Relevant bibliographies by topics / Tubulointerstitial fibrosis

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  1. Journal articles
  2. Dissertations / Theses
  3. Books
  4. Book chapters
  5. Conference papers

Academic literature on the topic 'Tubulointerstitial fibrosis'

Author: Grafiati
Published: 4 June 2021
Last updated: 8 February 2022

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Journal articles on the topic "Tubulointerstitial fibrosis"

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O'Donnell, Michael P. "Renal tubulointerstitial fibrosis." Postgraduate Medicine 108, no. 1 (July 2000): 159–72. http://dx.doi.org/10.3810/pgm.2000.07.1155.

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Zeisberg, Michael, and Eric G. Neilson. "Mechanisms of Tubulointerstitial Fibrosis." Journal of the American Society of Nephrology 21, no. 11 (September 23, 2010): 1819–34. http://dx.doi.org/10.1681/asn.2010080793.

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Kuncio, Gerald S., Eric G. Neilson, and Thomas Haverty. "Mechanisms of tubulointerstitial fibrosis." Kidney International 39, no. 3 (March 1991): 550–56. http://dx.doi.org/10.1038/ki.1991.63.

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Iwano, Masayuki, and Eric G. Neilson. "Mechanisms of tubulointerstitial fibrosis." Current Opinion in Nephrology and Hypertension 13, no. 3 (May 2004): 279–84. http://dx.doi.org/10.1097/00041552-200405000-00003.

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VIELHAUER, VOLKER, HANS-JOACHIM ANDERS, MATTHIAS MACK, JOSEF CIHAK, FRANK STRUTZ, MANFRED STANGASSINGER, BRUNO LUCKOW, HERMANN-JOSEF GRÖNE, and DETLEF SCHLÖNDORFF. "Obstructive Nephropathy in the Mouse: Progressive Fibrosis Correlates with Tubulointerstitial Chemokine Expression and Accumulation of CC Chemokine Receptor 2- and 5-Positive Leukocytes." Journal of the American Society of Nephrology 12, no. 6 (June 2001): 1173–87. http://dx.doi.org/10.1681/asn.v1261173.

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Abstract. The infiltration of leukocytes plays a major role in mediating tubulointerstitial inflammation and fibrosis in chronic renal disease. CC chemokines participate in leukocyte migration and infiltration into inflamed renal tissue. Because CC chemokine-directed leukocyte migration is mediated by target cell expression of a group of CC chemokine receptors, this study examined the expression of CC chemokines and their receptors during initiation of tubulointerstitial fibrosis after unilateral ureteral obstruction in C57BL/6 mice. Obstructed kidneys developed hydronephrosis, tubular cell da
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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 (February 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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Ito, Hideyuki, Xiaoxiang Yan, Nanae Nagata, Kosuke Aritake, Yoshinori Katsumata, Tomohiro Matsuhashi, Masataka Nakamura, et al. "PGD2-CRTH2 Pathway Promotes Tubulointerstitial Fibrosis." Journal of the American Society of Nephrology 23, no. 11 (September 20, 2012): 1797–809. http://dx.doi.org/10.1681/asn.2012020126.

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Boor, Peter, Andrzej Konieczny, Luigi Villa, Anna-Lisa Schult, Eva Bücher, Song Rong, Uta Kunter, et al. "Complement C5 Mediates Experimental Tubulointerstitial Fibrosis." Journal of the American Society of Nephrology 18, no. 5 (March 27, 2007): 1508–15. http://dx.doi.org/10.1681/asn.2006121343.

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Sakamoto, Izumi, Yasuhiko Ito, Masashi Mizuno, Yasuhiro Suzuki, Akiho Sawai, Akio Tanaka, Shoichi Maruyama, Yoshifumi Takei, Yukio Yuzawa, and Seiichi Matsuo. "Lymphatic vessels develop during tubulointerstitial fibrosis." Kidney International 75, no. 8 (April 2009): 828–38. http://dx.doi.org/10.1038/ki.2008.661.

