Relevant bibliographies by topics / Fibrosi renale

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Academic literature on the topic 'Fibrosi renale'

Author: Grafiati
Published: 9 March 2023
Last updated: 10 March 2023

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Journal articles on the topic "Fibrosi renale"

1

Curci, C., and G. Castellano. "Fibrosi renale ed anemia: una storia tutta da scoprire." Giornale di Clinica Nefrologica e Dialisi 24, no. 1 (January 24, 2018): 27–28. http://dx.doi.org/10.33393/gcnd.2012.1111.

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Ad oggi l'origine dei fibroblasti, le principali cellule responsabili dello sviluppo della fibrosi renale, è ancora incerta. In un recente lavoro pubblicato da Asada e colleghi, gli Autori dimostrano che la maggior parte dei fibroblasti secernenti eritropoietina nel rene normale hanno un'origine extra renale e provengono da cellule della Cresta Neurale. Durante lo sviluppo della fibrosi renale, queste cellule trans-differenziano in miofibroblasti, perdendo la loro capacità intrinseca di produrre eritropoietina. Questi interessanti dati potrebbero rappresentare il punto di partenza per lo sviluppo di nuovi farmaci capaci da un lato di ridurre la fibrosi renale e dall'altro di preservare la produzione di eritropoietina.
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2

Lombardi, Duccio. "Rigenerazione e Proteinuria, Quando L'albumina Fa La Differenza." Giornale di Clinica Nefrologica e Dialisi 26, no. 1 (October 3, 2014): 65–68. http://dx.doi.org/10.33393/gcnd.2014.864.

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Nella malattia renale cronica, il rischio di fallimento d’organo dipende dal grado di severità della proteinuria, la quale è determinata dal numero di podociti persi e dalla conseguente fibrosi glomerulare. Esistono, tuttavia, numerose evidenze cliniche e sperimentali che suggeriscono la possibilità di remissione della malattia renale e, in alcuni casi, persino di regressione del danno, quando ancora l’istologia dell’organo non risulti totalmente compromessa. Tali risultati sono ottenuti in particolare mediante l’impiego di terapie con effetti anti-proteinurici. Nuove evidenze sperimentali suggeriscono perché il blocco della perdita di proteine urinarie permetta la remissione della malattia renale cronica. In un recente articolo di Peired et al., è, per la prima volta, dimostrato come l’albuminuria blocchi il processo rigenerativo a causa del sequestro attuato dall’albumina ai danni della vitamina A, noto agente differenziativo per popolazioni di progenitori staminali presenti in vari organi. La conseguente perdita della vitamina A, complessata all’albumina, con le urine, impedisce, quindi, l’attivazione dei progenitori renali residenti nella capsula di Bowman, bloccando sul nascere la risposta rigenerativa e permettendo la progressione della malattia renale cronica.
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3

Di Lullo, L., F. Floccari, R. Rivera, A. Bellasi, E. Ferramosca, A. De Pascalis, M. Timio, M. Malaguti, and A. Santoboni. "La patologia del pericardio e la malattia renale cronica." Giornale di Clinica Nefrologica e Dialisi 24, no. 2 (January 26, 2018): 62–70. http://dx.doi.org/10.33393/gcnd.2012.1141.

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I pazienti affetti da malattia renale cronica possono andare incontro a tutta una serie di patologie che colpiscono il pericardio ma, sicuramente, alcune entità nosologiche sono più frequenti di altre. Gli ultimi decenni hanno assistito, per fortuna nostra e dei nostri pazienti, a un netto miglioramento per quanto concerne i protocolli terapeutici per i pazienti nefropatici e le forme tipiche di pericardite uremica, così frequenti negli anni passati, sono ormai uno sbiadito ricordo. È tuttora frequente osservare pazienti con versamento pericardico (idiopatico, ovvero secondario a malattie sistemiche), soprattutto per quanto concerne i pazienti sottoposti a trattamenti depurativi extracorporei ed i pazienti che iniziano il trattamento dialitico in condizioni di emergenza/urgenza (ad esempio, pazienti affetti da scompenso cardiaco congestizio); il versamento pericardico viene schematicamente classificato in lieve, moderato e severo in base all'interessamento più o meno globale del pericardio. Meno frequenti sono gli episodi di pericardite acuta (anch'essa idiopatica o secondaria), spesso su base virale, neoplasticae/o immunologica (vedi pazienti trapiantati in terapia immunosoppressiva). Le forme di pericardite costrittiva sono più rare a documentarsi in corso di malattia renale cronica e, in genere, rappresentano lo stadio finale di diverse patologie sistemiche: l'esito finale è, in genere, la fibrosi pericardica. (Cardionephrology)
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4

Masola, V., S. Granata, M. Proglio, G. Gambaro, A. Lupo, and G. Zaza. "Eparanasi: un nuovo biomarker di fibrosi e un potenziale target farmacologico per ridurre la progressione del danno renale cronico." Giornale di Clinica Nefrologica e Dialisi 24, no. 2 (January 26, 2018): 10–15. http://dx.doi.org/10.33393/gcnd.2012.1131.

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Il trattamento poli-farmacologico ha determinato, nel corso degli anni, un significativo rallentamento della progressione della malattia renale cronica verso lo stadio di uremia terminale, ma siamo ancora distanti dallo sviluppo di interventi terapeutici in grado di bloccare questo inesorabile e irreversibile processo. Studi clinico-patologici hanno chiaramente dimostrato che il principale elemento coinvolto nel danno renale è la fibrosi tubulo-interstiziale e che il meccanismo patogenetico alla base di questa condizione ha inizio in larga parte nel compartimento tubulare. In particolare, il processo di transizione epitelio-mesenchimale gioca un ruolo importante nella genesi del danno cronico. Durante questo processo, le cellule epiteliali tubulari subiscono un incremento significativo di markers di superficie di natura mesenchimale e, grazie al rimodellamento del citoscheletro e alla degradazione della membrana basale, sono in grado di migrare nell'interstizio dove svolgono un ruolo chiave nel processo patogenetico. In questo contesto, sembra avere un ruolo chiave l'enzima eparanasi, una endo-β-D-glucuronidasi che taglia le catene dell'eparan-solfato a livello di siti specifici intracatena, e partecipa attivamente alla degradazione e al rimodellamento della matrice extracellulare. La degradazione dei vari costituenti dell'ECM, inclusi i proteoglicani eparan-solfato fa-vorisce il rilascio di fattori trofici quali il FGF-2 che induce l'espressione dei marcatori mesenchimali alfa-SMA, VIM e FN, porta alla degradazione della membrana basale mediante la secrezione di metalloproteinasi della matrice ed aumenta la motilità cellulare. L'epressione dell'eparanasi è regolata da fattori di trascrizione, dalla metilazione del DNA e da varie molecole endogene. L'importanza di questo enzima è stata confermata clinicamente dal riscontro di una sua iperespressione in preparati istologici di biopsie effettuate in soggetti affetti da nefropatie croniche (per esempio, nefropatia diabetica). Pertanto visto l'importante ruolo dell'eparanasi sono in fase di standardizzazione numerose strategie per inibire la sua espressione genica e/o la sua attività enzimatica. Infine, è stato proposto il suo possibile utilizzo come biomarker di progressione del danno tubulo-interstiziale da utilizzare routinariamente in ambito nefrologico.
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Galiza, Aline Xavier Fialho, Luísa Mariano Cerqueira da Silva, Luísa Grecco Correa, Eduardo Gonçalves, Aline do Amaral, Pâmela Caye, Júlia Vargas Miranda, et al. "Perfil epidemiológico e alterações anatomopatológicas de biópsias de rins esquerdos de sete cães acometidos por Dioctophyme renale em rim direito." Research, Society and Development 10, no. 6 (June 8, 2021): e50310615703. http://dx.doi.org/10.33448/rsd-v10i6.15703.

