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1
Curci, C., and G. Castellano. "Fibrosi renale ed anemia: una storia tutta da scoprire." Giornale di Clinica Nefrologica e Dialisi 24, no. 1 (January 24, 2018): 27–28. http://dx.doi.org/10.33393/gcnd.2012.1111.
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Ad oggi l'origine dei fibroblasti, le principali cellule responsabili dello sviluppo della fibrosi renale, è ancora incerta. In un recente lavoro pubblicato da Asada e colleghi, gli Autori dimostrano che la maggior parte dei fibroblasti secernenti eritropoietina nel rene normale hanno un'origine extra renale e provengono da cellule della Cresta Neurale. Durante lo sviluppo della fibrosi renale, queste cellule trans-differenziano in miofibroblasti, perdendo la loro capacità intrinseca di produrre eritropoietina. Questi interessanti dati potrebbero rappresentare il punto di partenza per lo sviluppo di nuovi farmaci capaci da un lato di ridurre la fibrosi renale e dall'altro di preservare la produzione di eritropoietina.
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Lombardi, Duccio. "Rigenerazione e Proteinuria, Quando L'albumina Fa La Differenza." Giornale di Clinica Nefrologica e Dialisi 26, no. 1 (October 3, 2014): 65–68. http://dx.doi.org/10.33393/gcnd.2014.864.
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Nella malattia renale cronica, il rischio di fallimento d’organo dipende dal grado di severità della proteinuria, la quale è determinata dal numero di podociti persi e dalla conseguente fibrosi glomerulare. Esistono, tuttavia, numerose evidenze cliniche e sperimentali che suggeriscono la possibilità di remissione della malattia renale e, in alcuni casi, persino di regressione del danno, quando ancora l’istologia dell’organo non risulti totalmente compromessa. Tali risultati sono ottenuti in particolare mediante l’impiego di terapie con effetti anti-proteinurici. Nuove evidenze sperimentali suggeriscono perché il blocco della perdita di proteine urinarie permetta la remissione della malattia renale cronica. In un recente articolo di Peired et al., è, per la prima volta, dimostrato come l’albuminuria blocchi il processo rigenerativo a causa del sequestro attuato dall’albumina ai danni della vitamina A, noto agente differenziativo per popolazioni di progenitori staminali presenti in vari organi. La conseguente perdita della vitamina A, complessata all’albumina, con le urine, impedisce, quindi, l’attivazione dei progenitori renali residenti nella capsula di Bowman, bloccando sul nascere la risposta rigenerativa e permettendo la progressione della malattia renale cronica.
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Di Lullo, L., F. Floccari, R. Rivera, A. Bellasi, E. Ferramosca, A. De Pascalis, M. Timio, M. Malaguti, and A. Santoboni. "La patologia del pericardio e la malattia renale cronica." Giornale di Clinica Nefrologica e Dialisi 24, no. 2 (January 26, 2018): 62–70. http://dx.doi.org/10.33393/gcnd.2012.1141.
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I pazienti affetti da malattia renale cronica possono andare incontro a tutta una serie di patologie che colpiscono il pericardio ma, sicuramente, alcune entità nosologiche sono più frequenti di altre. Gli ultimi decenni hanno assistito, per fortuna nostra e dei nostri pazienti, a un netto miglioramento per quanto concerne i protocolli terapeutici per i pazienti nefropatici e le forme tipiche di pericardite uremica, così frequenti negli anni passati, sono ormai uno sbiadito ricordo. È tuttora frequente osservare pazienti con versamento pericardico (idiopatico, ovvero secondario a malattie sistemiche), soprattutto per quanto concerne i pazienti sottoposti a trattamenti depurativi extracorporei ed i pazienti che iniziano il trattamento dialitico in condizioni di emergenza/urgenza (ad esempio, pazienti affetti da scompenso cardiaco congestizio); il versamento pericardico viene schematicamente classificato in lieve, moderato e severo in base all'interessamento più o meno globale del pericardio. Meno frequenti sono gli episodi di pericardite acuta (anch'essa idiopatica o secondaria), spesso su base virale, neoplasticae/o immunologica (vedi pazienti trapiantati in terapia immunosoppressiva). Le forme di pericardite costrittiva sono più rare a documentarsi in corso di malattia renale cronica e, in genere, rappresentano lo stadio finale di diverse patologie sistemiche: l'esito finale è, in genere, la fibrosi pericardica. (Cardionephrology)
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Masola, V., S. Granata, M. Proglio, G. Gambaro, A. Lupo, and G. Zaza. "Eparanasi: un nuovo biomarker di fibrosi e un potenziale target farmacologico per ridurre la progressione del danno renale cronico." Giornale di Clinica Nefrologica e Dialisi 24, no. 2 (January 26, 2018): 10–15. http://dx.doi.org/10.33393/gcnd.2012.1131.
