Academic literature on the topic 'Tubulointerstitial fibrosis'
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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 damage, interstitial inflammation, and fibrosis. From days 2 to 10, a progressive interstitial influx of F4/80+ macrophages and CD3+ lymphocytes occurred (macrophages, 4-fold; lymphocytes, 20-fold at day 10, compared with contralateral control kidneys). In parallel, the number of activated fibroblast-specific protein 1+ fibroblasts and interstitial collagen IV accumulation increased from days 2 to 10. The mRNA expression of CC chemokines (predominantly monocyte chemoattractant protein-1 [MCP-1]/CCL2, RANTES/CCL5) and their receptors CCR1, CCR2, CCR5 increased progressively from days 2 to 10. Byin situhybridization, a prominent interstitial mRNA expression of MCP-1 and RANTES and their receptors CCR2 and CCR5 localized to interstitial mononuclear cell infiltrates. MCP-1 and RANTES expression was also seen in tubular epithelial cells. Fluorescence-activated cell sorter analysis of single-cell suspensions from obstructed kidneys revealed a prominent expression of CCR2 and CCR5 by infiltrating macrophages, whereas most lymphocytes expressed CCR5 only. These data demonstrate an increased expression of MCP-1/CCL2 and RANTES/CCL5 at sites of tubulointerstitial damage and progressive fibrosis during unilateral ureteral obstruction that correlates with simultaneous accumulation of interstitial macrophages and T lymphocytes expressing the respective surface receptors CCR2 and CCR5. The chemokine receptor—mediated leukocyte influx into the tubulointerstitium could offer a new potential target for therapeutic intervention in progressive renal tubulointerstitial fibrosis.
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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 deposition. Aging rats demonstrated immunostaining for endothelial nitric oxide synthase (eNOSIII) in renal tubular epithelial cells and infiltrating mononuclear cells in areas of tubulointerstitial injury, with a relative loss of staining of the peritubular capillaries compared with young rats. The aging rats also displayed focal loss of peritubular capillaries (as noted by focally decreased RECA-1 and OX-2 staining) in areas of tubulointerstitial injury. The areas of fibrosis and hypocellularity were associated with increased apoptosis of tubular and interstitial cells compared with young (3 mo) rats (25.4 +/- 5.3 versus 3.5 +/- 2.5 TUNEL-positive cells/0.25 mm2 in old versus young rats, P = 0.0001). It is concluded that tubulointerstitial fibrosis in aging is an active process associated with interstitial inflammation and fibroblast activation. The progressive loss of cells in areas of fibrosis may be due to accelerated apoptosis. Furthermore, the tubulointerstitial injury may be the consequence of ischemia secondary to peritubular capillary injury and altered eNOS expression.
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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 levels of transforming growth factor-β by Northern blot analysis. Nuclear factor-κB activity was assessed by gel shift assay. UUO in wild mice resulted in a marked expansion of relative volume of the tubulointerstitium, together with increased deposition of collagen types III and IV and number of infiltrated monocytes/macrophages in the interstitium, relative to sham-operated mice. In comparison, these changes were significantly lower in mutant mice with UUO. The mRNA level of transforming growth factor-β was significantly higher in the OBK of wild mice with UUO compared with sham-operated mice. In contrast, the increase in mRNA level in the OBK of mutant mice was significantly less than in wild mice. Finally, UUO resulted in activation of nuclear factor-κB in wild mice but was inhibited in the OBK of mutant mice. The results provide direct evidence that angiotensin II acting via the AT1a plays a pivotal role in the development of tubulointerstitial fibrosis in UUO.