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A dioctofimatose é uma doença causada pelo nematódeo Dioctophyme renale, que acomete principalmente rins direitos de cães e ao penetrar na cápsula renal causa destruição e atrofia do parênquima, podendo restar apenas uma cápsula fibrosa do rim afetado. Dessa forma, buscando estabelecer as condições histológicas do rim contralateral (RCL) dos animais acometidos pela parasitose, o objetivo desse estudo foi descrever o perfil epidemiológico e alterações anatomopatológicas encontradas em biópsias de rins esquerdos de sete cães submetidos a nefrectomia em decorrência de parasitismo por Dioctophyme renale em rim direito. Informações referentes à raça, sexo, faixa etária, histórico clínico, e alterações histológicas, foram tabulados e avaliados. Para as biópsias foi utilizado o método incisional. Microscopicamente em três amostras (3/7) havia glomerulonefrite membranosa, em quatro (4/7) observou-se infiltrado inflamatório de células mononucleadas e fibrose focal em duas amostras analisadas (2/7). Em uma amostra havia glomeruloesclerose segmentar focal e em outra não havia alteração histológica. Foram contabilizadas mais de uma alteração em uma única amostra. As alterações encontradas nas biópsias indicam algum comprometimento do rim remanescente e sugerindo que possa haver ação sistêmica, ou pelo menos inter-renais das enzimas esofágicas produzidas pelo parasito Este estudo espera contribuir para o estadiamento das funções renais do rim remanescente e auxiliar no estabelecimento do tratamento em cada caso.
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Wolf, G., and G. Lehmann. "Knochenhistologie bei renaler Osteodystrophie." Osteologie 17, no. 03 (2008): 107–11. http://dx.doi.org/10.1055/s-0037-1619855.

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ZusammenfassungChronische Nierenfunktionseinschränkungen führen am Knochen zu Stoffwechsel- und Strukturschäden, deren differenzierte Beurteilung vor allem durch die histologische Aufarbeitung von Knochenbioptaten möglich ist. Die internationale Klassifikation unterscheidet vier Formen der renalen Osteodystrophie (ROD). Dabei wird zwischen renalem Hyperparathyreoidismus (Osteitis fibrosa), Osteomalazie, gemischter urämischer Osteodystrophie und adynamer renaler Knochenerkrankung unterschieden. In der Arbeit werden die Methoden der Knochenentnahme und -bearbeitung, typische histologische Befunde sowie die Indikationen zur osteologischen Beckenkammbiopsie dargestellt.
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7

Solomon, Garron J., Elizabeth Wu, and Paul Peter Rosen. "Nephrogenic Systemic Fibrosis Mimicking Inflammatory Breast Carcinoma." Archives of Pathology & Laboratory Medicine 131, no. 1 (January 1, 2007): 145–48. http://dx.doi.org/10.5858/2007-131-145-nsfmib.

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Abstract Nephrogenic systemic fibrosis, previously known as nephrogenic fibrosing dermopathy, is a newly recognized systemic fibrosing disorder primarily affecting patients with chronic renal failure. Patients with skin involvement often develop papules and plaques with peau d'orange surface changes. The lower extremities and trunk are most commonly affected. The most important histologic differential diagnosis is with scleromyxedema. To our knowledge, we report the first case of nephrogenic systemic fibrosis involving the breasts of a 61-year-old woman with end-stage renal disease, clinically mimicking inflammatory breast carcinoma. We propose that nephrogenic systemic fibrosis be considered in the differential diagnosis as a rare possibility when cutaneous changes in the breast suggest inflammatory breast carcinoma in a patient with renal failure.
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Gibson, Sarah E., Carol F. Farver, and Richard A. Prayson. "Multiorgan Involvement in Nephrogenic Fibrosing Dermopathy: An Autopsy Case and Review of the Literature." Archives of Pathology & Laboratory Medicine 130, no. 2 (February 1, 2006): 209–12. http://dx.doi.org/10.5858/2006-130-209-miinfd.

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Abstract Nephrogenic fibrosing dermopathy is a recently recognized, scleromyxedema-like fibrosing skin condition that occurs in individuals with acute or chronic renal failure. Although the early descriptions of this disorder describe a purely cutaneous disease process, 2 recent autopsy reports have identified apparent multiorgan fibrosis with involvement of skeletal muscle, myocardium, lungs, kidneys, and testes. We describe a 23-year-old man with nephrogenic fibrosing dermopathy and significant fibrosis of the atrial myocardium and dura mater, which was identified at autopsy. Dural fibrosis is a previously undescribed systemic manifestation of nephrogenic fibrosing dermopathy. The literature is reviewed.
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9

D'Attoma, N., E. Residori, R. Mariotto, R. Cerini, M. Gregianin, and A. Lotto. "L'imaging della fibrosi retroperitoneale primitiva: Primitive retroperitoneal fibrosis imaging." Urologia Journal 65, no. 2 (April 1998): 276–86. http://dx.doi.org/10.1177/039156039806500216.

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Idiopathic retroperitoneal fibrosis (RPF) is characterised by the development of a fibrotic mass in the prelumbar or presacral area which becomes clinically significant when it causes ureteral obstruction. New imaging techniques have improved accuracy of the morphological approach to the disease, but urography and sequential renal scintigraphy are still important for assessing ureteral involvement. The role of imaging techniques is discussed and current diagnostic and therapeutic tools are evaluated.
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10

Valle, Bruna dos Santos, Pamela Caye, Carolina da Fonseca Sapin, Luisa Mariano Cerqueira da Silva, Júlia Vargas Miranda, Gustavo Antonio Boff, Luísa Grecco Corrêa, Josaine Cristina da Silva Rappeti, Cristina Geverh Fernandes, and Fabiane Borelli Grecco. "Alterações anatomopatológicas e parâmetros bioquímicos séricos e urinários em cães com diagnóstico de Dioctophyme renale." Research, Society and Development 11, no. 12 (September 22, 2022): e515111234874. http://dx.doi.org/10.33448/rsd-v11i12.34874.

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Animais acometidos por Dioctophyme renale geralmente são assintomáticos e o diagnóstico definitivo é o exame de imagem e o anatomopatológico. Desta forma, este estudo tem como objetivo descrever os parâmetros bioquímicos de sangue e urina e exames anatomopatológicos de 15 cães diagnosticados com D. renale na região de Pelotas-Rio Grande do Sul-RS. Foram obtidos dados de anamnese e exames laboratoriais sorológicos e urinários de protocolos de atendimento de animais no Hospital de Clínicas Veterinárias da Universidade Federal de Pelotas-UFPel, e análises anatomopatológicas pelo Serviço de oncologia SOVET/UFPEL. Foram observadas alterações macroscópicas em todas as amostras, sendo a atrofia do parênquima renal e espessamento da cápsula as mais frequentes. O exame histopatológico revelou substituição do tecido renal por fibrose, glomeruloesclerose e eventualmente presença de ovos do parasito. Em relação aos parâmetros sanguíneos e urinários, apenas um dos animais apresentou alteração nos valores de referência de ureia sérica e todos apresentaram creatinina dentro dos parâmetros considerados normais. Na urinálise havia presença de proteínas, sangue oculto, cilindros granulares, cristais e ovos do parasito. Os testes estatísticos mostraram correlação entre a evolução e grau das lesões renais com parâmetros alterados, porém mesmo em cães que apresentavam lesões de insuficiência renal aguda (IRA), haviam lesões concomitantes de insuficiência renal crônica (IRC). Como conclusão dos dados obtidos, parâmetros séricos e urinários isoladamente não refletem o real comprometimento do rim afetado, mas associados ao grau de lesão renal são aliados para um melhor estadiamento dos animais acometidos.
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Dissertations / Theses on the topic "Fibrosi renale"

1

Bedino, Giulia <1980&gt. "La terapia combinata di cellule mesenchimali stromali e aceinibitori riduce la fibrosi renale in un modello animale di ostruzione ureterale unilaterale." Doctoral thesis, Alma Mater Studiorum - Università di Bologna, 2014. http://amsdottorato.unibo.it/6297/1/bedino_giulia_tesi.pdf.