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Il trattamento poli-farmacologico ha determinato, nel corso degli anni, un significativo rallentamento della progressione della malattia renale cronica verso lo stadio di uremia terminale, ma siamo ancora distanti dallo sviluppo di interventi terapeutici in grado di bloccare questo inesorabile e irreversibile processo. Studi clinico-patologici hanno chiaramente dimostrato che il principale elemento coinvolto nel danno renale è la fibrosi tubulo-interstiziale e che il meccanismo patogenetico alla base di questa condizione ha inizio in larga parte nel compartimento tubulare. In particolare, il processo di transizione epitelio-mesenchimale gioca un ruolo importante nella genesi del danno cronico. Durante questo processo, le cellule epiteliali tubulari subiscono un incremento significativo di markers di superficie di natura mesenchimale e, grazie al rimodellamento del citoscheletro e alla degradazione della membrana basale, sono in grado di migrare nell'interstizio dove svolgono un ruolo chiave nel processo patogenetico. In questo contesto, sembra avere un ruolo chiave l'enzima eparanasi, una endo-β-D-glucuronidasi che taglia le catene dell'eparan-solfato a livello di siti specifici intracatena, e partecipa attivamente alla degradazione e al rimodellamento della matrice extracellulare. La degradazione dei vari costituenti dell'ECM, inclusi i proteoglicani eparan-solfato fa-vorisce il rilascio di fattori trofici quali il FGF-2 che induce l'espressione dei marcatori mesenchimali alfa-SMA, VIM e FN, porta alla degradazione della membrana basale mediante la secrezione di metalloproteinasi della matrice ed aumenta la motilità cellulare. L'epressione dell'eparanasi è regolata da fattori di trascrizione, dalla metilazione del DNA e da varie molecole endogene. L'importanza di questo enzima è stata confermata clinicamente dal riscontro di una sua iperespressione in preparati istologici di biopsie effettuate in soggetti affetti da nefropatie croniche (per esempio, nefropatia diabetica). Pertanto visto l'importante ruolo dell'eparanasi sono in fase di standardizzazione numerose strategie per inibire la sua espressione genica e/o la sua attività enzimatica. Infine, è stato proposto il suo possibile utilizzo come biomarker di progressione del danno tubulo-interstiziale da utilizzare routinariamente in ambito nefrologico.
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Galiza, Aline Xavier Fialho, Luísa Mariano Cerqueira da Silva, Luísa Grecco Correa, Eduardo Gonçalves, Aline do Amaral, Pâmela Caye, Júlia Vargas Miranda, et al. "Perfil epidemiológico e alterações anatomopatológicas de biópsias de rins esquerdos de sete cães acometidos por Dioctophyme renale em rim direito." Research, Society and Development 10, no. 6 (June 8, 2021): e50310615703. http://dx.doi.org/10.33448/rsd-v10i6.15703.
