of new potential therapeutic targets.
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35

Honkanen, Eero. « Membranous glomerulonephritis a clinical, morphological, and experimental study / ». Hki : Societas scientiarum Fennica : Academic Bookstore [jakaja], 1987. http://catalog.hathitrust.org/api/volumes/oclc/57853993.html.

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36

André, Marie-Luce. « Glomerulonephrite extra membraneuse en tant que syndrome paraneoplasique : a propos d'un cas associant glomerulonephrite extra membraneuse, adenocarcinome renal et hamartome splenique ». Lyon 1, 1991. http://www.theses.fr/1991LYO1M194.

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37

Sedaghat, Sam. « Analyse des Nephropathiespektrums am Universitätsklinikum Leipzig von 1983 bis 2010 ». Doctoral thesis, Universitätsbibliothek Leipzig, 2015. http://nbn-resolving.de/urn:nbn:de:bsz:15-qucosa-172299.

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Diese retrospektiv-deskriptive Analyse befasste sich mit dem Nephropathiespektrum des Universitätsklinikums Leipzig von 1983 bis 2010. Anders als in manch anderen Ländern existiert in Deutschland kein zentrales Register, welches bundesweit Daten zu Nephropathien sammelt und verwertet. Es wurden 467 Biopsien ausgewertet. Knapp 60% der Patienten waren männlich (n=278), 40% weiblich (n=186). Das mittlere Alter betrug 46 Jahre. Das Durchschnittsalter bei Männern betrug 47 Jahre, bei Frauen 45 Jahre. Insgesamt waren 293 primäre GN, 118 sekundäre GN und 17 INP vorhanden. Die häufigste Diagnose war die IgAN (17% der ges. NP), gefolgt von der RPGN (13 % der ges. NP), der HTNP (10%), der MCGN (9%) und der MGN (9%). Die IgAN war mit 28% aller prim. GN die häufigste primäre GN, gefolgt von der RPGN (21% der prim. GN), der MCGN (14%), der MGN (14%) und der FSGS (5%). Die HTNP war die häufigste sekundäre GN (38% der sek. GN), gefolgt von der Lupus-Nephritis (27%) und der DNP (15%). Die häufigste INP war die Calcineurin-Hemmer-NP (29% der INP), gefolgt von der TMA und der Sklerodermie-NP (jeweils 18%), der Oxalatkristall-NP und der Medikamententoxischen NP (jeweils 12%). Die mittlere Inzidenz der IgAN lag bei 0,8/100.000 Einwohner, der MesP bei 0,7/100.000 Einwohner, der MCGN bei 0,6/100.000 Einwohner, der MGN bei 0,5/100.000 Einwohner, der MPGN bei 0,3/100.000 Einwohner, der FSGS bei 1,0/100.000 Einwohner, der RPGN bei 0,7/100.000 Einwohner, der LNP bei 0,5/100.000 Einwohner, der HTNP bei 0,7/100.000 Einwohner und der DNP bei 0,4/100.000 Einwohner. Beim Vergleich des Zeitraums von 1983 bis 1990 mit dem von 1990 bis 2010 fiel eine Abnahme der IgAN von 29% auf 16%, eine Zunahme der FSGS von 0 auf 4% und der RPGN von 6% auf 14% auf. Auch die DNP nahm von 2% auf 4% zu. Unter den vom Pathologischen Institut des Uniklinikums Hamburg-Eppendorf befundeten Nierenbiopsien war die IgAN die häufigste NP, gefolgt von der RPGN. Dagegen war unter den vom Pathologischen Institut des Uniklinikums Erlangen befundeten Biopsien die FSGS die Häufigste, gefolgt von der RPGN. Der Erkrankungsgipfel lag bei der IgAN zwischen dem 29. und 48. Lebensjahr, bei der MCGN zwischen dem 28. und 58. Lebensjahr, bei der MGN zwischen dem 38. und 67. Lebensjahr und bei der FSGS zwischen dem 47. und 73. Lebensjahr. Die RPGN hatte ihren Erkrankungsgipfel zwischen der 4. und 6. Lebensdekade, die Lupus-Nephritis zwischen dem 22. und 40. Lebensjahr und die HTNP zwischen dem 41. und 61. Lebensjahr. Das mittlere Alter bei der DNP lag bei 57 Jahren. Insgesamt waren von 1983 bis 2010 Veränderungen im Nephropathiespektrum zu beobachten. Eine Zunahme der Inzidenz der FSGS, wie in außereuropäischen Ländern beschrieben, konnte festgestellt werden. Auch die Inzidenz der RPGN stieg über die letzten Jahre deutlich an und löste, gemeinsam mit der FSGS, die IgAN ab 2009 als die bis dahin häufigste Diagnose ab.
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Ye, Yisha, et 葉伊莎. « Proteomics study of the effects of fish oil and corn oil enriched dieton membranous nephritis ». Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 2008. http://hub.hku.hk/bib/B40887753.