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Le cellule mesenchimali stromali (MSC) sono cellule multipotenti e numerosi studi hanno mostrato i loro effetti benefici nel danno renale acuto ma non sono ancora stati dimostrati potenziali effetti nella malattia renale cronica. L'ostruzione ureterale unilaterale (UUO) è un modello di fibrosi interstiziale nel quale l'attivazione di molecole vasoattive, citochine profibrotiche e infiammatorie gioca un ruolo patogenetico nello sviluppo dell'apoptosi e atrofia tubulare. Il sistema renina-angiotensina (RAS) gioca un ruolo chiave nello sviluppo della fibrosi renale e i farmaci che hanno come target l'angiotensina II, principale mediatore del RAS, sono attualmente la terapia più efficace nel ridurre la progressione della malattia renale cronica. E' noto che gli ACE-inibitori (ACEi) inducono un aumento compensatorio della renina plasmatica per la mancaza del feedback negativo sulla sua produzione. Tuttavia, la renina (R) promuove il danno renale non solo stimolando la produzione di ANGII, ma anche up-regolando geni profibrotici attraverso l'attivazione del recettore renina/prorenina. Lo scopo dello studio è stato indagare se l'infusione di MSC riduceva il danno renalein un modello animale di UUO e comparare gli eventuali effetti protettivi di ACEi e MSC in UUO. Abbiamo studiato 5 gruppi di ratti. A: sham operati. B: ratti sottoposti a UUO che ricevevano soluzione salina. C: ratti sottoposti a UUO che ricevavano MSC 3X106 nella vena della coda al giorno 0. D:ratti sottoposti a UUO che ricevevano lisinopril dal g 1 al g 21. E: ratti sottoposti a UUO che ricevevano MSC 3X106 nella vena della coda al giorno 0 e lisinopril dal g 1 al g 21. I ratti sono stati sacrificati al giorno 7 e 21. I risultati dello studio mostrano che MSC in UUO prevengono l'aumento della renina, riducono la generazione di ANGII e che in terapia combinata con ACEi riducono ulteriormente l'ANGII, determinando una sinergia nel miglioramento della fibrosi renale.
Mesenchymal stromal cells (MSC) are multipotent cells with immunomodulant and anti-inflammatory effect. Several studies have shown MSC beneficial effect in acute kidney injury but are not yet known MSC effects in chronic kidney disease. Unilateral ureteral obstruction (UUO) is a model of renal interstitial fibrosis, the final common pathway for progressive renal diseases where the activation of vasoactive molecules, inflammatory and profibrotic cytokines plays a pathogenetic role in the development of cell apoptosis and tubular atrophy. Renin-angiotensin system (RAS) plays a pivotal role in renal fibrosis and agents that target angiotensin II, principal mediator of RAS, are the most effective therapy to reduce progression of chronic kidney disease. Its known that angiotensin-converting enzyme inhibitors (ACEi) induce a compensatory increase in plasma renin levels because of the disruption of the negative feedback of its production. However renin (R) promotes renal injury not only by stimulating angiotensin II (ANG II) generation, but also up-regulating pro-fibrotic genes through renin/prorenin receptor activation. The aim of the study was to investigate whether MSC infusion attenuate renal injury in a rat model of UUO and to compare the protective effects of ACEi and MSC in UUO. We studied 5 groups of rats. A: rats sham operated. B: rats UUO received saline solution on day 0 (vehicle control). C: rats UUO received MSC 3X106 on day 0 via tail vein. D: rats UUO received lisinopril from d 1 to 21. E: rats UUO received MSC on d 0, and lisinopril from d 1 to 21. Rats were sacrified on d 7 and 21. Our results show that MSC in UUO rat model prevent renin increase, reduce angiotensin II generation and in combination therapy with ACEi suppress further angiotensin II block, thereby lead to a synergy in ameliorating renal fibrosis.
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2

Bedino, Giulia <1980&gt. "La terapia combinata di cellule mesenchimali stromali e aceinibitori riduce la fibrosi renale in un modello animale di ostruzione ureterale unilaterale." Doctoral thesis, Alma Mater Studiorum - Università di Bologna, 2014. http://amsdottorato.unibo.it/6297/.

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Le cellule mesenchimali stromali (MSC) sono cellule multipotenti e numerosi studi hanno mostrato i loro effetti benefici nel danno renale acuto ma non sono ancora stati dimostrati potenziali effetti nella malattia renale cronica. L'ostruzione ureterale unilaterale (UUO) è un modello di fibrosi interstiziale nel quale l'attivazione di molecole vasoattive, citochine profibrotiche e infiammatorie gioca un ruolo patogenetico nello sviluppo dell'apoptosi e atrofia tubulare. Il sistema renina-angiotensina (RAS) gioca un ruolo chiave nello sviluppo della fibrosi renale e i farmaci che hanno come target l'angiotensina II, principale mediatore del RAS, sono attualmente la terapia più efficace nel ridurre la progressione della malattia renale cronica. E' noto che gli ACE-inibitori (ACEi) inducono un aumento compensatorio della renina plasmatica per la mancaza del feedback negativo sulla sua produzione. Tuttavia, la renina (R) promuove il danno renale non solo stimolando la produzione di ANGII, ma anche up-regolando geni profibrotici attraverso l'attivazione del recettore renina/prorenina. Lo scopo dello studio è stato indagare se l'infusione di MSC riduceva il danno renalein un modello animale di UUO e comparare gli eventuali effetti protettivi di ACEi e MSC in UUO. Abbiamo studiato 5 gruppi di ratti. A: sham operati. B: ratti sottoposti a UUO che ricevevano soluzione salina. C: ratti sottoposti a UUO che ricevavano MSC 3X106 nella vena della coda al giorno 0. D:ratti sottoposti a UUO che ricevevano lisinopril dal g 1 al g 21. E: ratti sottoposti a UUO che ricevevano MSC 3X106 nella vena della coda al giorno 0 e lisinopril dal g 1 al g 21. I ratti sono stati sacrificati al giorno 7 e 21. I risultati dello studio mostrano che MSC in UUO prevengono l'aumento della renina, riducono la generazione di ANGII e che in terapia combinata con ACEi riducono ulteriormente l'ANGII, determinando una sinergia nel miglioramento della fibrosi renale.
Mesenchymal stromal cells (MSC) are multipotent cells with immunomodulant and anti-inflammatory effect. Several studies have shown MSC beneficial effect in acute kidney injury but are not yet known MSC effects in chronic kidney disease. Unilateral ureteral obstruction (UUO) is a model of renal interstitial fibrosis, the final common pathway for progressive renal diseases where the activation of vasoactive molecules, inflammatory and profibrotic cytokines plays a pathogenetic role in the development of cell apoptosis and tubular atrophy. Renin-angiotensin system (RAS) plays a pivotal role in renal fibrosis and agents that target angiotensin II, principal mediator of RAS, are the most effective therapy to reduce progression of chronic kidney disease. Its known that angiotensin-converting enzyme inhibitors (ACEi) induce a compensatory increase in plasma renin levels because of the disruption of the negative feedback of its production. However renin (R) promotes renal injury not only by stimulating angiotensin II (ANG II) generation, but also up-regulating pro-fibrotic genes through renin/prorenin receptor activation. The aim of the study was to investigate whether MSC infusion attenuate renal injury in a rat model of UUO and to compare the protective effects of ACEi and MSC in UUO. We studied 5 groups of rats. A: rats sham operated. B: rats UUO received saline solution on day 0 (vehicle control). C: rats UUO received MSC 3X106 on day 0 via tail vein. D: rats UUO received lisinopril from d 1 to 21. E: rats UUO received MSC on d 0, and lisinopril from d 1 to 21. Rats were sacrified on d 7 and 21. Our results show that MSC in UUO rat model prevent renin increase, reduce angiotensin II generation and in combination therapy with ACEi suppress further angiotensin II block, thereby lead to a synergy in ameliorating renal fibrosis.
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3