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A dioctofimatose é uma doença causada pelo nematódeo Dioctophyme renale, que acomete principalmente rins direitos de cães e ao penetrar na cápsula renal causa destruição e atrofia do parênquima, podendo restar apenas uma cápsula fibrosa do rim afetado. Dessa forma, buscando estabelecer as condições histológicas do rim contralateral (RCL) dos animais acometidos pela parasitose, o objetivo desse estudo foi descrever o perfil epidemiológico e alterações anatomopatológicas encontradas em biópsias de rins esquerdos de sete cães submetidos a nefrectomia em decorrência de parasitismo por Dioctophyme renale em rim direito. Informações referentes à raça, sexo, faixa etária, histórico clínico, e alterações histológicas, foram tabulados e avaliados. Para as biópsias foi utilizado o método incisional. Microscopicamente em três amostras (3/7) havia glomerulonefrite membranosa, em quatro (4/7) observou-se infiltrado inflamatório de células mononucleadas e fibrose focal em duas amostras analisadas (2/7). Em uma amostra havia glomeruloesclerose segmentar focal e em outra não havia alteração histológica. Foram contabilizadas mais de uma alteração em uma única amostra. As alterações encontradas nas biópsias indicam algum comprometimento do rim remanescente e sugerindo que possa haver ação sistêmica, ou pelo menos inter-renais das enzimas esofágicas produzidas pelo parasito Este estudo espera contribuir para o estadiamento das funções renais do rim remanescente e auxiliar no estabelecimento do tratamento em cada caso.
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Wolf, G., and G. Lehmann. "Knochenhistologie bei renaler Osteodystrophie." Osteologie 17, no. 03 (2008): 107–11. http://dx.doi.org/10.1055/s-0037-1619855.
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ZusammenfassungChronische Nierenfunktionseinschränkungen führen am Knochen zu Stoffwechsel- und Strukturschäden, deren differenzierte Beurteilung vor allem durch die histologische Aufarbeitung von Knochenbioptaten möglich ist. Die internationale Klassifikation unterscheidet vier Formen der renalen Osteodystrophie (ROD). Dabei wird zwischen renalem Hyperparathyreoidismus (Osteitis fibrosa), Osteomalazie, gemischter urämischer Osteodystrophie und adynamer renaler Knochenerkrankung unterschieden. In der Arbeit werden die Methoden der Knochenentnahme und -bearbeitung, typische histologische Befunde sowie die Indikationen zur osteologischen Beckenkammbiopsie dargestellt.
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Solomon, Garron J., Elizabeth Wu, and Paul Peter Rosen. "Nephrogenic Systemic Fibrosis Mimicking Inflammatory Breast Carcinoma." Archives of Pathology & Laboratory Medicine 131, no. 1 (January 1, 2007): 145–48. http://dx.doi.org/10.5858/2007-131-145-nsfmib.
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Abstract Nephrogenic systemic fibrosis, previously known as nephrogenic fibrosing dermopathy, is a newly recognized systemic fibrosing disorder primarily affecting patients with chronic renal failure. Patients with skin involvement often develop papules and plaques with peau d'orange surface changes. The lower extremities and trunk are most commonly affected. The most important histologic differential diagnosis is with scleromyxedema. To our knowledge, we report the first case of nephrogenic systemic fibrosis involving the breasts of a 61-year-old woman with end-stage renal disease, clinically mimicking inflammatory breast carcinoma. We propose that nephrogenic systemic fibrosis be considered in the differential diagnosis as a rare possibility when cutaneous changes in the breast suggest inflammatory breast carcinoma in a patient with renal failure.
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Gibson, Sarah E., Carol F. Farver, and Richard A. Prayson. "Multiorgan Involvement in Nephrogenic Fibrosing Dermopathy: An Autopsy Case and Review of the Literature." Archives of Pathology & Laboratory Medicine 130, no. 2 (February 1, 2006): 209–12. http://dx.doi.org/10.5858/2006-130-209-miinfd.
