Bibliografías temáticas / Tubular-interstitial fibrosis

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Literatura académica sobre el tema "Tubular-interstitial fibrosis"

Autor: Grafiati
Publicado: 19 de octubre de 2024
Última modificación: 31 de julio de 2025

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Artículos de revistas sobre el tema "Tubular-interstitial fibrosis"

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Wyczanska, Maja, Jana Rohling, Ursula Keller, Marcus R. Benz, Carsten Kirschning, and Bärbel Lange-Sperandio. "TLR2 mediates renal apoptosis in neonatal mice subjected experimentally to obstructive nephropathy." PLOS ONE 18, no. 11 (2023): e0294142. http://dx.doi.org/10.1371/journal.pone.0294142.

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Urinary tract obstruction during renal development leads to inflammation, tubular apoptosis, and interstitial fibrosis. Toll like receptors (TLRs) expressed on leukocytes, myofibroblasts and renal cells play a central role in acute inflammation. TLR2 is activated by endogenous danger signals in the kidney; its contribution to renal injury in early life is still a controversial topic. We analyzed TLR2 for a potential role in the neonatal mouse model of congenital obstructive nephropathy. Inborn obstructive nephropathies are a leading cause of end-stage kidney disease in children. Thus, newborn
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Rascio, Federica, Paola Pontrelli, Giuseppe Stefano Netti, et al. "IgE-Mediated Immune Response and Antibody-Mediated Rejection." Clinical Journal of the American Society of Nephrology 15, no. 10 (2020): 1474–83. http://dx.doi.org/10.2215/cjn.02870320.

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Background and objectivesActive antibody-mediated rejection is the main cause of kidney transplant loss, sharing with SLE the alloimmune response and the systemic activation of the IFN-α pathway. IgE-mediated immune response plays a key role in the development of SLE nephritis and is associated with IFN-α secretion. The aim of our study was to investigate IgE-mediated immune response in antibody-mediated rejection.Design, setting, participants, & measurementsThis was a cross-sectional study of 56 biopsy-proven antibody-mediated rejection study participants, 80 recipients with normal graft
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Christensen, Erik I., and Pierre J. Verroust. "Interstitial fibrosis: tubular hypothesis versus glomerular hypothesis." Kidney International 74, no. 10 (2008): 1233–36. http://dx.doi.org/10.1038/ki.2008.421.

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Eskild-Jensen, Anni, Lene Fogt Paulsen, Lise Wogensen, et al. "AT1 receptor blockade prevents interstitial and glomerular apoptosis but not fibrosis in pigs with neonatal induced partial unilateral ureteral obstruction." American Journal of Physiology-Renal Physiology 292, no. 6 (2007): F1771—F1781. http://dx.doi.org/10.1152/ajprenal.00479.2006.

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Obstruction-induced fibrosis is a leading cause of end-stage renal failure in children. The pathophysiological mechanisms may involve apoptosis and the renin-angiotensin system. We studied apoptosis and fibrosis in a well-established neonatal pig model with unilateral partial ureteral obstruction (PUUO) induced during ongoing nephrogenesis in 2-day-old piglets. The role of angiotensin II (ANG II) was studied using the AT1 receptor blocker CV-11974 (0.12 mg/h candesartan from age 23 to 30 days). At day 30 the kidneys were perfusion fixed and fibrosis, apoptosis, and tubular lengths were quantit
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Wang, Shi-Nong, and Raimund Hirschberg. "Growth factor ultrafiltration in experimental diabetic nephropathy contributes to interstitial fibrosis." American Journal of Physiology-Renal Physiology 278, no. 4 (2000): F554—F560. http://dx.doi.org/10.1152/ajprenal.2000.278.4.f554.

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Glomerular proteinuria is a risk factor for progression of chronic renal failure and contributes to renal interstitial fibrosis. In experimental diabetic glomerular sclerosis, there is translocation of high-molecular-weight growth factors, namely, hepatocyte growth factor (HGF) and transforming growth factor (TGF)-β, from plasma into tubular fluid, both of which act on tubular cells through apical membrane receptors. In the present studies, the hypothesis is examined that ultrafiltered HGF and TGF-β induce increased expression of extracellular matrix (ECM) proteins directly in tubular cells, o
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Thomas, S. E., S. Anderson, K. L. Gordon, T. T. Oyama, S. J. Shankland, and R. J. Johnson. "Tubulointerstitial disease in aging: evidence for underlying peritubular capillary damage, a potential role for renal ischemia." Journal of the American Society of Nephrology 9, no. 2 (1998): 231–42. http://dx.doi.org/10.1681/asn.v92231.