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 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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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'équipe avaient montré que le LPA contribuait, via le récepteur LPA1, au développement de la fibrose tubulointerstitio (TIF) dans un modèle de MRC chez la souris : l'obstruction urétérale. Dans la première partie de la thèse nous avons étudié l'implication du LPA dans un modèle plus avancé de MRC: la néphrectomie subtotale (SNX) chez la souris. Nos travaux ont montré que 5 mois après chirurgie les souris (SNX) développaient une albuminurie massive associée à une TIF sévère et à une hypertrophie glomérulaire. Chez ces souris la concentration en LPA mesurée par chromatographie liquide en spectrométrie de masse en tandem était augmentée dans l'urine et étroitement corrélée à l'albuminurie et à la TIF. En parallèle, nous avons observé une diminution de l'expression rénale des Lipid-Phosphate Phosphatases (LPP 1, 2 et 3) responsables de l'inactivation du LPA. Nous avons également observé que l'expression rénale des récepteurs LPA1, 2, 3 et 4 était diminuée chez les souris Snx. Nous avons conclu que les effets délétères éventuels du LPA dans le développement de la MRC chez les souris SNX était vraisemblablement lié à une augmentation de sa production rénale plutôt qu'à une sensibilité accrue du rein au LPA. Des travaux antérieurs avaient montré que l'injection de LPA protégeait contre l'apparition des lésions rénales induites par ischémie/reperfusion chez la souris. Une autre étude avait montré que le LPA permettait d'atténuer l'inflammation systémique et les dommages aux organes induits par un choc septique. Dans la deuxième partie de la thèse, nous avons étudié l'influence du LPA sur l'IRA induite par une endotoxémie au LPS (lipopolysaccharide) chez la souris. Nous avons observé que l'injection de LPA permettait d'atténuer l'élévation d'urée et de créatinine plasmatiques, ainsi que l'augmentation d'expression rénale de cytokines inflammatoires (IL-6, TNFa, MCP-1) induites par le LPS. Le LPA a également empêché la baisse d'expression rénale du facteur PGC1a ainsi que les altérations ultra-structurales des mitochondries rénales induites par le LPS. In vitro, le LPA atténue l'augmentation d'expression des cytokines pro-inflammatoires (TNFa et MCP-1) induite par le LPS dans les macrophages RAW264. Enfin, nos travaux ont montré que l'endotoxémie au LPS chez la souris entrainait une réduction de la concentration urinaire de LPA associée à une réduction des enzymes anaboliques LPA (autotaxine et acylglycérol kinase) et une élévation de l'expression de de LPP2, dans le cortex rénal. Nous en avons conclu que l'IRA associée à l'endotoxémie pourrait être liée, au moins en partie, à une réduction de la production rénale de LPA et, par voix de conséquence, de ses effets anti-inflammatoires protecteurs de la fonction rénale. En conclusion, notre travail montre que les variations de production rénale de LPA pourraient jouer un rôle important dans le développement des maladies rénales. L'augmentation du LPA dans les MRC favoriserait ses effets délétères (fibrose, inflammation). Sa réduction dans l'IRA réduirait ses effets anti-inflammatoires. Cibler le catabolisme LPA pourrait donc être une approche intéressante dans le traitement des maladies rénalesBoth chronic kidney diseases (CKD) with consecutive development of end stage renal disease (ESRD) and acute kidney injury (AKI) represent worrying problems for healthcare system due to its increased frequency and the lack of efficient treatments. Lysophosphatidic acid (LPA) is a bioactive lysophospholipid that elicits a wide range of cell responses (proliferation, migration, transformation, contraction etc.) through the activation of specific G protein-coupled receptors (LPA1 to LPA6). In this work we were interested in involvement of the LPA and changes in its metabolism in CKD and AKI. Previous works showed that LPA exerts pro-fibrotic activity and contributes to development of tubulointerstitioal fibrosis (TIF) after ureteral obstruction through activation of LPA1 receptors. In the first part of the thesis we were interested whether LPA signalization is involved in more advanced model of the disease. We found that 5 months after subtotal nephrectomy (SNX) mice develop massive albuminuria, TIF and glomerular hypertrophy compared to control animals. LPA concentration measured by liquid chromatography tandem mass spectrometry was increased in urine but not in plasma of animals. That increase in LPA significantly correlated with albuminuria and TIF. In addition we found a decreased renal expression of lipid phosphate phosphatases (LPP1, 2 and 3) that are responsible for the degradation of LPA by dephosphorylation. Moreover, the expression of LPA1-LPA4 receptors is down-regulated, whereas LPA5 and LPA6 are unchanged. We concluded here that the possible deleterious effect of LPA in the development of CKD in SNX mice was likely related to its increased production rather than an increased sensitivity of the