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Dissertations / Theses on the topic 'Glomeruloskleroz'

Author: Grafiati

Published: 7 June 2025

Last updated: 11 July 2025

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1

Weichert, Wilko. "Fokal segmentale Glomerulosklerose und juxtaglomerulärer Apparat der hypertensiven "Fawn-hooded"-Ratte." [S.l.] : [s.n.], 2001. http://deposit.ddb.de/cgi-bin/dokserv?idn=963647989.

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2

Weichert, Wilko. "Fokal segmentale Glomerulosklerose und juxtaglomerulärer Apparat der hypertensiven "fawn-hooded" Ratte." Doctoral thesis, Humboldt-Universität zu Berlin, Medizinische Fakultät - Universitätsklinikum Charité, 2001. http://dx.doi.org/10.18452/14679.

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In dieser Arbeit wurden 8 und 16 Wochen alte, hypertensive "fawn-hooded" Ratten (FHH8, FHH16) mit genetisch ähnlichen 16 Wochen alten "fawn-hooded" Ratten mit nur geringgradiger Blutdruckerhöhung (FHL16, Kontrollgruppe) hinsichtlich der pathologisch-anatomischen Veränderungen der Nierenmorphologie und hinsichtlich der Expression von NO-Synthase-1 (NOS1), Cyclooxygenase-2 (COX-2) und Renin am juxtaglomerulären Apparat (JGA) verglichen. Die histopathologischen Veränderungen bei FHH16 umfassten die klassischen Schädigungszeichen der fokal segmentalen Glomerulosklerose (FSGS) mit fokaler Überexpression von Kollagen IV und eine moderate Arteriolopathie. Bei FHH8 ließen sich, wie bei FHL16 keine morphologischen Schädigungen nachweisen. Die NOS1-Aktivität an der Macula densa, untersucht mittels der NADPH-Diaphorasereaktion und die NOS1 mRNA Expression waren bei FHH8 (+153 and +88%; P < 0.05) und FHH16 (+93 and +98%; P < 0.05) im Vergleich zu FHL16 signifikant erhöht. Eine gleichgerichtete signifikante Erhöhung zeigte sich für die COX-2-Expression an der Macula densa von FHH8 (+166%; P < 0.05) und FHH16 (+157%; P < 0.05) im Vergleich zu FHL16. Des weiteren ließ sich eine signifikante, ebenfalls gleichgerichtete Überexpression von Renin in der afferenten Arteriole auf Protein- und mRNA-Ebene bei FHH8 (+51 and +166%; P < 0.05) und FHH16 (+105 and +136%; P < 0.05) im Vergleich zu FHL16 nachweisen. Somit konnte gezeigt werden, dass die gleichgerichtete Überexpression von NOS1, COX-2 und Renin am JGA bei der FHH-Ratte der Entwicklung einer fokal segmentalen Glomerulosklerose vorausgeht und damit möglicherweise pathogenetische Bedeutung für die Entstehung der Nierenschädigung bei diesem Rattenstamm hat.<br>This study describes elevated histochemical signals for nitric oxide synthase-1 (NOS1) and cyclooxygenase-2 (COX-2) in juxtaglomerular apparatus (JGA) and adjacent thick ascending limb of the kidney of fawn-hooded hypertensive rats (FHH). Two different age groups of FHH (8 and 16 wk; FHH8 and FHH16, respectively) were compared with genetically related fawn-hooded rats with close to normal blood pressure (FHL) that served as controls. Histopathological changes in FHH16 comprised focal segmental glomerulosclerosis (FSGS), focal matrix overexpression (mainly of collagen IV), and a moderate arteriolopathy with hypertrophy of the media, enhanced immunoreactivity for alpha-smooth muscle actin, and altered distribution of myofibrils. Macula densa NOS activity, as expressed by NADPH-diaphorase staining, and NOS1 mRNA abundance were significantly elevated in FHH8 (+153 and +88%; P < 0.05) and FHH16 (+93 and +98%; P < 0.05), respectively. Even higher elevations were registered for COX-2 immunoreactivity in FHH8 (+166%; P < 0.05) and FHH16 (+157%; P < 0.05). The intensity of renin immunoreactivity and renin mRNA expression in afferent arterioles was also elevated in FHH8 (+51 and +166%; P < 0.05) and FHH16 (+105 and +136%; P < 0.05), respectively. Thus we show that coordinate upregulation of tubular NOS1, COX-2, and renin expression precedes, and continues after, the manifestation of glomerulosclerotic damage in FHH. These observations may have implications in understanding the role of local paracrine mediators in glomerular disease.