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Aging is associated with a progressive decline in renal function and the development of glomerulosclerosis and interstitial fibrosis. Although many studies have addressed the cellular mechanisms of age-related glomerulosclerosis, less is known about the tubulointerstitial fibrosis. In this study, aging (24 mo) rats develop tubulointerstitial fibrosis characterized by tubular injury and focal tubular cell proliferation, myofibroblast activation, macrophage infiltration with increased immunostaining for the adhesive proteins osteopontin and intercellular adhesion molecule-1, and collagen IV depo
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Leong, Khai Gene, Elyce Ozols, John Kanellis, David J. Nikolic-Paterson, and Frank Y. Ma. "Cyclophilin A Promotes Inflammation in Acute Kidney Injury but Not in Renal Fibrosis." International Journal of Molecular Sciences 21, no. 10 (2020): 3667. http://dx.doi.org/10.3390/ijms21103667.

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Cyclophilin A (CypA) is a highly abundant protein in the cytoplasm of most mammalian cells. Beyond its homeostatic role in protein folding, CypA is a Damage-Associated Molecular Pattern which can promote inflammation during tissue injury. However, the role of CypA in kidney disease is largely unknown. This study investigates the contribution of CypA in two different types of kidney injury: acute tubular necrosis and progressive interstitial fibrosis. CypA (Ppia) gene deficient and wild type (WT) littermate controls underwent bilateral renal ischaemia/reperfusion injury (IRI) and were killed 24
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Wang, Shudan, Ming Wu, Luis Chiriboga, Chaim Putterman, Anna Broder, and H. Michael Belmont. "4336 Renal Tubular Complement C9 Deposition is Associated with Renal Tubular Damage and Fibrosis in Lupus Nephritis." Journal of Clinical and Translational Science 4, s1 (2020): 144. http://dx.doi.org/10.1017/cts.2020.424.

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OBJECTIVES/GOALS: Tubulointerstitial damage in lupus nephritis (LN) is a strong predictor of progression to chronic kidney disease and end stage renal disease (ESRD). While complement activation mediates glomerular injury, the role of complement in renal tubular damage has not been evaluated. We investigated the association between complement activation and tubulointerstitial fibrosis. METHODS/STUDY POPULATION: Patients with LN were selected randomly between July 2014 - July 2016. Chromogenic immunohistochemistry was performed on formalin-fixed, paraffin-embedded, 4-µm human renal biopsy secti
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Pichler, R. H., N. Franceschini, B. A. Young, et al. "Pathogenesis of cyclosporine nephropathy: roles of angiotensin II and osteopontin." Journal of the American Society of Nephrology 6, no. 4 (1995): 1186–96. http://dx.doi.org/10.1681/asn.v641186.

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Low-salt-diet, cyclosporine (CsA; 15 mg/kg per day)-treated rats develop striped interstitial fibrosis, arteriolar hyalinosis, and azotemia similar to the chronic nephropathy observed in humans. To examine the role of angiotensin II in this model, rats on a low-salt diet were given CsA, CsA and the angiotensin II receptor Type I antagonist Losartan (10 mg/kg per day), CsA and hydralazine/furosemide, or vehicle. At Day 35, CsA-treated rats had tubular injury, arteriolopathy of the afferent arteriole, increased expression of the monocyte-macrophage adhesive protein osteopontin, interstitial macr
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Wang, Hao, Yujiao Deng, Limeng He, Yan Deng, and Wei Zhang. "Renal Interstitial Fibrosis Detected on 18F-AlF-NOTA-FAPI-04 PET/CT in a Patient With Multiple Myeloma." Clinical Nuclear Medicine 48, no. 10 (2023): 896–98. http://dx.doi.org/10.1097/rlu.0000000000004804.

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Abstract 18F-AlF-NOTA-FAPI-04 PET/CT was performed on a 58-year-old woman newly diagnosed with multiple myeloma and acute renal insufficiency. 18F-AlF-NOTA-FAPI-04 PET/CT showed increased FAPI uptake in multiple osteolytic lesions and both kidneys. Subsequent renal aspiration biopsy confirmed renal interstitial fibrosis due to subacute tubular interstitial injury. This case suggests that 18F-AlF-NOTA-FAPI-04 PET/CT may be valuable in the evaluation of renal interstitial fibrosis in patients with multiple myeloma.
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Tesis sobre el tema "Tubular-interstitial fibrosis"

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Bletsos, Vassili S. "The Role of CD40 Signaling in Chronic Renal Allograft Rejection in a Hypertensive Rat Model." University of Toledo Health Science Campus / OhioLINK, 2018. http://rave.ohiolink.edu/etdc/view?acc_num=mco1532961455216765.