Mezzalira, Giorgia. "Studio delle patologie renali del cane." Doctoral thesis, Università degli studi di Padova, 2009. http://hdl.handle.net/11577/3425666.

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This study selected 40 canine patients with signalement, anamnesis, lab exams and renal biopsy or renal sample taken during necropsy. Renal sections stained with H&E, PAS, PASM, Masson's Thrichrome and AFOG was evaluated by three independent pathologists. Later, morphological diagnoses were correlated with lab exams.
Questo studio ha selezionato 40 cani completi di segnalamento, anamnesi, esami di laboratorio e campione bioptico renale prelevato tramite biopsia o post mortem, in sede necroscopica. Le sezioni istologiche ottenute e colorate con ematossilina ed eosina, PAS, PASM, Tricromica di Masson ed AFOG sono state valutate da tre patologi in sede separata. Le diagnosi morfologiche sono state poste poi in relazione con i dati laboratoristici in possesso.
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4

CORRADI, BARBARA. "Ruolo di N-Acetyl-Seryl-Aspartyl-Lysyl-Proline (Ac-SDKP) nella progressione della Nefropatia Diabetica." Doctoral thesis, Università degli Studi di Milano-Bicocca, 2013. http://hdl.handle.net/10281/43715.

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La nefropatia diabetica è la principale causa di insufficienza renale terminale. N-Acetyl-Seryl-Aspartyl-Lysyl-Proline (Ac-SDKP), tetrapeptide fisiologicamente presente nel plasma e nei tessuti, viene idrolizzato dall’ enzima di conversione dell’angiotensina. Il tetrapeptide ha un effetto antifibrotico sul sistema cardiovascolare e nel rene in modelli sperimentali di ipertensione, infarto del miocardio e nefropatie. Lo scopo del nostro lavoro è stato studiare gli effetti antifibrotici di Ac-SDKP in un modello sperimentale di nefropatia diabetica, e il potenziale effetto additivo del tetrapeptide, in aggiunta al singolo trattamento con ACE-inibitore, sulla progressione della fibrosi renale. A 28 ratti Sprague Dawley e’ stato indotto diabete con un’iniezione di streptozotocina, mentre a 10 ratti controllo e’ stata somministrata solo soluzione tampone. Dopo l’ insorgenza di diabete a 11 ratti è stato somministrato un inibitore dell’enzima di conversione dell’angiotensina (ACE-inibitore, ramipril 3 mg/Kg/die). Dopo 2 mesi di trattamento con ACE-inibitore a 7 ratti diabetici e a 6 ratti diabetici trattati con ramipril è stato somministrato per 8 settimane Ac-SDKP, alla dose di 1 mg/Kg/die, attraverso minipompe osmotiche impiantate nella regione infrascapolare. A 10 ratti controllo, a 10 ratti diabetici e a 5 ratti diabetici trattati con ramipril la minipompa osmotica rilasciava, per lo stesso periodo, solo soluzione fisiologica. Al termine del trattamento i ratti diabetici rispetto ai ratti del gruppo di controllo mostravano un significativo aumento del livello di glucosio, dell’ escrezione urinaria di albumina, della fibrosi renale e una significativa riduzione dell’espressione di nefrina a livello dei glomeruli. La somministrazione di Ac-SDKP riduceva significativamente la fibrosi renale nei ratti diabetici, ma non modificava significativamente l’escrezione urinaria di albumina. Il trattamento farmacologico con ACE-inibitore causava una significativa diminuzione dell’albuminuria e della fibrosi renale, ripristinando l’espressione della nefrina glomerulare. La somministrazione di Ac-SDKP, in aggiunta al trattamento con ACE-inibitore, riduceva ulteriormente la fibrosi renale rispetto al solo trattamento con ramipril, mentre non incrementava l’effetto antiproteinurico dell’ACE-inibitore. In conclusione questo studio ha dimostrato che la somministrazione di Ac-SDKP in un modello di nefropatia diabetica riduce la fibrosi renale. Il trattamento combinato (Ac-SDKP + ACE-inibitore) aumenta l’effetto antifibrotico dell’ACE-inibitore nel tessuto renale, suggerendo il benefico effetto di questa associazione farmacologica nel trattamento della nefropatia diabetica.
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Yi, Hao. "The Effect of Metformin on Inflammatory and Fibrotic Responses in Renal Fibrosis." Thesis, The University of Sydney, 2019. https://hdl.handle.net/2123/21855.

