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Dissertations / Theses on the topic 'Diabetes Insipidus'

Author: Grafiati

Published: 4 June 2021

Last updated: 25 July 2025

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1

Hedrich, Christian Michael, Agnieszka Zachurzok-Buczynska, Aneta Gawlik, et al. "Autosomal Dominant Neurohypophyseal Diabetes Insipidus in Two Families." Saechsische Landesbibliothek- Staats- und Universitaetsbibliothek Dresden, 2014. http://nbn-resolving.de/urn:nbn:de:bsz:14-qucosa-134493.

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Background: Autosomal dominant familial neurohypophyseal diabetes insipidus (adFNDI) is a rare disease with symptoms of polydipsia, polyuria and dehydration caused by arginine vasopressin deficiency. Disease onset is within infancy or adolescence. A variety of disease-causing mutations of the arginine vasopressin neurophysin II gene (AVP) on chromosome 20p13 have been described. Methods: Two Polish families with adFNDI were screened for mutations. Processing of wild-type (WT) and mutant AVP was monitored using immunocytochemical methods in stably transfected Neuro2A cells. AVP secretion into t

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2

Ho, Tsun-bond Horace. "Aldose reductase deficient mice develop nephrogenic diabetes insipidus /." Hong Kong : University of Hong Kong, 2000. http://sunzi.lib.hku.hk/hkuto/record.jsp?B21949074.

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3

Davies, Janet Elizabeth. "Towards a transgenic rat model of Familial Neurohypophysial Diabetes Insipidus." Thesis, University of Bristol, 2002. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.247860.

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4

Zaarouri, Kamel. "Closed-loop control of plasma osmolality in patients with central diabetes insipidus." Thesis, McGill University, 2010. http://digitool.Library.McGill.CA:8881/R/?func=dbin-jump-full&object_id=92300.

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5

Sanches, Talita Rojas Cunha. "Vias intracelulares da ação do Sildenafil no diabetes insipidus induzido pelo lítio." Universidade de São Paulo, 2012. http://www.teses.usp.br/teses/disponiveis/5/5148/tde-27082012-163342/.

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Os pacientes que usam lítio (Li) para tratamento do transtorno bipolar frequentemente apresentam poliúria e deficiência de concentração urinária, sintomas do Diabetes Insipidus Nefrogênico (DIN). Animais tratados com Li apresentam baixos níveis de produção de adenosina monofosfato cíclico (AMPc) em resposta ao hormônio antidiurético (HAD). O Sildenafil (Sil), um inibidor da fosfodiesterase 5 (PDE5), eleva os níveis intracelulares de guanosina monofosfato cíclico (GMPc), levando a inserção de aquaporina 2 (AQP2) na membrana plasmática das células do ducto coletor. Portanto, inibidores de PDE po

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6

Villarreal-Engelhardt, Gabriele. "Extensive glomerular immaturity associated with renal tubular acidosis, nephrogenic diabetes insipidus and nephrocalcinosis /." [S.l : s.n.], 1987. http://www.ub.unibe.ch/content/bibliotheken_sammlungen/sondersammlungen/dissen_bestellformular/index_ger.html.

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7

Sanches, Talita Rojas Cunha. "Estudo da ação do inibidor de fosfodiesterase (sildenafil) no diabetes insipidus induzido pelo lítio." Universidade de São Paulo, 2008. http://www.teses.usp.br/teses/disponiveis/5/5148/tde-20012009-112638/.

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Os pacientes que usam lítio (Li) para tratamento do transtorno bipolar freqüentemente apresentam poliúria e deficiência de concentração urinária, sintomas do Diabetes Insipidus nefrogênico (DIN). Animais tratados com Li apresentam baixos níveis de produção de adenosina monofosfato cíclico (AMPc) em resposta ao hormônio antidiurético (HAD). O Sildenafil (Sil), um inibidor da fosfodiesterase 5 (PDE5), eleva os níveis intracelulares de guanosina monofosfato cíclico (GMPc), levando a inserção de aquaporina 2 (AQP2) na membrana plasmática das células do ducto coletor. Portanto, inibidores de PDE po

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8

Poulsen, Søren Brandt, Tina Bøgelund Kristensen, Heddwen L. Brooks, Donald E. Kohan, Timo Rieg, and Robert A. Fenton. "Role of adenylyl cyclase 6 in the development of lithium-induced nephrogenic diabetes insipidus." AMER SOC CLINICAL INVESTIGATION INC, 2017. http://hdl.handle.net/10150/623931.