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Roger, Elena. "Rôle de la Connexine 43 dans les maladies rénales tubulaires expérimentales." Electronic Thesis or Diss., Sorbonne université, 2024. https://accesdistant.sorbonne-universite.fr/login?url=https://theses-intra.sorbonne-universite.fr/2024SORUS202.pdf.

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La maladie rénale chronique (MRC) est un problème majeur pour la santé publique, affectant des millions de personne dans le monde. Même si des progrès significatifs ont été réalisés, il n'existe aucun traitement spécifique permettant d'empêcher sa progression de manière probante, la découverte de nouvelles cibles thérapeutiques devenant cruciale pour mettre au point un traitement efficace. Notre objectif principal est de définir le rôle de la Connexine 43 (Cx43), protéine constitutive des jonctions gap, dans l'adaptation fonctionnelle et structurelle du rein en réponse à des agressions chroniq
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Hwang, Kuo-Chan, and 黃國展. "Proteome analysis of the effect of (+)-Catechin toward tubular interstitial fibrosis by fluorogenic derivatization-liquid chromatography-tandem mass spectrometry method." Thesis, 2012. http://ndltd.ncl.edu.tw/handle/18888450087904874418.

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Libros sobre el tema "Tubular-interstitial fibrosis"

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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 a
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Schiller, Adalbert, Adrian Covic, and Liviu Segall. Chronic tubulointerstitial nephritis. Edited by Adrian Covic. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780199592548.003.0086_update_001.

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Chronic tubulointerstitial nephropathies (CTINs) are a group of renal diseases, characterized by variable interstitial inflammation and fibrosis and tubular atrophy, and a slow course towards end-stage renal disease (ESRD). The causes of CTIN are numerous, including nephrotoxic drugs and chemicals, infections, autoimmune diseases, obstructive uropathies, and metabolic disorders. Taken together, CTIN are responsible for less than 10% of all ESRD cases requiring renal replacement therapy. The clinical manifestations of CTIN typically comprise low-grade proteinuria, leucocyturia, and variably red
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Radović, Milan, and Adalbert Schiller. Balkan endemic nephropathy. Edited by Adrian Covic. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780199592548.003.0090_update_001.

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Balkan endemic nephropathy (BEN) is a chronic, slowly progressive tubulointerstitial nephritis, with familial clustering, occurring in several endemic rural regions in countries of the Balkan Peninsula. BEN is characterized by anaemia, tubular proteinuria, renal shrinkage, and slowly declining glomerular filtration rate (GFR). Up to one-third of patients may also develop upper urothelial tumours. The aetiology of BEN is unclear; chronic exposure to aristolochic acid and a polygenic predisposition are the most likely contributing factors. The major pathological characteristics of BEN are symmet
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Hughes, Jeremy. Proteinuria as a direct cause of progression. Edited by David J. Goldsmith. Oxford University Press, 2015. http://dx.doi.org/10.1093/med/9780199592548.003.0137.

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Proximal tubular cells reabsorb any filtered proteins during health via cell surface receptors such as megalin and cubulin so that very low levels of protein are present in the excreted urine. Significant proteinuria is a common finding in patients with many renal diseases. Proteinuria is a marker of glomerular damage and podocyte loss and injury in particular. The degree of proteinuria at presentation or during the course of the disease correlates with long-term outcome in many renal diseases. Proteinuria per se may be nephrotoxic and thus directly relevant to the progression of renal disease
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Segall, Liviu, and Adrian Covic. Immune-mediated tubulointerstitial nephritis. Edited by Adrian Covic. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780199592548.003.0093_update_001.

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Immune-mediated tubulointerstitial nephritides (TINs) are generally encountered in the context of systemic or extrarenal autoimmune diseases, such as sarcoidosis, Sjögren syndrome, systemic lupus erythematosus, inflammatory bowel disease, TIN and uveitis (TINU) syndrome, and immunoglobulin G4-related disease. The pathogenesis of these TINs is complex and more or less unclear; it usually involves leucocyte activation, autoantibodies, immune complex deposition, complement activation, and release of inflammatory cytokines and growth factors. Tubulointerstitial inflammation most commonly has a chr
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Izzedine, Hassan, and Victor Gueutin. Drug-induced acute tubulointerstitial nephritis. Edited by Adrian Covic. Oxford University Press, 2015. http://dx.doi.org/10.1093/med/9780199592548.003.0084.