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MENTHON, SAID MARIE-HELENE. « Glomerulonephrites associees a mycoplasma pneumoniae chez l'enfant ». Lyon 1, 1994. http://www.theses.fr/1994LYO1M215.

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Scholz, Juliane. « Die Rolle dentritischer Zellen in der Pathogenese der Glomerulonephritis / ». Bonn, 2008. http://opac.nebis.ch/cgi-bin/showAbstract.pl?sys=000253892.

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Khan, Sarah Basir. « Mediators of inflammation and fibrosis in experimental crescentic glomerulonephritis ». Thesis, Imperial College London, 2005. http://hdl.handle.net/10044/1/11303.

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Habib-Nassif, Anne-Marie. « T cell receptor gene characterisation in experimental autoimmune glomerulonephritis ». Thesis, Imperial College London, 2004. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.412499.

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Chaudhry, Afzal Niaz. « Cell mediated immunity in the development of crescentic glomerulonephritis ». Thesis, Imperial College London, 2004. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.410025.

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Chan, Yuk-yee. « The role of angiotensin II and angiotensin receptors in the pathogenesis of IgA nephropathy ». Click to view the E-thesis via HKUTO, 2006. http://sunzi.lib.hku.hk/hkuto/record/B36612248.

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Ngai, H. Y. Heidi. « Proteomics analysis of potential biomarkers and pathogenic mechanisms of membranous nephropathy in a rat model of passive Heymann nephritis ». Click to view the E-thesis via HKUTO, 2007. http://sunzi.lib.hku.hk/hkuto/record/B38827372.

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Tein, Mark S. C. « Studies on basement membrane permeation : models of pathogenic mechanims of glomerulonephritis ». Thesis, University of Oxford, 1994. http://ora.ox.ac.uk/objects/uuid:22440bfc-e712-4f7c-a11d-2eed9b07bcb6.