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Abstract Nephrogenic fibrosing dermopathy is a recently recognized, scleromyxedema-like fibrosing skin condition that occurs in individuals with acute or chronic renal failure. Although the early descriptions of this disorder describe a purely cutaneous disease process, 2 recent autopsy reports have identified apparent multiorgan fibrosis with involvement of skeletal muscle, myocardium, lungs, kidneys, and testes. We describe a 23-year-old man with nephrogenic fibrosing dermopathy and significant fibrosis of the atrial myocardium and dura mater, which was identified at autopsy. Dural fibrosis is a previously undescribed systemic manifestation of nephrogenic fibrosing dermopathy. The literature is reviewed.
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D'Attoma, N., E. Residori, R. Mariotto, R. Cerini, M. Gregianin, and A. Lotto. "L'imaging della fibrosi retroperitoneale primitiva: Primitive retroperitoneal fibrosis imaging." Urologia Journal 65, no. 2 (April 1998): 276–86. http://dx.doi.org/10.1177/039156039806500216.
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Idiopathic retroperitoneal fibrosis (RPF) is characterised by the development of a fibrotic mass in the prelumbar or presacral area which becomes clinically significant when it causes ureteral obstruction. New imaging techniques have improved accuracy of the morphological approach to the disease, but urography and sequential renal scintigraphy are still important for assessing ureteral involvement. The role of imaging techniques is discussed and current diagnostic and therapeutic tools are evaluated.
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Valle, Bruna dos Santos, Pamela Caye, Carolina da Fonseca Sapin, Luisa Mariano Cerqueira da Silva, Júlia Vargas Miranda, Gustavo Antonio Boff, Luísa Grecco Corrêa, Josaine Cristina da Silva Rappeti, Cristina Geverh Fernandes, and Fabiane Borelli Grecco. "Alterações anatomopatológicas e parâmetros bioquímicos séricos e urinários em cães com diagnóstico de Dioctophyme renale." Research, Society and Development 11, no. 12 (September 22, 2022): e515111234874. http://dx.doi.org/10.33448/rsd-v11i12.34874.
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Animais acometidos por Dioctophyme renale geralmente são assintomáticos e o diagnóstico definitivo é o exame de imagem e o anatomopatológico. Desta forma, este estudo tem como objetivo descrever os parâmetros bioquímicos de sangue e urina e exames anatomopatológicos de 15 cães diagnosticados com D. renale na região de Pelotas-Rio Grande do Sul-RS. Foram obtidos dados de anamnese e exames laboratoriais sorológicos e urinários de protocolos de atendimento de animais no Hospital de Clínicas Veterinárias da Universidade Federal de Pelotas-UFPel, e análises anatomopatológicas pelo Serviço de oncologia SOVET/UFPEL. Foram observadas alterações macroscópicas em todas as amostras, sendo a atrofia do parênquima renal e espessamento da cápsula as mais frequentes. O exame histopatológico revelou substituição do tecido renal por fibrose, glomeruloesclerose e eventualmente presença de ovos do parasito. Em relação aos parâmetros sanguíneos e urinários, apenas um dos animais apresentou alteração nos valores de referência de ureia sérica e todos apresentaram creatinina dentro dos parâmetros considerados normais. Na urinálise havia presença de proteínas, sangue oculto, cilindros granulares, cristais e ovos do parasito. Os testes estatísticos mostraram correlação entre a evolução e grau das lesões renais com parâmetros alterados, porém mesmo em cães que apresentavam lesões de insuficiência renal aguda (IRA), haviam lesões concomitantes de insuficiência renal crônica (IRC). Como conclusão dos dados obtidos, parâmetros séricos e urinários isoladamente não refletem o real comprometimento do rim afetado, mas associados ao grau de lesão renal são aliados para um melhor estadiamento dos animais acometidos.
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McDonald, Glenn A., Pradip Sarkar, Helmut Rennke, Elaine Unemori, Raghu Kalluri, and Vikas P. Sukhatme. "Relaxin increases ubiquitin-dependent degradation of fibronectin in vitro and ameliorates renal fibrosis in vivo." American Journal of Physiology-Renal Physiology 285, no. 1 (July 2003): F59—F67. http://dx.doi.org/10.1152/ajprenal.00157.2002.