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Chronic kidney disease (CKD) is a worldwide public health problem, with adverse outcomes of kidney failure, cardiovascular disease, and premature death. It is well recognised that renal fibrosis is the unifying pathology in almost all forms of progressive CKD. To date, kidney transplantation and dialysis are the only options for the management of end-stage kidney disease, which results in a significant burden on the health system. Hence innovative strategies are needed to both prevent and treat CKD. It is well recognised that inflammatory pathways play a central role in the progression of CKD and TGFβ-1 is a profibrotic cytokine found in CKD regardless of aetiology, which initiates and modulates a variety of pathophysiological processes. In renal disease, TGFβ-1 is upregulated and induces renal cells to produce extracellular matrix proteins leading to glomerulosclerosis as well as tubulointerstitial fibrosis. Different types of renal cells undergo different pathophysiological changes induced by TGF-β1, leading to apoptosis, hypertrophy and abnormalities of podocyte foot processes, which ultimately result in renal dysfunction. Regardless of the cause of CKD, multiple cytokines, growth factors, pro-inflammatory and fibrotic signalling pathways participate in the development of the pathological process in the kidney. Excessive deposition of extracellular matrix (ECM) is the most striking and common feature of renal fibrosis. Hence, targeting inflammatory and fibrotic responses, and ECM deposition, holds promise to limit fibrosis. Metformin, a biguanide, is a widely used drug in the treatment of type 2 diabetes mellitus (T2DM). It has been well-reviewed that metformin plays an important role in limiting cardiac and vascular fibrosis. Increasing evidence studies indicates metformin may be protective in renal fibrosis. However, the exact mechanisms of protection in renal injury are not fully understood or experimentally investigated. Thus, I initially examined the effect of metformin in TGFβ-1 induced fibrosis in human proximal tubular cells line (HK2 cells). Therefore, I further examined the effect of metformin on renal fibrosis in two mouse models of acute kidney injury (AKI; Folic Acid model (FA)) and chronic kidney injury (CKI, Adenine model). The studies have shown that metformin inhibited monocyte chemoattractant protein-1 (MCP-1) expression and TGFβ-1 signalling pathways in kidney proximal tubular cells exposed to TGFβ-1 by reducing mRNA, protein levels or phosphorylation of signalling molecules of non-Smad and Smad signalling pathways. Metformin also inhibited TGFβ-1 induced extracellular matrix deposition by reducing the expression of fibronectin and collagen IV in kidney proximal tubular cells exposed to TGF-β1. In animal studies, the acute phase of renal fibrosis was successfully established by giving folic acid via intraperitoneal injection, and then the antifibrotic effect of metformin was assessed by administering animals metformin or control for 14 days. The acute renal fibrosis mice model was successfully established by given adenine via gavage, and then treated with or without metformin for 14 days. The in vivo data has shown that folic acid induced impairment of renal function and the overexpression of fibronectin and collagen IV and inflammatory molecular MCP-1, F4/80 and intercellular adhesion molecule-1 (ICAM1) in kidneys compared to control groups; and the impaired renal function and inflammatory and fibrotic response were at least partially attenuated by metformin treatment. The chronic renal fibrosis mice model was successfully established by giving adenine through gavage daily and treatment with or without metformin for 21 days. The data showed that adenine induced renal dysfunction and the overexpression of fibronectin and collagen IV and inflammatory molecular MCP-1, F4/80 and ICAM in kidneys compared to control groups. Renal dysfunction and the inflammatory and fibrotic responses were reversed by metformin treatment. Collectively, these results suggest that metformin may have potential therapeutic value for the treatment of renal fibrosis independent of the cause of CKD.
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DaSilva, Santos Iara Karlla. "Impacto de la inflamación y fibrosis en la función del injerto renal." Doctoral thesis, Universitat Autònoma de Barcelona, 2018. http://hdl.handle.net/10803/666855.

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A pesar de los grandes avances en el campo del trasplante renal (TR), los resultados a largo plazo aún no son óptimos. Varios estudios han demostrado que diversos factores como la inflamación precoz y/o la presencia de fibrosis intersticial (FI) están asociados a un peor pronóstico del injerto, pero todavía se trata de un tema controvertido. En este estudio analizamos el estado inflamatorio (Banff, macrófagos CD68+, fenotipos de macrófagos M1-M2) y la expresión génica de múltiples factores relacionados con la inflamación y FI (TGF-β1, metaloproteinasas, proteínas de matriz extracelular, entre otros) en injertos procedentes de donantes cadáver (DC) y los comparamos con un grupo control de donantes vivos (DV). Así mismo analizamos la potencial asociación de estos factores, ya desde antes de la implantación, con diversas variables clínicas y con la función renal a medio-largo plazo. Entre otros hallazgos, confirmamos que los órganos procedentes de DC presentan un mayor infiltrado intersticial de macrófagos CD68+ y describimos que tanto la expresión génica de varias proteínas pro-inflamatorias como pro-fibróticas se encuentran significativamente incrementadas en los DC incluso antes de la implantación. También observamos un aumento en la expresión génica de proteínas que promueven la infiltración leucocitaria, especialmente macrófagos, en el tejido (MCP-1, ICAM-1), así como de mediadores de inflamación como TNFα, IL1β. También se observó un aumento en la expresión génica de receptores de membrana de los macrófagos que les confiere el fenotipo inflamatorio (M1) así como el antinflamatorio (M2). En los DC también se observó un aumento significativo de los precursores y mediadores de FI. Es de destacar que muchos de estos parámetros (inflamatorios y pro-fibróticos) se asociaron a la función renal estimada (MDRD) en distintos tiempos de seguimiento. El análisis multivariante (regresión lineal múltiple) mostró que tanto la función retrasada del injerto como la expresión génica de TGF-β1 a los cuatro meses fueron predictores independientes de la función del injerto del último control (media 5.8 1.0 años). En conclusión, confirmamos la estrecha interconexión entre inflamación y fibrosis especialmente en el TR de DC, que ésta se inicia ya antes de la implantación y persiste post-TR y que estos factores muy precoces (potencialmente tratables) pueden determinar el pronóstico del injerto a largo plazo.
Despite great achievements in the field of renal transplantation (RT), long-term results are still not optimal. Several studies have shown that various factors such as early inflammation and/or the presence of interstitial fibrosis (IF) are associated with a worse graft prognosis, but this issue is still controversial and far from being resolved. In this study, we analyzed the inflammatory state (Banff, CD68 + macrophages, M1-M2 phenotypes, among others) and the gene expression of multiple factors related to both inflammation and IF (TGF-β1, metalloproteinases, extracellular matrix proteins, among others) in grafts from cadaveric donors (CD) and they were compared with a control group from living donors (LD). We also analyzed the potential association of all these factors with several clinical variables with medium and/or long-term renal function. Among other findings, we confirm that organs from CD have a greater CD68+ macrophage infiltration and we describe that the expression of several proinflammatory and and profibrotic molecules is significantly increased in CD even before grafting. We also observed an increased gene expression of proteins related to graft leukocyte infiltration, mainly macrophages, such as MCP-1 or ICAM-1, as well as of inflammatory mediators such as TNFα or IL1β. We also observed an increased gene expression of macrophage membrane cell receptors related to their inflammatory (M1) or anti-inflammatory (M2) phenotype. Finally, we described a significant increase of IF precursors and mediators in CD. It is noteworthy that multiple parameters (both inflammatory and profibrotic) were associated with the estimated glomerular filtration rate (MDRD) at different times. Multiple regression analysis revealed that delayed renal function as well as graft TGF-β1 gene expression four months after RT were independent predictors of the last renal function control during follow-up (5.8 1.0 years). In conclusion, we confirm the existence of an especially close interconnection between inflammation and fibrosis, especially in the CD RT setting, starting before engraftment and progressing after RT, and that these very early (potentially treatable) factors may already devise its long-term graft prognosis.
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Bigé, Naïke. "Rôle de la Thrombospondine-1 et du récepteur CD47 dans le développement de la fibrose rénale." Thesis, Paris 6, 2014. http://www.theses.fr/2014PA066705/document.