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Psychiatric patients treated with lithium (Li+) may develop nephrogenic diabetes insipidus (NDI). Although the etiology of Li+-induced NDI (Li-NDI) is poorly understood, it occurs partially due to reduced aquaporin-2 (AQP2) expression in the kidney collecting ducts. A mechanism postulated for this is that Li+ inhibits adenylyl cyclase (AC) activity, leading to decreased cAMP, reduced AQP2 abundance, and less membrane targeting. We hypothesized that Li-NDI would not develop in mice lacking AC6. Whole-body AC6 knockout (AC6(-/-)) mice and potentially novel connecting tubule/principal cell-specif

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9

Schliebe, Nicole. "Die molekulare Pathophysiologie der hypothalamisch-renalen Osmoregulation bei Mäusen mit X-chromosomalem nephrogenen Diabetes insipidus." Leipzig Leipziger Univ.-Verl, 2009. http://d-nb.info/998766585/04.

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10

Geddes, Brad J. "Adenovirus as gene therapy vectors in the CNS : evaluation in a model of hypothalamic diabetes insipidus." Thesis, University of Bristol, 1998. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.265302.

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11

Gasparotto, Ana Paula Devite Cardoso 1971. "Diabetes insipidus, sindrome perdedora de sal e sindrome da secreção inapropriada do hormonio antidiuretico em pacientes neurocirugicos." [s.n.], 2002. http://repositorio.unicamp.br/jspui/handle/REPOSIP/311134.

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Orientadores: Desanka Dragosavac, Antonio Luis Eiras Falcão, Sebastião Araujo<br>Dissertação (mestrado) - Universidade Estadual de Campinas, Faculdade de Ciências Médicas<br>Made available in DSpace on 2018-08-03T18:11:32Z (GMT). No. of bitstreams: 1 Gasparotto_AnaPaulaDeviteCardoso_M.pdf: 633497 bytes, checksum: c02e20dc885b6507d1ed4dc92372343f (MD5) Previous issue date: 2002<br>Resumo: Introdução - Alterações do sódio plasmático são freqüentemente encontradas no pós-operatório de pacientes submetidos à neurocirurgia e estão associadas à piora do estado neurológico desses pacientes. Essas a

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12

Hedrich, Christian Michael, Agnieszka Zachurzok-Buczynska, Aneta Gawlik, et al. "Autosomal Dominant Neurohypophyseal Diabetes Insipidus in Two Families: Molecular Analysis of the Vasopressin-Neurophysin II Gene and Functional Studies of Three Missense Mutations." Karger, 2009. https://tud.qucosa.de/id/qucosa%3A27572.

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Background: Autosomal dominant familial neurohypophyseal diabetes insipidus (adFNDI) is a rare disease with symptoms of polydipsia, polyuria and dehydration caused by arginine vasopressin deficiency. Disease onset is within infancy or adolescence. A variety of disease-causing mutations of the arginine vasopressin neurophysin II gene (AVP) on chromosome 20p13 have been described. Methods: Two Polish families with adFNDI were screened for mutations. Processing of wild-type (WT) and mutant AVP was monitored using immunocytochemical methods in stably transfected Neuro2A cells. AVP secretion into t

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13

Schrader, Caroline [Verfasser], Helmuth-Günther [Akademischer Betreuer] Dörr, and Helmuth-Günther [Gutachter] Dörr. "Betreuung von Kindern mit Diabetes insipidus zentralis in der endokrinologischen Ambulanz eines Universitätsklinikums / Caroline Schrader ; Gutachter: Helmuth-Günther Dörr ; Betreuer: Helmuth-Günther Dörr." Erlangen : Friedrich-Alexander-Universität Erlangen-Nürnberg (FAU), 2021. http://d-nb.info/1239419082/34.

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14

Bragança, Ana Carolina de. "Efeito da carbamazepina na reabsorção de água pelo ducto coletor medular interno de ratos normais e de ratos com diabetes insípido nefrogênico induzido pelo lítio." Universidade de São Paulo, 2010. http://www.teses.usp.br/teses/disponiveis/5/5148/tde-10052010-121705/.