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Fibronectin, a large adhesive glycoprotein, is a prominent constituent of the extracellular matrix. Abnormalities in fibronectin homeostasis occur in numerous disease states, ranging from primary fibrosing conditions to neoplastic transformation. We demonstrate that fibronectin is a target protein substrate for ubiquitin-dependent degradation. Coimmunoprecipitation experiments and confocal microscopy demonstrated ubiquitin-fibronectin interaction. In an in vitro model of renal fibrosis, relaxin, an insulin-like growth factor, increased ubiquitin-dependent fibronectin degradation. Relaxin also was evaluated in an anti-glomerular basement membrane model of renal fibrosis. Animals treated with relaxin experienced renoprotection, manifested by decreased serum creatinine and proteinuria. Histological evaluation of kidney sections from animals treated with relaxin showed decreased glomerulosclerosis and interstitial fibrosis. We conclude that relaxin might be developed as a useful agent for the treatment of renal fibrosis.
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M, Lubis, Alvarino Alvarino, Tofrizal Tofrizal, and Erkadius Erkadius. "Pengaruh Pemberian Valsartan Dan Kurkumin Terhadap Pembentukan Fibrosis Di Tubulus Proksimal Ginjal Akibat Obstruksi Ureter Unilateral pada Tikus Wistar." Jurnal Kesehatan Andalas 2, no. 1 (January 1, 2013): 01. http://dx.doi.org/10.25077/jka.v2i1.53.
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AbstrakPendahuluan: Obstruksi ureter adalah kondisi terhalangnya aliran urin dari ginjal ke buli-buli, adanya obstruksi pada ureter memperlambat laju filtrasi glomerulus dan dapat menyebabkan kerusakan parenkim ginjal. Fibrosis pada ginjal yang obstruksi timbul melalui dua mediator yaitu tumor nekrotik factor (TNF-α) dan angiotensin II. Penghambatan kedua mediator ini akan menurunkan tingkat fibrosis di tubulus proksimal ginjal akibat obstruksi. Zat yang bisa menghambat TNF-α salah satunya adalah kurkumin sedangkan Angitensin II dapat dihambat dengan valsatran. Metode: Penelitian ini merupakan penelitian eksperimental, tikus wistar dibagi dalam dua kelompok dengan jumlah tiap kelompok adalah 15 ekor. Proksimal ureter kanan diikat dan kelompok perlakuan 1 sebagai kontrol diberi valsatran, kelompok perlakuan2 diberi valsartan dan kurkumin. Pemberian oral, dimana obat dilakukan pengenceran. Hari ke lima belas dilakukan pengambilan ginjal tikus wistar, diperiksa histologi. Pembentukan fibrosis di tubulus proksimal dianalisa dengan uji statistik chisquare dengan koreksi Yates dan t test, sedang terbentuknya degenerasi hidrofik dan terbentuknya atrofi pada tubulus proksimal dianalisa dengan uji statistik t test. Hasil: Adanya perbedaan bermakna perubahan pembentukan fibrosis di tubulus proksimal ginjal antara kelompok perlakuan dan kontrol ( Chi Squqre didapat nilai p ≤ 0,001 dan dengan t test didapat nilai p ≤ 0,000). Terbentuknya degenerasi hidrofilik di tubulus proksimal ginjal terdapat perbedaan bermakna terbentuknya degenerasi hidrofilik kelompok perlakuan dan kelompok kontrol ( t test didapatkan nilai p ≤ 0,000). Terbentuknya atrofi di tubulus proksimal terdapatt perbedaan bermakna terbentuknya atrofi di tubulus proksimal ginjal kelompok perlakuan dan kelompok kontrol ( t test didapat nilai p ≤ 0,000). Kesimpulan: Ada perbedaan pengaruh pemberian valsartan dan valsartan + kurkumin terhadap pembentukan fibrosis di tubulus proksimal ginjal. Perbedaan bermakna terbentuKata kunci: Obstruksi ureter, Valsartan, Kurkumin, Fibrosis, Degenerasi hidrofilik, AtrofiAbstractIntroduction: ureter obstruction is a condition where is an obstacle for urine flow from renal to blast (vesica urinaria). The obstruction in ureter will decrease glomerulus filtration flow and it destroys renal parenchym. Fibroses