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La Thrombospondine-1 (TSP-1) représente l'un des principaux activateurs endogènes du TGF-?1 et possède des propriétés anti-angiogéniques et immunomodulatrices. L'un de ses récepteurs, le CD47, joue un rôle critique dans son effet anti-angiogénique et module l'inflammation. Après obstruction urétérale unilatérale (UUO), l'expression de la TSP-1 augmente, est corrélée à celle du TGF-?1 et du collagène III et décroît avec la réparation tissulaire qui accompagne la désobstruction urétérale. L'utilisation de souris knock-out pour la TSP-1 a permis de montrer qu'elle participe au développement des lésions tubulaires rénales en favorisant les altérations vasculaires et le recrutement des cellules inflammatoires. Cet effet pro-inflammatoire dépend, au moins en partie, du facteur chimiotactique MCP-1, de l'augmentation du rolling leucocytaire et de l'activation de la voie Th17. Les souris knock-out pour CD47 bénéficient également d'une protection tubulaire et vasculaire. Cependant, elles présentent une fibrose interstitielle accrue associée à une augmentation de l'expression de la TSP-1 et du TGF-?1 qui pourrait compromettre une éventuelle récupération rénale. L'étude préliminaire de modèles de néphroangiosclérose chez le rat et la souris révèle que la TSP-1 est surexprimée dans le parenchyme rénal au cours de l'hypertension artérielle. L'intensité de son expression est corrélée à la sévérité des lésions histologiques, suggérant son rôle physiopathologique. Ces résultats montrent que la TSP-1 et le récepteur CD47 participent au développement de la fibrose rénale et représentent donc des cibles thérapeutiques potentielles au cours des maladies rénales chroniques
Thrombospondin-1 (TSP-1) is a major endogenous activator of TGF-β1 and has anti-angiogenic and immunomodulatory properties. One of its partners, receptor CD47, plays a critical role in its anti-angiogenic activity and also regulates inflammation. After unilateral ureteral obstruction (UUO), TSP-1 expression increases, correlates to TGF-β1 and collagen III expression and decreases with renal repair after desobstruction. Use of TSP-1 knock-out mice allowed us to demonstrate that TSP-1 favours renal injury by increasing vascular lesions and inflammatory cells recruitment. This pro-inflammatory effect depends, at least in part, on chemotactic factor MCP-1, increasing in leukocyte rolling and engagement of T cells in Th17 pathway. CD47 knock-out mice also benefit from tubular and vascular protection after UUO. However, they exhibit increased interstitial fibrosis associated with higher expression of TSP-1 and TGF-β1, which could compromise renal repair. Preliminary study of nephroangiosclerosis models in rats and mice revealed that TSP-1 expression is induced in renal tissue by arterial hypertension and is correlated to the severity of histological lesions, suggesting its physiopathological role. These results show that TSP-1 and CD47 are involved in renal fibrosis and that they represent potential therapeutic target in the management of chronic kidney disease
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8

Pat, Betty Kila. "Signal transduction pathways in renal fibrosis /." St. Lucia, Qld, 2003. http://www.library.uq.edu.au/pdfserve.php?image=thesisabs/absthe17739.pdf.

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9

Winbanks, Catherine, and winbanks@unimelb edu au. "Novel Aspects of Renal Tubulointerstitial Fibrosis." RMIT University. Medical Sciences, 2007. http://adt.lib.rmit.edu.au/adt/public/adt-VIT20080617.143850.

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Tubulointerstitial fibrosis is the key histological predictor of the progression of declining renal function and the final common pathway of progressive kidney disease, regardless of aetiology. Despite its significance, there are currently no treatments available to abrogate this process and those that suffer with this burden eventually succumb to renal failure. Tubulointerstitial fibrosis is largely mediated by fibroblasts and myofibroblasts present in the interstitium. In response to injury, activated fibroblasts differentiate into myofibroblasts which serves as a histological hallmark of fibrosis. Myofibroblasts are characterised as the key contributors to interstitial volume and their presence ultimately leads to loss of renal function. The pathological entities leading to fibrosis inextricably depend on complex signalling pathways. Whilst many of the well-known growth factors that exert effects on renal fibroblasts (such as FGF, EGF and PDGF) involve the activation of receptor tyrosine kinases, the intracellular signalling events dictating the response of fibroblasts remain undefined. The kinase mTOR, responsible for integrating stress and amino acids and controlling cell growth, is increasingly recognised for its ability to integrate growth factor signals mediated through the upstream serine/threonine kinase PI3K. A number of recent studies have highlighted the role of PI3K and mTOR in the regulation of key events relevant to fibrosis, serving as a basis for Chapter 3: The role of PI3K and mTOR in the regulation of fibroblast proliferation and collagen synthesis, and the first part of Chapter 5: The role of PI3K and mTOR in the regulation of myofibroblast differentiation. These studies have identified a key role for PI3K and mTOR in the regulation of fibroblast proliferation, differentiation and collagen synthesis. The work described within has also attempted to examine the derivation of myofibroblasts via EMT. EMT is a process that is integral to embryogenesis and may act as an important source of myofibroblasts during fibrosis. This process is examined in Chapter 4: Development and validation of an ex vivo model of EMT. This model aims to better represent the in vivo environment and has also been used to identify novel regulators involved in EMT being utilised in the second part of Chapter 5: The role of PI3K and mTOR in EMT. Although cytokines and growth factors are thought to be chiefly responsible for tubulointerstitial fibrosis, we now know that serine proteases of the coagulation cascade may also play roles in renal disease. However, unlike their role in glomerular diseases, the role of coagulation in tubulointerstitial fibrosis is less well-known. The work described in Chapter 6: Constituents of the coagulation cascade are spatially and functionally related to experimental tubulointerstitial fibrosis has examined temporal and spatial in vivo relationships of coagulation factors and markers of fibrosis that aid our understanding of mechanisms of fibrosis. The aim of this thesis was to examine those facets of renal fibroblast function that are most devastating to renal function and culminate in an expansion of the renal interstitium during fibrosis. This work hopes to provide useful information to aid the understanding of the multifaceted mechanisms involved in renal tubulointerstitial fibrosis.
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10

Krupa, Aleksandra. "Role of microRNAs in renal fibrosis." Thesis, Cardiff University, 2010. http://orca.cf.ac.uk/54361/.

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This thesis examines the role of microRNAs in renal fibrosis. MicroRNAs constitute a large family of approximately 22-nucleotide-long non-coding RNAs, that in animal cells regulate gene expression posttranscriptionally. At the start of the project, microRNAs were emerging as potentially important factors in various physiological and pathological processes however, there was very little known about their expression and function in the kidney, in particular in tubulointerstitial fibrosis. In this thesis, global microRNA expression has been analysed in vitro in proximal tubular epithelial cells, and in vivo in formalin-fixed, paraffin-embedded kidney biopsy samples from patients with diabetic nephropathy. Among microRNAs altered by profibrotic stimuli, the greatest difference has been found in expression ofmiR-192, which is downregulated in severe diabetic nephropathy. Further examination of miR-192 in kidney biopsy samples has revealed that its expression correlates well with renal function and inversely correlates with fibrosis. A possible function of miR-192 has been then studied in vitro in proximal tubular epithelial cells. It has been found that treatment of the cells with the profibrotic cytokine TGF-β1 downregulates miR-192. Moreover, manipulation of miR-192 expression has shown that miR-192 is involved in E-cadherin regulation. The mechanism of that regulation has been investigated, pointing to two transcriptional repressors of E-cadherin, ZEB1 and ZEB2, as direct targets of miR-192. The presented data suggest that, in the kidney, miR-192 may prevent epithelial-to-mesenchymal transition, known to contribute to renal fibrosis. In parallel, global microRNA downregulation in proximal tubular epithelial cells has been attempted. However, knockdown of Dicer or TRBP, proteins involved in microRNA processing, has not been sufficient to induce changes in microRNA expression. The possible explanations have been discussed. Finally, microRNA role in direct regulation of TGF-β1 synthesis has been investigated. In particular, human microRNAs similar to viral hsv-miR-LAT, reported to directly target TGF-β1 mRNA, have been tested.
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Books on the topic "Fibrosi renale"

1

Liu, Bi-Cheng, Hui-Yao Lan, and Lin-Li Lv, eds. Renal Fibrosis: Mechanisms and Therapies. Singapore: Springer Singapore, 2019. http://dx.doi.org/10.1007/978-981-13-8871-2.