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3

Mühe, Anne [Verfasser], and Volker [Akademischer Betreuer] Vielhauer. "Entzündliche Mechanismen der Glomerulosklerose und sekundären interstitiellen Nierenschädigung: Rolle von Tumornekrosefaktor / Anne Mühe ; Betreuer: Volker Vielhauer." München : Universitätsbibliothek der Ludwig-Maximilians-Universität, 2016. http://d-nb.info/1121507840/34.

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4

Berning, Elias. "Die Blockade des Chemokinrezeptors CCR1 reduziert bei Mäusen mit Adriamycin-induzierter Glomerulosklerose die interstitielle Entzündung und Fibrose." Diss., lmu, 2006. http://nbn-resolving.de/urn:nbn:de:bvb:19-52189.

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5

Wilkening, Anja [Verfasser], and Volker [Akademischer Betreuer] Vielhauer. "Identifizierung einer pathophysiologischen Rolle des Chemokinrezeptors CCR2 bei der fokal segmentalen Glomerulosklerose / Anja Wilkening ; Betreuer: Volker Vielhauer." München : Universitätsbibliothek der Ludwig-Maximilians-Universität, 2019. http://d-nb.info/1202011799/34.

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6

Witthus, Marco [Verfasser]. "Rituximab als neue Therapieoption bei der primären Minimal-Change-Glomerulopathie und fokal segmentalen Glomerulosklerose des Erwachsenen / Marco Witthus." Köln : Deutsche Zentralbibliothek für Medizin, 2013. http://d-nb.info/1037399773/34.

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7

Schlichting, Daniel [Verfasser]. "Therapie der Minimal-Change-Nephropathie und der Fokal-Segmentalen Glomerulosklerose : Vergleich zweier Ciclosporin-A-Dosierungsregime im Langzeitverlauf / Daniel Schlichting." Ulm : Universität Ulm. Medizinische Fakultät, 2011. http://d-nb.info/1017117101/34.

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8

Bruns, Hauke Arne [Verfasser], and Hans-Joachim [Akademischer Betreuer] Anders. "Podozyten-spezifischer Murine Double Minute (MDM) 2 Knockout führt zu fokal segmentaler Glomerulosklerose / Hauke Arne Bruns ; Betreuer: Hans-Joachim Anders." München : Universitätsbibliothek der Ludwig-Maximilians-Universität, 2017. http://d-nb.info/1126968080/34.

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9

Weichert, Wilko [Verfasser], H. [Gutachter] Pavenstädt, H. J. [Gutachter] Gröne, and S. [Gutachter] Bachmann. "Fokal segmentale Glomerulosklerose und juxtaglomerulärer Apparat der hypertensiven "fawn-hooded" Ratte / Wilko Weichert ; Gutachter: H. Pavenstädt, H.-J. Gröne, S. Bachmann." Berlin : Humboldt-Universität zu Berlin, 2001. http://d-nb.info/1207656011/34.

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10

Brand, Daniel [Verfasser]. "Nephroprotektive Effekte des Angiotensin II Rezeptor Agonisten Compound 21 im Modell der Anti-Thy1-induzierten chronisch-progressiven Glomerulosklerose der Ratte / Daniel Brand." Berlin : Freie Universität Berlin, 2015. http://d-nb.info/1070819999/34.

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11

Lichtneger, Till-Simon [Verfasser], Andrea [Akademischer Betreuer] Hartner, Ines [Akademischer Betreuer] Marek, and Andrea [Gutachter] Hartner. "Einfluss von alpha8-Integrin auf die Regulation der Zellstressmechanismen Apoptose, Autophagie und ER-Stress, sowie Zellalterung und Proliferation bei renaler interstitieller Fibrose und Glomerulosklerose im Mausmodell / Till-Simon Lichtneger ; Gutachter: Andrea Hartner ; Andrea Hartner, Ines Marek." Erlangen : Friedrich-Alexander-Universität Erlangen-Nürnberg (FAU), 2021. http://d-nb.info/1230137637/34.

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12

Weichert, Wilko [Verfasser]. "Fokal segmentale Glomerulosklerose und juxtaglomerulärer Apparat der hypertensiven "Fawn-hooded"-Ratte / von Wilko Weichert." 2001. http://d-nb.info/963647989/34.

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13

Tossidou, Irini [Verfasser]. "Pathomechanismen der fokal segmentalen Glomerulosklerose (FSGS) : Charakterisierung von "Survival"- und Apoptose-Signalwegen / von Irini Tossidou." 2008. http://d-nb.info/989092828/34.