in obstructed renal present through two mediators, there are necrotizing tumor factors-α (TNF-α) and angiotension-II. Obstruction of this two mediators will decrease fibroses grading in proximal tubules of renal caused by obtruction. One of TNF-α inhibitors is curcumene and angiotension-II will be obstructed by valsartan. Methods: this experiment is kind of experimental type using animal experiment (Wistar Mice). Wistar Mice are divided into two groups, each group consist of 15 mice, so the total are 30 mice. This animals tighted with at proximal ureter The first group is control one, given valsartan. The second group is given valsartan and curcumene. Oral route and dilution before given. Medicine is given use 1 cc spuit. Giving action in 14 days. The fifteenth day, we take renal of Wistar and do histology examination. Significant difference between fibroses forming in proximal tubulus analyzed by Chi Square Statistic Test with correction of Yates and T-Test, beside that, hydofic degeneration and atrophy in proximal tubulus analyzed by T-Test Statistic Test. Result: there is significant difference in forming of fibroses in proximal tubules of renal between action group and controlled group (Chi Square with p ≤ 0.0001 and T-Test with p ≤ 0.000). In hydrophilic degeneration forming in proximal tubules gotten significant difference between two groups ( T-Test with p ≤ 0.000). In atrophy forming in proximal tubules, there is important difference between two groups (T-Test with p ≤ 0.000).Concultion. There is an effect in giving valsartan and curcumene to fibroses forming in proximal tubules of renal. There is significant difference in hydrophilic degeneration in proximal tubules of renal. And also there is important difference in atrophy forming in proximal tubules between two groups.Keywords:ureter obstruction, valsartan, curcumene, fibroses, hydrophilic degeneration, atrophy.
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Rossi, Y. A., D. C. Sousa, J. R. Rocha, V. Rodrigues, and F. G. G. Dias. "Fibrous osteodystrophy due to secondary renal hyperparathyroidism in a senile dog." Arquivo Brasileiro de Medicina Veterinária e Zootecnia 74, no. 6 (December 2022): 1089–95. http://dx.doi.org/10.1590/1678-4162-12713.
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ABSTRACT Renal hyperparathyroidism stands out among the complications of kidney disease in dogs due to phosphorus retention with a predisposition to hypocalcemia, parathyroid hormone stimulation with mobilization of calcium from the bones, characterizing fibrous osteodystrophy, unusual in the elderly. The objective was to report it in 12-year-old Labrador with polyuria, polydipsia, and emesis for five months due to maxillary and mandibular volume increase, followed by loosely fixed teeth, and facial deformity. Blood tests showed anemia, thrombocytosis, azotemia, hypoalbuminemia and hyperphosphatemia and urinalysis showed low density, glycosuria, proteinuria, and moderate caudate and transitional epithelial cells. Oral x-rays showed loss of dental bone support and decreased bone radiopacity. Chest radiographs showed decreased density in the ribs and costochondral junction; on the other hand, organs of the cardiorespiratory system showed no changes. The electrocardiogram and echocardiogram did not show impairment. Abdominal ultrasound revealed kidneys with asymmetry, increased echogenicity of the cortical and poorly preserved cortico-medullary definition. Oral histopathology showed intense fibroplasia associated with bone reabsorption. Support therapy was instituted, but the patient died ten days after consultation. Thus, although uncommon in the elderly, fibrous osteodystrophy should be investigated in dogs with advanced-stage chronic kidney disease and, even with conservative therapies, the prognosis is unfavorable.