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Journées Gabriel Richet (1994 Le Coudray Montceaux, France). Molecular and experimental aspects of renal fibrogenesis: Journées Gabriel Richet. Edited by Sraer Jean-Daniel, Ronco Pierre, and Rondeau Eric. [Cambridge, MA]: Blackwell Science, 1995.

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Hanssen, Lydia. Die pathophysiologische Bedeutung des Y-box-bindenden Proteins-1 (YB-1) in der renalen Fibrose. [S.l: s.n.], 2012.

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Razzaque, M. S., and T. Taguchi, eds. Renal Fibrosis. S. Karger AG, 2003. http://dx.doi.org/10.1159/isbn.978-3-318-00964-4.

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(Editor), Mohammed S. Razzaque, and Takashi Taguchi (Editor), eds. Renal Fibrosis (Contributions to Nephrology). S. Karger Publishers (USA), 2003.

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6

Liu, Bi-Cheng, Hui-Yao Lan, and Lin-Li Lv. Renal Fibrosis: Mechanisms and Therapies. Springer, 2020.

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Liu, Bi-Cheng, Hui-Yao Lan, and Lin-Li Lv. Renal Fibrosis: Mechanisms and Therapies. Springer, 2019.

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Liu, Bi-Cheng, Hui-Yao Lan, and Lin-Li Lv. Renal Fibrosis: Mechanisms and Therapies. Springer, 2019.

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9

Lan, Hui Y., and David J. Nikolic-Paterson, eds. Advances in Mechanisms of Renal Fibrosis. Frontiers Media SA, 2018. http://dx.doi.org/10.3389/978-2-88945-499-0.

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Herrington, William G., Aron Chakera, and Christopher A. O’Callaghan. Interstitial renal disease. Edited by Patrick Davey and David Sprigings. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780199568741.003.0160.

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Tubulointerstitial renal diseases affect the renal tubules and/or the supporting interstitial tissue around them. The glomeruli are typically spared in early disease. Acute interstitial nephritis is characterized by an inflammatory infiltrate (often containing eosinophils). Chronic tubulointerstitial nephritis (TIN) is characterized by extensive tubular atrophy and interstitial fibrosis. The processes are clinically distinct but a prolonged acute interstitial nephritis will develop into chronic disease. This chapter looks at the etiology of interstitial renal disease, as well as its symptoms and clinical features, demographics, complications, diagnosis, and treatment.
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Book chapters on the topic "Fibrosi renale"

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Serai, Suraj D., and Meng Yin. "MR Elastography of the Abdomen: Experimental Protocols." In Methods in Molecular Biology, 519–46. New York, NY: Springer US, 2021. http://dx.doi.org/10.1007/978-1-0716-0978-1_32.

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AbstractApplication of MRE for noninvasive evaluation of renal fibrosis has great potential for noninvasive assessment in patients with chronic kidney disease (CKD). CKD leads to severe complications, which require dialysis or kidney transplant and could even result in death. CKD in native kidneys and interstitial fibrosis in allograft kidneys are the two major kidney fibrotic pathologies where MRE may be clinically useful. Both these conditions can lead to extensive morbidity, mortality, and high health care costs. Currently, biopsy is the standard method for renal fibrosis staging. This method of diagnosis is painful, invasive, limited by sampling bias, exhibits inter- and intraobserver variability, requires prolonged hospitalization, poses risk of complications and significant bleeding, and could even lead to death. MRE based methods can potentially be useful to noninvasively detect, stage, and monitor renal fibrosis, reducing the need for renal biopsy. In this chapter, we describe experimental procedure and step by step instructions to run MRE along with some illustrative applications. We also includes sections on how to perform data quality check and analysis methods.This publication is based upon work from the COST Action PARENCHIMA, a community-driven network funded by the European Cooperation in Science and Technology (COST) program of the European Union, which aims to improve the reproducibility and standardization of renal MRI biomarkers.
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Razzaque, M. S., and T. Taguchi. "Factors That Influence and Contribute to the Regulation of Fibrosis." In Renal Fibrosis, 1–11. Basel: KARGER, 2003. http://dx.doi.org/10.1159/000071732.

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Oite, T., J. Yao, and T. Morioka. "Disturbance of Syncytial Cell Function in Glomerular Mesangial Cells Involved in the Progressive Glomerular Diseases." In Renal Fibrosis, 12–19. Basel: KARGER, 2003. http://dx.doi.org/10.1159/000071733.

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Matsuo, S., Y. Morita, S. Maruyama, L. Manchang, and Y. Yuzawa. "Proteinuria and Tubulointerstitial Injury: The Causative Factors for the Progression of Renal Diseases." In Renal Fibrosis, 20–31. Basel: KARGER, 2003. http://dx.doi.org/10.1159/000071734.

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Maeshima, Y., and H. Makino. "Molecular Mechanism of Cell Injury." In Renal Fibrosis, 32–43. Basel: KARGER, 2003. http://dx.doi.org/10.1159/000071735.

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Tamaki, K., and S. Okuda. "Role of TGF-β in the Progression of Renal Fibrosis." In Renal Fibrosis, 44–65. Basel: KARGER, 2003. http://dx.doi.org/10.1159/000071736.

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Yokoyama, H., T. Wada, and K. Furuichi. "Chemokines in Renal Fibrosis." In Renal Fibrosis, 66–89. Basel: KARGER, 2003. http://dx.doi.org/10.1159/000071737.

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Inan, M. S., M. S. Razzaque, and T. Taguchi. "Pathological Significance of Renal Expression of NF-κB." In Renal Fibrosis, 90–101. Basel: KARGER, 2003. http://dx.doi.org/10.1159/000071738.

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Cochrane, A. L., and S. D. Ricardo. "Oxidant Stress and Regulation of Chemokines in the Development of Renal Interstitial Fibrosis." In Renal Fibrosis, 102–19. Basel: KARGER, 2003. http://dx.doi.org/10.1159/000071739.

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Moriyama, T., and E. Imai. "Role of Myofibroblasts in Progressive Renal Diseases." In Renal Fibrosis, 120–40. Basel: KARGER, 2003. http://dx.doi.org/10.1159/000071740.

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Conference papers on the topic "Fibrosi renale"

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Nascimento, Giovanna Bezerra do, Júlia Yasmin Alves Silva, Max Victor Arruda Alves, and Amanda Soares de Vasconcelos. "ASPECTOS HISTOLÓGICOS DA NEFROTOXICIDADE CAUSADA PELO CONSUMO DE CARAMBOLA EM PESSOAS COM FUNÇÃO RENAL ALTERADA." In I Congresso On-line Nacional de Histologia e Embriologia Humana. Revista Multidisciplinar em Saúde, 2022. http://dx.doi.org/10.51161/rems/3222.