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SATOH, MINORU, NAOKI KASHIHARA, YASUSHI YAMASAKI, KEISUKE MARUYAMA, KAZUNORI OKAMOTO, YOUHEI MAESHIMA, HITOSHI SUGIYAMA, TAKESHI SUGAYA, KAZUO MURAKAMI, and HIROFUMI MAKINO. "Renal Interstitial Fibrosis Is Reduced in Angiotensin II Type 1a Receptor-Deficient Mice." Journal of the American Society of Nephrology 12, no. 2 (February 2001): 317–25. http://dx.doi.org/10.1681/asn.v122317.

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Abstract. Unilateral ureteral obstruction (UUO) results in tubulointerstitial fibrosis of the affected kidney by stimulating the renin-angiotensin system. This study established a UUO model in angiotensin type 1a receptor (AT1a) deficient (mutant) mice to elucidate the role of angiotensin II through AT1a on the fibrosis of the obstructed kidney (OBK). The relative volume of the tubulointerstitium was measured by an image analyzer; deposition of collagen types III and IV and monocyte/macrophage infiltration were histologically examined using specific antibodies. Also determined were the mRNA le
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Dissertations / Theses on the topic "Tubulointerstitial fibrosis"

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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
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Yokoi, Hideki. "Role of connective tissue growth factor in renal tubulointerstitial fibrosis." Kyoto University, 2005. http://hdl.handle.net/2433/144757.

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Mirzoyan, Koryun. "The role of LPA in kidney pathologies." Thesis, Toulouse 3, 2017. http://www.theses.fr/2017TOU30073/document.

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Les maladies rénales chroniques (MRC) et l'insuffisance rénale aiguë (IRA) sont des problèmes essentiels de santé publique en raison de l'augmentation continue de leur fréquence et du manque de solutions thérapeutiques contre ces maladies. L'acide lysophosphatidique (LPA) est un lysophospholipide bioactif qui induit un large éventail de réponses cellulaires par le biais de récepteurs membranaires spécifiques (LPA1 à LPA6) couplés aux protéines G. Dans ce travail, nous nous sommes intéressés aux effets biologiques et au métabolisme du LPA dans les MRC et l'IRA. Des travaux antérieurs de l'équip
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Wan-ChunChen and 陳宛君. "Role of matrix stiffness in the regulation of primary proximal tubular cell proliferation and differentiation:implication in chronic tubulointerstitial fibrosis." Thesis, 2015. http://ndltd.ncl.edu.tw/handle/rnwsq7.

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博士<br>國立成功大學<br>基礎醫學研究所<br>103<br>Normally, differentiated renal proximal tubular epithelial cells (PTECs) reside on soft basement membrane containing laminin-rich extracellular matrix (ECM). Chronic tubulointerstitial fibrosis is characterized by the accumulation of collagen with tissue stiffening and finally leads to the end-stage renal disease. Previous studies showed that transforming growth factor-beta 1 (TGF-beta1) played the potent initiator and/or enhancer for fibrogenesis. However, accumulated studies also indicate that the matrix stiffness also regulate cell behaviors, i.e. developme
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Takes, Julia. "Der Einfluss von Interleukin-1 und des Interleukin-1-Rezeptorantagonisten (Anakinra) auf die epithelial-mesenchymale Transition von Tubulusepithelzellen in vitro." Doctoral thesis, 2011. http://hdl.handle.net/11858/00-1735-0000-0006-B25C-C.

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Ghosh, Anindya. "Mécanisme(s) d'action de l'insuline dans la prévention de l'hypertension et la progression de la tubulopathie dans le diabète : rôle de hnRNP F, Nrf2 et Bmf." Thèse, 2018. http://hdl.handle.net/1866/21837.

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Shi, Yixuan. "Caractérisation du gène de l'enzyme de conversion de l'angiotensine-2 dans le rein diabétique et implication dans le développement de la néphropathie diabétique et de l'hypertension." Thèse, 2014. http://hdl.handle.net/1866/11828.

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De nombreuses études ont bien démontré que l’activation du système rénine-angiotensine (RAS) joue un rôle important dans le développement de l’hypertension et de la néphropathie diabétique (DN). La découverte de l’enzyme de conversion de l’angiotensine-2 (ACE2) et l’identification du récepteur MAS, spécifique pour l’angiotensine 1-7 (Ang 1-7), ont permis d’identifier deux nouveaux membres du RAS. L’axe ACE2/Ang 1-7/MAS contrebalance les effets de l’axe ACE/Ang II/AT1. Plusieurs évidences impliquent la contribution du RAS intrarénal dans la DN. Des études réalisées dans notre laboratoire avec d
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Books on the topic "Tubulointerstitial fibrosis"

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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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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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Izzedine, Hassan, and Victor Gueutin. Drug-induced chronic tubulointerstitial nephritis. Edited by Adrian Covic. Oxford University Press, 2015. http://dx.doi.org/10.1093/med/9780199592548.003.0087.