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Carbamazepina (Carba) é um anticonvulsivante, uma droga psicotrópica muito utilizada no tratamento de pacientes com distúrbios intelectuais. Esta droga foi utilizada para diminuir o volume urinário no Diabetes Insípido (DI), pois possui um efeito antidiurético, mas a incidência de hiponatremia é uma ocorrência comum. O lítio é uma das drogas mais importantes para o tratamento do distúrbio bipolar. No entanto, ele tem uma grande capacidade de induzir DI dificultando o seu uso em pacientes debilitados psicologicamente. Atualmente, a associação destas drogas é frequentemente utilizada para o trat

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15

Cunin, Claude. "Greffes intracérébroventriculaires de noyaux hypothalamiques : Études histophysiologiques chez le rat brattleboro déficient génétique en vasopressine." Nancy 1, 1986. http://www.theses.fr/1986NAN10009.

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L'étude immunocytochimique du développement du greffon a mis en évidence de la vasopressine, de l'ocytocine des neurophysines I et II associées. Examen des paramètres de la fonction rénale. La technique de greffe serait susceptible de recréer une restauration fonctionnelle au niveau du système nerveux diencéphalique

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16

PORTE, DENIS. "Histiocytose x pulmonaire de l'adulte : a propos d'une observation avec diabete insipide." Lille 2, 1990. http://www.theses.fr/1990LIL2M193.

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17

KASSIS, KEGHAM. "Association d'un diabete insipide nephrogenique et d'un syndrome de fahr : a propos d'une observation." Besançon, 1992. http://www.theses.fr/1992BESA3026.

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18

Sanchez, Patrick. "Diabete insipide central associe a un deficit corticotrope : a propos d'une observation." Toulouse 3, 1988. http://www.theses.fr/1988TOU31287.

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19

Morin, Denis. "Le récepteur V2 humain de la vasopressine : perte de fonction et gain de fonction. Du Diabète Insipide Néphrogénique à un récepteur V2 constitutivement actif." Montpellier 1, 1999. http://www.theses.fr/1999MON1T007.

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20

Winiszewski, Anne-Marie. "Diabète insipide néphrogénique induit par le lithium : à propos de deux observations." Université Louis Pasteur (Strasbourg) (1971-2008), 1990. http://www.theses.fr/1990STR1M021.

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21

CRETENET, XAVIER. "La pathologie post-hypophysaire post-traumatique." Dijon, 1994. http://www.theses.fr/1994DIJOM107.

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22

Guérin-Jacob, Delphine. "Diabète insipide central de révélation néonatale : à propos de deux observations." Bordeaux 2, 1999. http://www.theses.fr/1999BOR20302.

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23

Debrand, Nicolas. "Caractérisation et étude d'un élément régulateur du gène codant pour le récepteur à la vasopressine de type 2." Phd thesis, Université Pierre et Marie Curie - Paris VI, 2008. http://tel.archives-ouvertes.fr/tel-00485725.

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Le contrôle de la transcription constitue le principal niveau de la régulation de l'expression des gènes dans les cellules eucaryotes. Le laboratoire a identifié 6 familles indépendantes avec un diabète insipide néphrogénique (DIN) lié à l'X portant de grandes délétions en amont du gène de l'AVPR2. Dans chacune de ces familles, les gènes AVPR2 et AQP2 sont intacts et les hommes sont atteints de DIN lié à l'X dans sa forme rénale « classique ». Le séquençage et l'analyse de 61 kilobases en amont et en aval de l'AVPR2 ont permis l'identification de 6 zones délétées chez 6 familles indépendantes,

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24

Vargas-Poussou, Rosa. "Etude genetique et moleculaire de deux tubulopathies de l'enfant : diabete insipide nephrogenique et syndrome de bartter (doctorat : bases cellulaires et moleculaires du fonctionnement renal normal et pathologique)." Paris 5, 1998. http://www.theses.fr/1998PA05N148.

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25

Arbez, Marc. "Le syndrome d'interruption de la tige pituitaire : à propos de deux observations, avec déficit multiple hypophysaire : revue de la littérature." Bordeaux 2, 1993. http://www.theses.fr/1993BOR2M211.