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Oelzner, Peter, Kerstin Amann, and Gunter Wolf. "Nierenbeteiligung bei Kollagenosen – Teil 2: Antiphospholipid-Syndrom, primäres Sjögren-Syndrom, systemische Sklerose." Aktuelle Rheumatologie 45, no. 02 (March 12, 2020): 163–72. http://dx.doi.org/10.1055/a-1089-7347.
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ZusammenfassungRenale Manifestationen bei Antiphospholipid-Syndrom (APS), primärem Sjögren-Syndrom (pSS) und systemischer Sklerose (SSc) unterscheiden sich erheblich in Pathogenese, Histologie, klinischem Erscheinungsbild, Prognose und therapeutischer Konsequenz. Die Häufigkeit APS-assoziierter Nierenveränderungen wird mit 10–40% angegeben. Das APS kann sich an der Niere in Form von renaler Hypertonie, Thrombosen oder Stenosen der Nierenarterien, Niereninfarkten, Nierenvenenthrombose und intrarenaler Vaskulopathie (APS-Nephropathie) manifestieren. Gerade beim sekundären APS ist die Differenzialdiagnose zur Lupusnephritis mittels Nierenbiopsie wichtig, da das APS eine Antikoagulation und in der Regel keine Immunsuppression erfordert. Auch beim pSS werden renale Affektionen mit 20–40% relativ häufig beobachtet. Die typische und auch häufigste Manifestation ist die interstitielle Nephritis mit distal tubulärer Azidose Typ 1. Sie verläuft oft asymptomatisch, kann aber zu Hypokaliämie und Osteomalazie führen. Während interstitielle Nephritis und die seltenere Glomerulonephritis in der Regel gut auf eine Immunsuppression ansprechen, wird die distal-tubuläre Azidose durch Immunsuppression nur unzureichend beeinflusst. Bei SSc werden Nierenfunktionseinschränkungen und Proteinurie als Ausdruck einer renalen Affektion in bis zu 36% beobachtet. Diese histologisch durch sklerosierte Glomeruli, tubuläre Atrophie und interstitielle Fibrose charakterisierte und häufig multifaktorielle Nephropathie hat jedoch im Hinblick auf die Nierenfunktion eine gute Prognose. Deutlich seltener ist mit 4–11% die renale Krise, welche histologisch durch eine obstruktive Vaskulopathie und klinisch durch akzelerierte arterielle Hypertonie und progrediente Niereninsuffizienz gekennzeichnet ist. Risikofaktoren der renalen Krise bei SSc sind das Vorliegen einer diffus cutanen SSc, höheres Alter, männliches Geschlecht, Einnahme von Glukokortikoiden, Perikarderguss sowie der Nachweis von Antikörpern gegen RNA-Polymerase III. Die Therapie der hypertensiven renalen Krise besteht in einer Blutdrucksenkung um ca. 10% pro Tag unter Vermeidung längerer Perioden einer Hypotension bis in den Normbereich unter bevorzugtem Einsatz von ACE-Hemmern. Bei unzureichender Blutdrucksenkung unter ausdosiertem ACE-Hemmer kommen zusätzlich Alpha-Blocker, Kalziumantagonisten und Minoxidil zum Einsatz. Nützlich sind ferner die intravenöse Gabe von Prostacyclin zur Verbesserung der renalen Perfusion und die Anwendung des Endothelin-Rezeptor-Antagonisten Bosentan. Die Einführung von ACE-Hemmern hat zwar die Mortalität infolge einer renalen Krise erheblich reduziert, allerdings ist in 40–50% ein Fortschreiten zur terminalen Niereninsuffizienz zu erwarten.
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Zhang, Ranran, and William Nicholas Rose. "Photopheresis Provides Significant Long-Lasting Benefit in Nephrogenic Systemic Fibrosis." Case Reports in Dermatological Medicine 2017 (2017): 1–4. http://dx.doi.org/10.1155/2017/3240287.