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The chronic form of drug-induced tubulointerstitial nephritis (CTIN) is an insidious disease and most probably represents the common final response pattern of the kidney to a variety of agents (including analgesics, lithium, antineoplastic chemotherapeutic agents, like cisplatin and nitrosoureas, and immunosuppressive drugs, such as ciclosporin and tacrolimus). Drug-induced CTIN is usually asymptomatic, presenting with slowly progressive renal impairment. Because of its insidious nature, CTIN is often diagnosed incidentally on routine laboratory screening or evaluation of CKD. The diagnosis of
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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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Kang, Duk-Hee, and Mehmet Kanbay. Urate nephropathy. Edited by Adrian Covic. Oxford University Press, 2015. http://dx.doi.org/10.1093/med/9780199592548.003.0092.

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Gout is a disorder of purine metabolism, characterized by hyperuricaemia and urate crystal deposition within and around the joints. The recognition of increased comorbidity burden in patients with gout rendered it as a systemic disorder rather than simply a musculoskeletal condition. Gout nephropathy (also known as chronic uric acid nephropathy or urate nephropathy) is a form of chronic tubulointerstitial nephritis, induced by deposition of monosodium urate crystals in the distal collecting ducts and the medullary interstitium, associated with a secondary inflammatory reaction. Other renal his
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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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Book chapters on the topic "Tubulointerstitial fibrosis"

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Li, Zuo-Lin, and Bi-Cheng Liu. "Hypoxia and Renal Tubulointerstitial Fibrosis." In Advances in Experimental Medicine and Biology, 467–85. Singapore: Springer Singapore, 2019. http://dx.doi.org/10.1007/978-981-13-8871-2_23.

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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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Dodd, S. "The Pathogenesis of Tubulointerstitial Disease and Mechanisms of Fibrosis." In Current Topics in Pathology, 51–67. Berlin, Heidelberg: Springer Berlin Heidelberg, 1995. http://dx.doi.org/10.1007/978-3-642-79517-6_2.

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De Broe, Marc E., Patrick C. D’Haese, and Monique M. Elseviers. "Chronic tubulointerstitial nephritis." In Oxford Textbook of Medicine, 4005–20. Oxford University Press, 2010. http://dx.doi.org/10.1093/med/9780199204854.003.210902_update_001.

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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 (&lt;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....
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Koratala, Abhilash, Girish Singhania, and A. Ahsan Ejaz. "Tubulointerstitial Nephropathies." In Kidney Protection, edited by Vijay Lapsia, Bernard G. Jaar, and A. Ahsan Ejaz, 427–38. Oxford University Press, 2019. http://dx.doi.org/10.1093/med/9780190611620.003.0043.