kidney to LPA. Since LPA was reported previously to protect kidney damage in the course of ischemia/reperfusion injury, and that it was able to mitigate the systemic inflammation and organ damage in sepsis, we were interested in second part of the thesis to determine whether exogenous and/or endogenous LPA might protect against sepsis-associated AKI. C57BL/6 mice were treated with exogenous LPA 18:1 1 hour before being injected with the lipopolysaccharide (LPS) and AKI was analyzed after 24h. LPA pre-treatment significantly mitigated the LPS-induced elevation of plasma urea and creatinine, lessened the up-regulation of inflammatory cytokines (IL-6, TNFa, MCP-1) and completely prevented the down-regulation of peroxisome proliferator-activated receptor gamma coactivator 1-alpha (PGC1a) in kidney. LPA also prevented LPS-mediated alterations of renal mitochondria ultrastructure. In vitro, pre-treatment with LPA 18:1 (10 µM) significantly attenuated LPS-induced up-regulation of the pro-inflammatory cytokines (TNFa and MCP-1) in RAW264 macrophages. In addition we found that LPS led to the reduction of urinary LPA concentration that was associated with a reduction in LPA anabolic enzymes (autotaxin and acylglycerol kinase), and an elevation in LPA catabolic enzyme (lipid phosphate phosphatase 2) expression in kidney cortex. We concluded hereby that exogenous LPA exerts protection against endotoxemia-induced kidney injury. Moreover, the observation that LPS reduces the renal production of LPA suggests that sepsis-associated AKI could be mediated, at least in part, by alleviation of the protective action of endogenous LPA. In general our work shows that LPA local metabolism is altered in both forms of kidney diseases. In course of sepsis-induced AKI LPS leads to increased local catabolism of LPA leading to low availability of the phospholipid and alleviating its protective effect whereas in advanced CKD the local catabolism of the phospholipid is decreased with subsequent increase of urine LPA that favors development of the disease. Targeting LPA catabolism can be an interesting approach in treatment of kidney diseases
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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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博士國立成功大學
基礎醫學研究所
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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. development, proliferation, differentiation, apoptosis and tumorigenesis. We were curious about the role of matrix stiffness in the physiological and pathological development in the kidney. In the first part of study, we focused on the interplay between chemical cues and physical cues from ECM on the regulation of cell behaviors. Primary culture of mice PTECs (mPTECs) gradually lost their tubular morphology and differentiated properties with the increase of cell spreading and proliferation when cultured on stiff matrix. Furthermore, the cells responded to TGF-beta1 and underwent epithelial-mesenchymal transition (EMT) under stiff matrix. However, these phenomena were reversed when cells were cultured on soft matrix. On the other hand, an increase of collagen amount in soft matrix also facilitated cell spreading, de-differentiation, proliferation, and TGF-beta1-induced EMT, indicating that both soft matrix and basement membrane signals were required for the maintenance of the physiological function of mPTECs. Furthermore, we identified that ERK activation controlled by stiff matrix contributed to all the cellular behaviors regulated by stiff matrix. In the second part of study, we attempted to verify the novel mechanism of how matrix stiffness controls cell proliferation and its significance on the pathogenesis of chronic tubulointerstitial fibrosis. Based on the results obtained from oligo-microarray and experiments, we purposed Krüppel-like factors 5 (Klf5) and Krüppel-like factors (Klf4) as the possible candidates. Stiff matrix upregulated Klf5 and downregulated Klf4 in mRNA and protein levels via ERK signal. Suppression of Klf5 or forced expression of Klf4 stunted stiff matrix-induced cell proliferation as confirmed by nuclear Cyclin D1 and EdU intensity, indicating that Klf5/Klf4 served as the positive/negative regulators of cell proliferation, respectively. Furthermore, we suggested that mechanosensitive Yes-associated protein 1 (YAP1) may contribute to stiff matrix induced Klf5 upregulation through preventing Klf5 degradation. Finally, we applied the in vivo model of unilateral ureteral obstruction to induce fibrosis. Notably, alleviation of tissue stiffening by blocking collagen crosslinker efficiently suppressed tubular dilatation and abnormal proliferation with the upregulation of ERK/YAP1/Klf5/Cyclin D1 axis and the downregulation of Klf4. In conclusion, we demonstrate that how mechanical cues are involved in the regulation of renal physiological functions and pathological progression via mechanosensitive transcription factors. This study provides us a new insight into the pathogenesis of chronic tubulointerstitial fibrosis from the physical view.