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Le diagnostic de syndrome d'interruption de la tige pituitaire n'est possible que depuis l'avènement de l'IRM. Il se caractérise par une tige pituitaire interrompue ou hypoplasique, une antéhypophyse souvant de petite taille, et la formation d'une posthypophyse ectopique, qui semble remplacer la neurohypophyse absente. Ce syndrome et ses variantes entraînent le plus souvent un déficit multiple hypophysaire notamment thyréotrope et parfois un diabète insipide (DI). L'azxe somatotrope est le premier atteint. Ce syndrome est plus fréquent chez les garçons. L'hypothèse étiologique congénitale de r

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26

Castelão, João Pedro Constâncio. "Diabetes insipidus central : um caso clínico." Master's thesis, 2019. http://hdl.handle.net/10451/43186.

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Trabalho Final do Curso de Mestrado Integrado em Medicina, Faculdade de Medicina, Universidade de Lisboa, 2019<br>A Diabetes Insipidus (DI) central é uma doença rara com múltiplas etiologias possíveis. Descreve-se neste trabalho final de mestrado um caso clínico complexo, seguindo a marcha diagnóstica pediátrica da avaliação da poliúria e polidipsia numa criança de 5 anos, com abordagem do diagnóstico diferencial, benefícios e riscos da terapêutica e procedimentos diagnósticos, englobando também a vertente social e ética. Este caso demonstra como é essencial saber gerir a complexidade clínica

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27

Chen, Wen-Yu, and 陳文瑜. "Molecular Genetic Study of Nephrogenic Diabetes Insipidus." Thesis, 1999. http://ndltd.ncl.edu.tw/handle/94175207870572591848.

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碩士<br>國立陽明大學<br>遺傳學研究所<br>87<br>Nephrogenic Diabetes Insipidus (NDI) is a rare X-linked recessive renal disorder (MIM No. 304800) due to resistance to antidiuretic action of arginine vasopression (AVP) hormone. NDI is characterized with clinical symptoms of polyuria, polydipsia and dehydration. Previous studies have demonstrated that the NDI is caused by the defects of vasopressin 2 receptor (V2R) in renal tubules. The V2R belongs to the family of G-protein coupled receptors that contain seven distinct transmembrane domains. The gene encoding V2R has been cloned and sequenced, which facili

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28

Simões, Andreia Inês Amado. "Abordagem clínica à Diabetes Insipidus em cães e gatos." Master's thesis, 2021. http://hdl.handle.net/10400.26/38133.

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A Diabetes Insipidus (DI) é uma doença metabólica, pouco frequente na clínica de animais de companhia, e resulta na alteração do balanço hídrico do organismo. A DI ocorre devido a uma alteração na síntese ou secreção da hormona antidiurética (ADH), neste caso designada de diabetes insipidus central, ou devido a uma insensibilidade renal à ação da mesma hormona, designada de diabetes insipidus nefrogénica. Estas alterações resultam na falha da reabsorção tubular de água e na produção de grandes volumes de urina diluída, ou poliúria. De modo a evitar a desidratação, o animal desenvolve polidipsi

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29

Francisco, Ângela Sofia Fernandes Alves. "Identification of genetic mutations in patients with familial central diabetes insipidus." Master's thesis, 2012. http://hdl.handle.net/10400.6/3266.

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Diabetes insipidus (DI) is associated with defects that involve the secretion and the action of hormone arginine vasopressin (AVP) resulting in the excretion of abnormally large volumes of diluted urine. The most common defect that results in disease development is the deficient secretion of the hormone AVP and the disease is referred to as central or neurohypophyseal DI. The AVP hormone is synthesized in magnocellular neurons, that originate in the supraoptic and paraventricular nuclei of the hypothalamus and are projected to neurohypophysis, and the destruction of these neurons leads to a de

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30

Yu, Shang-Shiuan, and 游上萱. "The KSP-Cre transgenic mice：A potential mouse model for nephrogenic diabetes insipidus." Thesis, 2005. http://ndltd.ncl.edu.tw/handle/44773213192223646716.