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14

Köbler, Sven [Verfasser]. "Podozytenspezifischer Atg5-Knock-Out führt zu altersabhängiger Glomerulosklerose in der Maus / vorgelegt von Sven Köbler." 2010. http://d-nb.info/1009465473/34.

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15

Berning, Elias [Verfasser]. "Die Blockade des Chemokinrezeptors CCR1 reduziert bei Mäusen mit Adriamycin-induzierter Glomerulosklerose die interstitielle Entzündung und Fibrose / vorgelegt von Elias Berning." 2006. http://d-nb.info/979795753/34.

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16

Obeidová, Lena. "Mutační analýza genu TRPC6 u pacientů s nefrotickým syndromem." Master's thesis, 2011. http://www.nusl.cz/ntk/nusl-312695.

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Focal segmental glomerulosclerosis is one of the commonest cause of the nephrotic syndrome in adults patients. It is a damage of glomerulus characterized by leakage of proteins to urine and oedemas which usually develops into the end-stage renal disease within 10 years. Recently have been described familial forms of this disease which arise from injury to proteins making up filtration barrier of kidney. In 2005 non-selective ion channel TRPC6 was assigned among these proteins. In this thesis I focused on summarizing existing knowledge of the nephrotic syndrome, focal segmental glomerulosclerosis and involvement of TRPC6 in their origin. Second part of this work is devoted to the screening analysis of TRPC6 gene to discover possible mutations and polymorfisms in 47 patients with histologically proven focal segmental glomerulosclerosis or minimal change disease. The used methods were high resolution melting and direct sequencing. In the group of patients was detected no pathogenic mutation, only 2 known polymorfisms P15S and A404V and few changes which do not result in alteration of amino acid. So it seems TRPC6 gene mutations are a rare cause of the focal segmental glomerulosclerosis in adult patients in the Czech Republic.

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17

Šafaříková, Markéta. "Genetické faktory ovlivňující průběh vybraných forem nefrotického syndromu." Master's thesis, 2011. http://www.nusl.cz/ntk/nusl-312728.

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Nephrotic syndrome (NS) is characterized by proteinuria, hypalbuminemia and edemas. It occurs during first and second glomerulopathies. This disease can be divided into two groups: primary (idiopathic) and secondary. The heredity of the familial nephrotic syndrome is autosomal dominant and autosomal recessive. There are four most important genes that condition the formation of hereditary nephrotic syndrome in adult patienst. These genes are ACTN4, CD2AP, NPHS2 and TRPC6. The gene ACTN4, which encodes protein α-actinin 4, is responsible for the autosomal dominant form of focal segmental glomerulosclerosis (FSGS). FSGS is included in first glomerulopathies. α-Actinin 4 was also researched for some types of carcinomas. There was performed the mutational analysis of the gene ACTN4 on the set of 48 patients with nephrotic syndrome in this diploma thesis. High resolution melting (HRM) analysis and sequencing selected samples were used during this mutation detection. During this process many published and unpublished SNPs and one unpublished candidate mutation that could have causal associations with FSGS were found.

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18

Šafaříková, Markéta. "Geneticky podmíněné faktory progrese vybraných forem chronických nefropatií." Doctoral thesis, 2019. http://www.nusl.cz/ntk/nusl-396192.

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Nephrotic syndrome is characterized by proteinuria, hypoproteinemia, edemas and hyperlipidemia. It occurs in primary (e.g. focal segmental glomerulosclerosis, FSGS or minimal change disease, MCD) and in secondary glomerulopathies (e.g. kidney amyloidosis). In primary forms, great attention is paid to the potential genetic background of the disease and due to new molecular genetic methods genes, whose mutations cause different nephropathies (e.g. ACTN4 or INF2) were identified. The aims of presented doctoral thesis were following. Firstly, to continue the mutational analysis of ACTN4 that was described in the author's diploma thesis in other glomerulopathies. Secondly, to implement the mutational analysis of INF2 and subsequently analyse this gene in patients with FSGS/MCD and in patients from special group characterized by positive family history for end stage renal disease (ESRD) in combination with advanced chronic kidney disease (CKD) or already developed ESRD at the time of diagnosis. Thirdly, mutational analysis of NPHS2 and TRPC6 (methods implemented in laboratory earlier) in selected patients from the special group. Finally, expression analyses of genes important for podocyte function or connected with human immune system. This part also verifies the applicability of NPHS2/SYNPO expression...

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