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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 des souris transgéniques surexprimant l’angiotensinogène de rat dans les cellules de leurs tubules proximaux rénaux (RPTCs) ont permis de démontrer l’importance du RAS intrarénal dans l’induction de l’hypertension et les dommages rénaux. Nous avons également observé que l’expression rénale de l’ACE2 et les niveaux urinaires d’ANG 1-7 sont plus faibles chez les souris Akita (diabète de type 1) et qu’un traitement avec des bloqueurs du RAS permet de normaliser l’expression de l’ACE2 et de prévenir le développement de l’hypertension dans le modèle des souris Akita. Dans un milieu diabétique, à la fois la glycémie et l’angiotensine II (Ang II) peuvent induire la génération des espèces réactives de l’oxygène (ROS), contribuant ainsi aux dommages rénaux. Afin d’explorer la relation entre les ROS, ACE2 et la DN, nous avons créé des souris Akita transgéniques surexprimant la catalase (Cat) dans les RPTCs, en croisant des souris Akita diabétique de type 1 à notre modèle de souris transgéniques surexprimant la Cat de rat dans les RPTCs. Dans une seconde étude, des souris Akita ont été traitées avec l’Ang 1-7 ou une combinaison d’Ang 1-7 et de son antagoniste, A779, afin d’étudier la relation entre l’action de l’Ang 1-7, l’hypertension systolique (sHTN), le stress oxydatif, les dommages rénaux, ACE2 et l’expression du récepteur Mas.
Nos résultats ont montré que la surexpression de Cat atténue le stress oxydatif rénal; prévient l’hypertension, améliore le taux de filtration glomérulaire, l’albuminurie, l’hypertrophie rénale, la fibrose tubulo-interstitielle et l’apoptose tubulaire; et supprime l’expression des gènes profibrotiques et proapoptotiques dans les RPTCs des souris Akita Cat-Tg lorsque comparées aux souris Akita. De plus, la surexpression de Cat dans les RPTC des souris Akita normalise l’expression rénale de l’ACE2 et les niveaux urinaires d’Ang 1-7.
D’autre part, l’administration d’Ang 1-7 prévient l’hypertension systémique, normalise le ratio albumine/créatinine urinaire et atténue l’hyperfiltration glomérulaire des souris Akita, sans affecter la glycémie sanguine. De plus, le traitement avec l’Ang 1-7 atténue aussi le stress oxydatif et l’expression de la NADPH oxydase, Agt, ACE, TGF-β1 (transforming growth factor-β1) et collagène IV, tout en augmentant l’expression de l’ACE2 et du récepteur Mas dans les reins des souris Akita. Ces effets sont renversés par la co-admininstration d’A779.