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碩士<br>國立陽明大學<br>生物化學研究所<br>93<br>To study kidney-specific gene targeting, it is necessary to generate a mouse strain that expresses Cre recombinase under the control of a tissue-specific gene promoter. To direct the expression of Cre, we used the promoter of the kidney-specific cadherin gene (Ksp-cadherin, cadherin 16). This gene is uniquely expressed in the basolateral membrane of tubular epithelial cells in the kidney. Transgenic mice carrying the Ksp promoter linked to the Cre recombinase gene were produced by pronuclear microinjection. RT-PCR and immunoblot analysis showed that Ksp-Cre mic

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31

Carvalho, João Gomes. "Diabetes insipidus no pós cirurgia de adenomas da hipófise: casuística dos CHUC." Master's thesis, 2016. http://hdl.handle.net/10316/36962.

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Trabalho final do 6º ano médico com vista à atribuição do grau de mestre (área científica de neurocirurgia) no âmbito do ciclo de estudos de Mestrado Integrado em Medicina .<br>A diabetes insipidus (DI) é uma das complicações mais frequentes após manipulação cirúrgica da sela turca, nomeadamente devido a adenomas da hipófise. Este estudo retrospetivo a 5 anos avaliou a incidência desta complicação após cirurgia de adenomas da hipófise, no Centro Hospitalar Universitário de Coimbra (CHUC), e procurou a sua associação com sexo, idade, tamanho do adenoma, recidiva, apresentação clínica e complica

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32

Möller, Andreas [Verfasser]. "Molekulargenetische Untersuchung von Kindern mit der Verdachtsdiagnose eines nephrogenen Diabetes insipidus / vorgelegt von Andreas Möller." 2009. http://d-nb.info/993325335/34.

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33

Leduc-Nadeau, Alexandre. "Analyse fonctionnelle de deux nouvelles mutations récessives de l’AQP2 impliquées dans le diabète insipide néphrogénique par expression dans les ovocytes de Xenopus laevis." Thèse, 2009. http://hdl.handle.net/1866/4379.

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Le diabète insipide néphrogénique (DIN) autosomal peut être causé par les mutations du gène codant pour le canal à eau aquaporine-2 (AQP2). Un modèle couramment utilisé pour l’étude des protéines membranaires telle l’AQP2 est l’expression hétérologue dans les ovocytes de Xenopus laevis. Malheureusement, les techniques déjà existantes de purification de membranes plasmiques sont soit trop longues, trop difficiles ou demandent trop de matériel, ne permettent pas l’analyse adéquate du ciblage des formes sauvage comme mutantes, un élément crucial de ce type d’étude. Nous avons donc dans un premier

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34

Matar, Jessica. "Caractérisation biochimique et fonctionnelle du mutant T179N de l’aquaporine-2 humaine." Thèse, 2014. http://hdl.handle.net/1866/11793.

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L’aquaporine-2 (AQP2) est le canal responsable de la réabsorption finale d’eau au niveau du tubule collecteur du rein. À la base, contenue dans des vésicules internes, l’AQP2 est acheminée à la membrane apicale des cellules principales du tubule collecteur suite à une stimulation par l’hormone antidiurétique (ADH). L’incapacité à accomplir cette fonction entraîne le diabète insipide néphrogénique (DIN), une maladie caractérisée par l’inhabileté du rein à concentrer l’urine, entraînant une production de volumes urinaires élevés. Alors que les mutations récessives génèrent des protéines mal stru

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35

Carpentier, Eric. "Conséquences fonctionnelles de mutations affectant le récepteur de la vasopressine de type 2 et implications thérapeutiques." Thèse, 2011. http://hdl.handle.net/1866/6268.

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Le récepteur de la vasopressine de type 2 (V2R) joue un rôle crucial dans l’homéostasie hydrique. Exprimé principalement au niveau du rein, son activation par l’hormone antidiurétique arginine-vasopressine (AVP) favorise la réabsorption d’eau, participant ainsi à diminuer la diurèse. Plus de 200 mutations dans le gène du V2R ont été associées au diabète néphrogénique insipide congénital (DINc), une maladie causée par une perte de fonction du récepteur. À l’opposé, trois mutations découvertes récemment induisent un gain de fonction du V2R, et sont la cause du syndrome néphrogénique de l’ant

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