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Drug-induced acute tubulointerstitial nephritis (ATIN) is the most common aetiology of ATIN and a potentially correctable cause of acute kidney injury (AKI). An interval of 7–10 days typically exists between drug exposure and development of AKI, but this interval can be considerably shorter following re-challenge or markedly longer with certain drugs. It occurs in an idiosyncratic and non-dose-dependent manner. Antibiotics, NSAIDs, and proton pump inhibitors are the most frequently involved agents, but the list of drugs that can induce ATIN is continuously increasing. The mechanism of renal in
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Capítulos de libros sobre el tema "Tubular-interstitial fibrosis"

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Gartler, Stanley M., R. Scott Hansen, Vinzenz Oji, et al. "Interstitial Fibrosis/Tubular Atrophy." In Encyclopedia of Molecular Mechanisms of Disease. Springer Berlin Heidelberg, 2009. http://dx.doi.org/10.1007/978-3-540-29676-8_7797.

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"Tubular and interstitial disease." In Oxford Desk Reference Nephrology, edited by Jonathan Barratt, Peter Topham, Sue Carr, Mustafa Arici, and Adrian Liew. Oxford University Press, 2021. http://dx.doi.org/10.1093/med/9780198777182.003.0005.

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Tubulointerstitial diseases refer to a group of disorders in which inflammatory cell infiltrates within the kidney interstitium and/or tubular epithelium are seen on kidney biopsy. These disorders constitute an important group of kidney diseases with varying prevalences and presentations due to a number of causes. It is difficult to estimate the worldwide incidence of tubular and interstitial disease as it is a histological diagnosis and biopsy rates vary substantially around the world. Increasing incidence of tubulointerstitial nephritis has been related to polypharmacy, particularly in the o
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Harris, Kevin P. G. "Proteinuria: Implications for Progression and Management." In Mechanisms and Clinical Management of Chronic Renal Failure. Oxford University PressNew York, NY, 2000. http://dx.doi.org/10.1093/oso/9780192629333.003.0005.

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Abstract It is a well established observation from both human and animal studies of renal disease, that once a degree of renal damage has occurred then the progression of kidney failure is inexorable, even if the original injurious process has resolved [1]. Such observations have led to the hypothesis that following renal damage of any aetiology a maladaptive response occurs in the remaining nephrons which results in their eventual destruction by a common pathogenic mechanism. In support of this, the histological appearance of the kidney in end-stage renal disease is similar whatever the initi
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De Broe, Marc E., Channa Jayasumana, Patrick C. D’Haese, Monique M. Elseviers, and Benjamin Vervaet. "Chronic tubulointerstitial nephritis." In Oxford Textbook of Medicine, edited by John D. Firth. Oxford University Press, 2020. http://dx.doi.org/10.1093/med/9780198746690.003.0490.

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Chronic tubulointerstitial nephritis is usually asymptomatic, presenting with slowly progressive renal impairment. Urinalysis may be normal or show low-grade proteinuria (<1.5 g/day) and/or pyuria. Diagnosis depends on renal biopsy, which reveals variable cellular infiltration of the interstitium, tubular atrophy, and fibrosis. There are many causes including sarcoidosis, drugs (prescribed and nonprescribed), irradiation, toxins, and metabolic disorders. Analgesic nephropathy—characterized by renal papillary necrosis and chronic interstitial nephritis and caused by the prolonged and excessi
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Actas de conferencias sobre el tema "Tubular-interstitial fibrosis"

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Kammardi Shashiprakash, Avinash, Brendon Lutnick, Brandon Ginley, et al. "A distributed system improves inter-observer and AI concordance in annotating interstitial fibrosis and tubular atrophy." In Digital and Computational Pathology, edited by John E. Tomaszewski and Aaron D. Ward. SPIE, 2021. http://dx.doi.org/10.1117/12.2581789.

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CABRAL, HIANNY RIBEIRO, ARTHUR LIRA ARAÚJO, PAULO ROBERTO SILVA JÚNIOR, et al. "FOCAL TUBULAR ATROPHY AND INTERSTITIAL FIBROSIS RELATED TO THE USE OF LEFLUNOMIDE IN A PATIENT WITH RHEUMATOID ARTHRITIS: A CASE REPORT." In 36º Congresso Brasileiro de Reumatologia. Editora Blucher, 2019. http://dx.doi.org/10.5151/sbr2019-104.

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