Ces résultats démontrent que la surexpression de Cat prévient l’hypertension et la progression de la néphropathie, en plus de mettre en lumière l’importance du stress oxydatif intrarénal et l’expression de l’ACE2 comme facteurs contribuant à l’hypertension et les dommages rénaux observés dans le diabète. En outre, nos données suggèrent que l’Ang 1-7 joue un rôle protecteur dans l’hypertension et les dommages aux RPTC dans le diabète, principalement en réduisant les voies de signalisations du stress oxydatif dans les reins et en normalisant l’expression de l’ACE2 et du récepteur Mas. Nos résultats indiquent aussi que l’Ang 1-7 pourrait agir comme un agent thérapeutique potentiel dans le traitement de l’hypertension systémique et les dommages rénaux observés dans le diabète. En conséquence, l’Ang 1-7 est responsable du rôle protecteur de l’ACE2 dans l’hypertension et la DN.It is well accepted that renin-angiotensin system (RAS) activation plays an important role in the development of hypertension and diabetic nephropathy (DN). With the discovery of angiotensin-converting enzyme-2 (ACE2) and recognition of MAS as the receptor of Angiotensin 1-7 (Ang 1-7), new players in RAS, ACE2/Ang 1-7/MAS axis, have been identified to counteract the effect of ACE/Ang II/ AT1 axis. Evidence implicates the intrarenal RAS’s contribution to DN. Previous studies from our laboratory using transgenic mice overexpressing rat Angiotensinogen (Agt) in their renal proximal tubular cells (RPTCs) have demonstrated the importance of the intrarenal RAS in renal damage and the induction of hypertension. We also recently observed that renal ACE2 expression and urinary Ang 1–7 were lower in type 1 diabetic Akita mice and that treatment with RAS blockers normalized ACE2 expression and prevented hypertension development in these Akita mice. In the diabetic milieu, both glycemia and angiotensin II (Ang II) can induce reactive oxygen species (ROS) generation, which contributes to kidney injury. To explore the relationship among ROS, ACE2 and DN, we created Akita transgenic mice overexpressing catalase (Cat) in RPTCs by crossbreeding type I diabetic Akita mice with our established transgenic mice overexpressing rat Cat in RPTCs. In another study, Akita mice were treated with Ang 1-7 or combination of Ang 1-7 and its antagonist, A779, to investigate the relations between Ang 1-7 action, systolic hypertension (sHTN), oxidative stress, kidney injury, ACE2 and Mas receptor expression. Our results showed that overexpression of Cat attenuated renal oxidative stress; prevented hypertension; ameliorated glomerular filtration rate, albuminuria, kidney hypertrophy, tubulointerstitial fibrosis, and tubular apoptosis; and suppressed profibrotic and proapoptotic gene expression in RPTCs of Akita Cat-Tg mice compared with Akita mice. Furthermore, overexpression of Cat in RPTCs of Akita mice normalized renal ACE2 expression and urinary Ang 1–7 levels. On the other hand, Ang 1-7 administration prevented systemic hypertension, normalized urinary albumin/creatinine ratio and attenuated glomerular hyperfiltration without affecting blood glucose levels in Akita mice. Furthermore, Ang 1-7 treatment also attenuated oxidative stress and the expression of NADPH oxidase 4, Agt, ACE, transforming growth factor-β1 (TGF-β1) and collagen IV, and increased the expression of ACE2 and Mas receptor in Akita mouse kidneys. These effects were reversed by co-administration of A779. These data demonstrated that Cat overexpression prevents hypertension and progression of nephropathy and highlight the importance of intrarenal oxidative stress and ACE2 expression contributing to hypertension and renal injury in diabetes. Furthermore, our data suggest that Ang 1-7 plays a protective role in hypertension and RPTC injury in diabetes, predominantly through decreasing renal oxidative stress-mediated signaling and normalizing ACE2 and Mas receptor expression. Our results also indicate Ang 1-7 as a potential therapeutic agent for treatment of systemic hypertension and kidney injury in diabetes. Therefore, Ang 1-7 mediates the major protective role of ACE2 in the hypertension and DN.
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 reduced glomerular filtration rate (GFR), whereas the blood pressure is usually normal or moderately increased. Tubular abnormalities are common, including type 2 (proximal) renal tubular acidosis, Fanconi syndrome, nephrogenic diabetes insipidus, and type 1 (distal) renal tubular acidosis, with hypokalaemia and nephrolithiasis. Radiology exams reveal shrunken kidneys, sometimes with irregular outlines. A renal biopsy is often required for the diagnosis of CTIN and its aetiology. The treatment of CTIN mainly involves discontinuation of exposure to nephrotoxins and specific therapy of renal infections, urinary tract obstruction, or underlying systemic diseases. Agents like ACE inhibitors and pirfenidone, which might reduce interstitial inflammation and fibrosis, are still under clinical evaluation.