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Introdução: A carambola (Averrhoa carambola) é uma fruta comum em países tropicais, a exemplo do Brasil. Rica em fontes minerais e vitaminas, bem como em caramboxina e ácido oxálico. Esses últimos podem causar efeitos negativos no corpo humano, resultando na deposição de cristais de oxalato nos túbulos renais, com potencial de gerar lesão tubular renal aguda, quando essa fruta é consumida em excesso ou quando há alteração da função renal. Existem 2 tipos de carambola: a azeda, com o teor de oxalato em torno de 7 mg/g; e a doce, na qual a concentração corresponde a 0,4-0,8 mg/g. Objetivo: Compreender o mecanismo pelo qual a carambola ocasiona danos aos túbulos renais do ponto de vista histológico. Metodologia: Revisão de literatura utilizando as bases de dados ScienceDirect e Pubmed. Foram escolhidos os artigos referentes ao intervalo de tempo 2017-2022, nos idiomas português, inglês e espanhol, através dos termos da área de busca: (“lesão renal” OR “acute kidney injury”) AND (carambola OR “fruit star”). Artigos que tangenciassem o tema, não abordando o objetivo de estudo foram excluídos. Resultados e discussão: A literatura encontrada relaciona a ingestão de carambola com lesões renais a partir da formação de cristais de oxalato nesta região. Nos trabalhos analisados observou-se que o consumo dessa fruta em excesso pode acarretar danos à fisiologia renal, majoritariamente a pacientes portadores de alguma patologia pré-existente nos rins, estando estes mais propícios a evoluir para um quadro de doença renal crônica. Na visão histológica, os artigos observados trazem que os cristais de oxalato de cálcio, vistos através da birrefringência sob luz polarizada, quando depositados ocasionam uma reação inflamatória que resulta em edema e fibrose dos túbulos renais, o que prejudica a função renal; podendo, inclusive, evoluir com necrose tecidual. A filtração e a secreção tubular de oxalato causam aumento excessivo na sua concentração local, o que induz a citotoxicidade do tecido dos túbulos renais com perda deste epitélio. Conclusão: Apesar das evidências, mais estudos são necessários para caracterizar o mecanismo fisiopatológico da toxicidade dos componentes da carambola.
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Tey, Wei Keat, Ye Chow Kuang, Joon Joon Khoo, Melanie Po-Leen Ooi, and Serge Demidenko. "Automatic renal interstitial fibrosis quantification system." In 2017 IEEE International Instrumentation and Measurement Technology Conference (I2MTC). IEEE, 2017. http://dx.doi.org/10.1109/i2mtc.2017.7969716.

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McSorley, Anita, Andrew M. Jones, A. Kevin Webb, P. Nagaraj Rao, and John P. Kavanagh. "Calcium Stone Growth in Urine from Cystic Fibrosis Patients and Healthy Controls." In RENAL STONE DISEASE: 1st Annual International Urolithiasis Research Symposium. AIP, 2007. http://dx.doi.org/10.1063/1.2723576.

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"Study on the Mechanism of Renal Interstitial Fibrosis." In 2018 International Conference on Medicine, Biology, Materials and Manufacturing. Francis Academic Press, 2018. http://dx.doi.org/10.25236/icmbmm.2018.02.

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Shahin, Walaa, Ahmed Badr, Walaa Rabie, Rawdah Ahmed, Mona Mohsen, and Mona El-Falaki. "Early renal involvement in children with cystic fibrosis." In ERS International Congress 2018 abstracts. European Respiratory Society, 2018. http://dx.doi.org/10.1183/13993003.congress-2018.pa4627.

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Reed, Cassandra L., Shree G. Sharma, Sandra P. Prieto, and Timothy J. Muldoon. "Quantitative Analysis of Renal Fibrosis Using a Colorimetric System." In 2018 IEEE Conference on Multimedia Information Processing and Retrieval (MIPR). IEEE, 2018. http://dx.doi.org/10.1109/mipr.2018.00040.

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Peng, Yan, Jieli Huang, Jie Luo, Chen Yu, and Yiming Zhu. "Identifying Endogenous Biomarker in Renal fibrosis by Terahertz Spectroscopy." In 2019 44th International Conference on Infrared, Millimeter, and Terahertz Waves (IRMMW-THz). IEEE, 2019. http://dx.doi.org/10.1109/irmmw-thz.2019.8873713.

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Agouni, Abdelali, Duck Y. Lee, Assaad A. Eid, Yves Gorin, and Kumar Sharma. "The Protective Role of Sestrin2 in High Fat Diet-Induced Nephropathy." In Qatar University Annual Research Forum & Exhibition. Qatar University Press, 2020. http://dx.doi.org/10.29117/quarfe.2020.0134.

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Introduction: Obesity is a major risk factor for type-2 diabetes predisposing patients to diabetic nephropathy (DN), the leading cause of end-stage renal failure. Glomerular injury is a prominent pathological feature of DN. Sestrin2 (Sesn2) is a stress-induced protein, but its role in DN has not been investigated. Therefore, we have determined the impact of Sesn2 deletion in a mouse model of obesityinduced nephropathy. Materials and methods: We examined the effects of Sesn2-deficiency in a longterm (22 weeks) mouse model of high fat diet (HFD)-induced obesity on glomerular structure. The severity of renal injury and fibrosis in wild type (Sesn2+/+) mice (fed HFD or chow diets) was compared to that in Sesn2-deficient mice (Sesn2-/- ) fed HFD or chow diets. Animal work was carried out under an IACUC-approved protocol. Results: Data showed that Sesn2 ablation exacerbated HFD-induced glomerular fibrotic injury as evidenced by mesangial matrix hypertrophy and accumulation of both fibronectin and collagen IV. Western blot analysis revealed that HFD- or chow-fed Sesn2-/- mice exhibited higher protein expression of key lipogenic enzymes, fatty acid translocase CD36 (an indicator of lipid uptake), fatty acid synthase and ATP citrate lyase. Sesn2-deficiency in obese mice resulted in podocyte loss as indicated by reduced expression of synaptopodin. Glomerular lesions like those observed in HFD-fed wild-type mice were detected in Sesn2-/-mice fed a chow diet, indicating that the basal deletion of Sesn2 is deleterious by itself. Conclusions: We provide the first evidence that Sesn2 is renoprotective in obesity-induced nephropathy by diminishing lipid accumulation and blocking excessive lipid uptake and de novo lipid synthesis. Understanding the protective of Sesn2 should yield novel therapeutic interventions to effectively preserve glomerular function in obesity and diabetes.
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Luo, Jie, Yan Peng, Tianyi Kou, Chengjun Shi, and Yiming Zhu. "Terahertz s pectroscop ic identification of biomarker in renal fibrosis." In International Symposium on Ultrafast Phenomena and Terahertz Waves. Washington, D.C.: OSA, 2018. http://dx.doi.org/10.1364/isuptw.2018.wi16.

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"Research Progress on the Occurrence Mechanism of Renal Interstitial Fibrosis." In 2018 International Conference on Medicine, Biology, Materials and Manufacturing. Francis Academic Press, 2018. http://dx.doi.org/10.25236/icmbmm.2018.52.

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Reports on the topic "Fibrosi renale"

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Hua, Zi Bo, and Lv Yuan Chen. Human UCB MSC versus placebo for effect on kidney fibrosis. INPLASY - International Platform of Registered Systematic Review and Meta-analysis Protocols, October 2022. http://dx.doi.org/10.37766/inplasy2022.10.0104.

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Review question / Objective: Human UCB MSC versus placebo for effect on kidney fibrosis Condition being studied: Renal fibrosis is the final outcome of long-term chronic kidney disease, and the kidney will lose its basic function. This experiment will explore the effect of Human UCB MSC for effect on kidney fibrosis. Main outcome(s): Correlation analysis of Human UCB MSC treatment on renalfibrosis.
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Yu, Guang, Mao Guo, Junju Zou, Xiaotao Zhou, and Yuerong Ma. The Efficacy of Taking Traditional Chinese Medicine Orally In Renal Interstitial Fibrosis: Protocol for A Systematic Review and Meta-Analysis. INPLASY - International Platform of Registered Systematic Review and Meta-analysis Protocols, August 2020. http://dx.doi.org/10.37766/inplasy2020.8.0042.

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