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The effects of the biological cross-linker transglutaminase, the neutrophil oxidant hydrogen peroxide, and neutrophil proteinases on glomerular basement membrane permeability have been examined using an in vitro model of glomerular ultrafiltration. The main focus of the study lies in determining whether any of the test agents were able to render glomerular basement membrane more permeable to protein. Guinea pig liver transglutaminase was used as a model enzyme to test for the effect of biological cross-linkers on glomerular basement membrane permeability. It cross-linked glomerular basement membrane proteins, caused membrane contraction, and rendered glomerular basement membrane less permeable both to water and the low molecular weight protein marker myoglobin but had no effect on the membrane permeability to the high molecular weight marker protein bovine serum albumin or serum protein. The pathophysiological relevance of the effect is discussed. Hydrogen peroxide increased glomerular basement membrane permeability to water and proteins but the effect depended on hydrogen peroxide concentration and incubation time. The minimum concentration needed to render glomerular basement membrane more permeable to bovine serum albumin and serum protein was 1 M and the minimum incubation time needed was 6 hrs. A respiratory burst analysis of activated neutrophils showed that the average concentration of hydrogen peroxide that could be generated by the neutrophils was less than 50 mM and the time taken for extracellular hydrogen peroxide concentration to fall off to zero was less than 1 hr. Therefore, neutrophils seemed unable to generate and sustain a sufficiently high hydrogen peroxide concentration to render glomerular basement membrane more permeable to protein in vivo. Proteinases extracted from pig neutrophil granules were used to assess their effect on glomerular basement membrane permeability. The extract showed activity against glomerular basement membrane and the activity was primarily attributed to the serine proteinases elastase and cathepsin G, judged from substrate and inhibitor analyses. The proteinase extract also contain latent metalloproteinases, activatable by the organomercurial 4-aminophenyl mercuric acetate and calcium ions. Once activated, they also showed activity against glomerular basement membrane. The extract rendered glomerular basement membrane more permeable to water, myoglobin, bovine serum albumin, and serum protein. The increase in membrane permeability to water and proteins was due to membrane thinning and an increase in the intrinsic porosity of the membrane. When the serine and metalloproteinases were allowed to act in concert, they synergistically degraded glomerular basement membrane and increased the membrane permeability to serum protein and water. The study provides the first direct evidence that pathophysiological amounts of serine and metalloproteinases are able to render glomerular basement membrane more permeable to protein and suggests they may be capable of promoting proteinuria in neutrophil-dependent forms of immune glomerulonephritis.
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Brown, Paul A. J. « The plasminogen activator/plasmin system in the normal and diseased glomerulus ». Thesis, University of Aberdeen, 1995. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.362277.

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My studies have investigated the possible involvement of the plasminogen activator/plasmin system in glomerular physiology and pathology. Urokinase plasminogen activator and its cellular receptor are not found immunocytochemically within the normal or diseased glomerulus in vivo. Plasminogen activator inhibitor-1, an inhibitor of urokinase plasminogen activator was, however, identified in crescents from cases of crescentic glomerulonephritis, but not within the glomerular tuft proper. Culture of human glomerular cells initially revealed urokinase plasminogen activator and plasminogen activator-1 proteins within the supernatant of epithelial cells and mesangial cells, as measured by ELISA. However, immunocytochemical characterisation of each of the cell cultures showed that there was contamination of some of the mesangial cell cultures by epithelial cells. Pure cultures of both types of cell produced plasminogen activator inhibitor-1. However, measurement of urokinase plasminogen activator activity by zymography confirmed that this molecule was not present within supernatants obtained from pure mesangial cell cultures. Furthermore, the use of combined non-isotopic in situ hybridisation and immunocytochemistry allowed identification of urokinase plasminogen activator mRNA only within human cultured glomerular epithelial cells and not within mesangial cells. This finding proved that contaminating epithelial cells were responsible for urokinase plasminogen activator production in cultures thought to be made up of pure mesangial cells. Thus there is excellent evidence for synthesis of this molecule only by epithelial cells. Non-isotopic and radioactive in situ hybridisation were unsuccessful in identifying urokinase plasminogen activator within human kidney sections and the difficulties involved in the methodology of this technique, and the implications of the culture cell work for the role of the plasminogen activator/plasmin system in the glomerulus, are discussed.
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LUMBROSO, CATHERINE. « Atteintes glomerulaires au cours de l'infection par le virus d'immunodeficience humaine ». Toulouse 3, 1991. http://www.theses.fr/1991TOU31551.

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Cheung, Tsoek-yee Giselle. « The role of homocysteine in the development of glomerulosclerosis : stimulation of monocyte chemoattractant protein-1 in rat mesangial cells / ». Click to view the E-thesis via HKUTO, 2002. http://sunzi.lib.hku.hk/hkuto/record/B42576465.

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Robson, Michael Gregory. « The role of the complement system in experimental murine glomerulonephritis ». Thesis, Imperial College London, 2000. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.394030.

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