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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 chronic pattern, although acute forms of TIN may also occur. Furthermore, inflammation may be granulomatous (as in sarcoidosis or Crohn’s disease) or non-granulomatous. Immunofluorescence staining can sometimes reveal immune complex deposits and even antitubular basement membrane autoantibodies. Systemic immunosuppressive therapies are almost always required to prevent progression to irreversible interstitial fibrosis, tubular atrophy, and end-stage renal disease.
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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 injury is postulated to involve cell-mediated immunity, supported by the observation that T cells are the predominant cell type comprising the interstitial infiltrate. A humoral response underlies rare cases of ATIN, in which a portion of a drug molecule (i.e. methicillin) may act as a hapten, bind to the tubular basement membrane (TBM), and elicit anti-TBM antibodies. The classic symptoms of fever, rash, and arthralgia may be absent in up to two-thirds of patients. Diagnostic studies, such as urine eosinophils and renal gallium-67 scanning provide only suggestive evidence. Renal biopsy remains the gold standard for diagnosis, but it may not be required in mild cases or when clinical improvement is rapid after removal of an offending medication. Pathologic findings include interstitial inflammation, oedema, and tubulitis. The time until removal of such agents and the severity of renal biopsy findings provide the best prognostic value for the return to baseline renal function. Poor prognostic indicators are the long duration of AKI (> 3 weeks), a patient’s advanced age, and the high degree of interstitial fibrosis. Early recognition and appropriate therapy are essential to the management of drug-induced ATIN, because patients can ultimately develop chronic kidney disease. The mainstay of therapy is timely discontinuation of the causative agent, whereas controversy persists about the role of steroids.
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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 drug-induced CTIN largely depends on the history of exposure to a nephrotoxic drug. Clinical investigations may show modest elevation in serum creatinine, evidence of tubular dysfunction (e.g. renal tubular acidosis), or Fanconi syndrome (i.e. aminoaciduria, glycosuria, hypophosphataemia, and hypouricaemia). 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. Analgesic nephropathy is possibly still the most common category of CTIN worldwide. The amount of phenacetin-acetaminophen combination required to cause CTIN has been estimated to be at least 2–3 kg over many years. Lithium-induced CTIN occurs in a small subset of patients receiving long-term lithium therapy, who have had repeated episodes of lithium toxicity, with high serum drug levels. CTIN induced by ciclosporin or tacrolimus is common among patients receiving kidney, heart, liver, and pancreas transplants. The mechanism appears to be dependent largely on the potent vasoconstrictive effects of these drugs. The recognition of a potential association between a patient’s renal disease and exposure to a drug is crucial, because, unlike many other forms of renal disease, drug-induced CTIN can be prevented and even reversed, by avoiding additional drug exposure.
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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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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 histologic changes include arteriolosclerosis, glomerulosclerosis, and tubulointerstitial fibrosis. In patients with urate nephropathy, hypertension is common, but usually there is only mild proteinuria and a slight increase in serum creatinine. The reduction of serum uric acid, using xanthine oxidase inhibitors and perhaps low-purine diet, is the mainstay of therapy. There is current research around the question of whether it is beneficial to lower serum uric acid in asymptomatic patients with renal disease or with cardiovascular risk factors.
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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 symmetrically shrunken, smooth-shaped kidneys, with interstitial fibrosis, mild interstitial inflammation, and tubular atrophy. Diagnosis is usually based upon positive family history of BEN, past or current residence in endemic regions, tubular proteinuria, tubular dysfunctions (such as urine acidification defects, salt wasting, and impaired excretion of ammonia, uric acid, and phosphate), scant urinary sediment, bilateral and symmetrically reduced kidney size, accompanied by severe anaemia, disproportionate to the degree of GFR reduction. There is no specific therapy for BEN; patients should therefore be treated as all patients with chronic kidney disease, in general. The use of distant water supplies or moving to another residence area should be advised to affected families. Careful evaluation for urothelial cancers is mandatory in patients with haematuria.
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 (<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 (<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 (>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 (<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.
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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