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Tubulointerstitial nephropathies encompass diverse disease processes involving the part of the renal parenchyma that consists of the tubules and interstitium. Tubulointerstitial diseases can occur as primary or secondary (to a systemic disease) processes, and patients can present with either acute or chronic disease. Depending on the offending agent, the disease may have a particular predilection for the proximal tubules, the distal tubules, or both. Definitive diagnosis is by renal biopsy, which typically reveals variable degrees of cellular infiltration of the interstitium, tubular atrophy, and fibrosis, depending on the chronicity. There are several causes, including drugs, infections, environmental toxins, and immunologic processes. This chapter classifies tubulointerstitial nephropathies and briefly discusses the important individual entities. In addition, an approach for renoprotection in these cases based on the available data is suggested.
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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, 4956–74. 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 (&lt;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 excessive consumption of combinations of analgesics, mostly including phenacetin. Nonsteroidal anti-inflammatory drugs—the most frequent cause of permanent renal insufficiency after acute interstitial nephritis. Aristolochic acid nephropathy—(1) Chinese herb nephropathy—caused in most cases (but perhaps not all) by aristolochic acid, and is associated with a high incidence of urothelial malignancy. (2) Balkan endemic nephropathy—a chronic, familial, noninflammatory tubulointerstitial disease of the kidneys that is associated with a high frequency of urothelial atypia, occasionally culminating in tumours of the renal pelvis and urethra. 5-Aminosalicylic acid—used in the treatment of chronic inflammatory bowel disease and causes clinical nephrotoxicity in approximately 1 in 4000 patients/year. Chronic interstitial nephritis in agricultural communities (CINAC) —nonproteinuric chronic kidney disease that presents in young, agricultural workers in Central America and Sri Lanka in the absence of any clear aetiology. Lithium—the most common renal side effect is to cause nephrogenic diabetes insipidus. Radiation nephropathy—preventive shielding of the kidneys in patients receiving radiation therapy generally prevents radiation nephropathy, but total body irradiation preceding bone marrow transplantation leads 20% to develop chronic renal failure in the long term. Nephropathies induced by toxins (including lead and cadmium) or by metabolic disorders (chronic hypokalaemia and chronic urate nephropathy).
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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, 140–84. 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 older population. Tubulointerstitial nephritis may present acutely as an immunologically mediated hypersensitivity reaction to an inciting agent—typically a drug or infection—or chronically as a part of a disease process leading to chronic interstitial fibrosis and tubular atrophy. Allergic interstitial nephritis, analgesic nephropathy, nephrotoxic metals, hyperuricemia, Balkan nephropathy, Mesoamerican nephropathy, aristolochic acid nephropathy, and other rare causes of tubulointerstitial nephritis are covered in this section. Isolated defects of tubular function, tubular disorder-related nephropathies, and electrolyte derangements also constitute important aspects of tubulointerstitial diseases.
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Bilous, Rudolf. "Diabetes mellitus and the kidney." In Oxford Textbook of Medicine, edited by John D. Firth, 4975–87. Oxford University Press, 2020. http://dx.doi.org/10.1093/med/9780198746690.003.0491.

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Diabetic nephropathy is the commonest cause of endstage renal disease in the developed world. Aetiology and pathology—causation is related to glycaemic control, hypertension, inflammation, genetic factors, and dietary and other environmental factors. Pathological hallmarks in the glomerulus are thickening of the glomerular basement membrane and mesangial expansion, with or without nodule formation, secondary to an accumulation of extracellular matrix. Many patients have a varying severity of tubulointerstitial inflammation and fibrosis. Staging and natural history—is classically described in terms of urinary albumin excretion rate (UAER). Clinical features—most patients (&gt;60%) will have a normal UAER throughout their diabetic life, but 1 to 2% of the remainder develop persistent moderately increased albuminuria each year. Once UAER exceeds 200 µg/min, there tends to be a relentless increase in proteinuria and glomerular filtration rate declines progressively at a rate that largely depends upon blood pressure control. Prevention—tight glycaemic control can prevent moderately increased albuminuria in both type 1 and type 2 diabetes. Whether intensive blood pressure control using angiotensin-converting enzyme (ACE) inhibitors can also prevent this remains controversial. In both type 1 and type 2 diabetes, intensive blood pressure control using ACE inhibitors or angiotensin II receptor blockers (ARBs) slows progression from moderately to severely increased albuminuria and also slows the rate of decline in glomerular filtration rate in those with severely increased albuminuria. Management—aims for (1) control of glycaemia, (2) control of hypertension (&lt;130/80 mmHg) using an ACE inhibitor or an ARB as first line; and (3) other interventions, including some or all of serum lipid lowering, smoking cessation, and reduction of dietary protein and salt.
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Conference papers on the topic "Tubulointerstitial fibrosis"

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Persy, Veerle P., Anja Verhulst, Sven R. Vercauteren, and Marc E. De Broe. "LESS MACROPHAGE INFILTRATION AND TUBULOINTERSTITIAL FIBROSIS IN OSTEOPONTIN KNOCKOUT MICE WITH CHRONIC RENAL FAILURE." In 3rd International Conference on Osteopontin and SIBLING (Small Integrin-Binding Ligand, N-linked Glycoprotein) Proteins, 2002. TheScientificWorld Ltd, 2002. http://dx.doi.org/10.1100/tsw.2002.329.

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