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Nephrogenic systemic fibrosis (NSF), previously known as nephrogenic fibrosing dermopathy, is a rare complication of exposure to gadolinium-based contrast agents in patients who have significantly decreased renal function. Manifestations include fibrosis of the skin and other tissues. Effective therapies are lacking. Photopheresis has been tried with variable rates of improvement, and small numbers of cases (20 as of 2016) have been reported of NSF patients treated with photopheresis. We report a case of patient with nephrogenic systemic fibrosis who was treated with photopheresis and demonstrated significant lasting improvements.
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Kommers, Glaucia Denise, Márcia Regina da Silva Ilha, and Claudio Severo Lombardo de Barros. "Dioctofimose em cães: 16 casos." Ciência Rural 29, no. 3 (September 1999): 517–22. http://dx.doi.org/10.1590/s0103-84781999000300023.
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No período de 1978 a 1996, de um total de 3.259 cães necropsiados, 16 (0,49%) apresentaram parasitismo por Dioctophyma renale. Desses, 12 (75%) eram cães de rua. Em 13 cães (81, 2%), um ou vários parasitas localizavam-se no rim direito. Em 3 casos (18,7%), o parasita foi observado na cavidade abdominal. Nos casos de parasitismo renal, observou-se acentuada atrofia do parênquima, transformando o rim numa bolsa fibrosa contendo o parasita em meio a exsudato necro-hemorrágico semilíquido. Foi observada hipertrofia renal compensatória contralateral em 5 casos. O ciclo evolutivo de D. renale é complexo e incompletamente entendido. Envolve um hospedeiro intermediário e hospedeiros paratênicos. A alta ocorrência da doença em cães de rua sugere que a infecção seja relacionada aos hábitos alimentares pouco seletivos desses animais.
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Shin, Sug Kyun, Do Hun Kim, Heung Su Kim, Kyu Tae Shin, Kyung Ae Ma, Sung Jung Kim, Youn Sik Kwak, Seung Kyu Ha, and Donald J. Sherrard. "Renal Osteodystrophy in Pre-Dialysis Patients: Ethnic Difference?" Peritoneal Dialysis International: Journal of the International Society for Peritoneal Dialysis 19, no. 2_suppl (February 1999): 402–7. http://dx.doi.org/10.1177/089686089901902s65.
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The purpose of the present study is to investigate whether an ethnic difference exists in the incidence of renal osteodystrophy between Asian and Western countries in end-stage renal disease (ESRD) patients. We evaluated bone histology in 58 pre-dialysis patients (28 male, 30 female; mean age: 47.7 years). All patients had bone biopsies with quantitative histomorphometry and sero-logical parameters such as intact PTH, osteocalcin, total alkaline phosphatase, and basal and deferoxamine-stimulated serum aluminum levels. We observed that 91.4% of all evaluated patients showed renal osteodystrophy before the start of dialytic therapy. Mild osteitis fibrosa were observed in 21 patients (36.2%), severe osteitis fibrosa in 5 patients (8.6%), mixed lesions in 7 patients (12.1 %), osteomalacia in 6 patients (10.3%), aplastic bone disease in 14 patients (24.1%), and normal bone in 5 patients (8.6%). Among the bone histomorphometric parameters, fibrosis area rate (%) showed the best correlation with intact PTH, and osteocalcin and osteoid area rate (%) with total alkaline phosphatase. Aluminum-related bone disease was not observed. Among patients with aplastic bone disease, only 14.3% showed aluminum deposition of any significance (5% < stainable bone surface aluminum < 25%). In the diabetic patients, aplastic bone disease was most common, but no case was related to aluminum intoxication. In conclusion, the distribution of renal osteodystrophy in our study was different from that of Western countries in pre-dialysis patients. Our patients tended to have more mild-form osteitis fibrosa and normal findings, and less severe-form osteitis fibrosa and aplastic bone disease. Aluminum-related bone disease was not observed.
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Tang, Ignatius Y. S., Natasha Walzer, Nidhi Aggarwal, Ivo Tzvetanov, Scott Cotler, and Enrico Benedetti. "Management of the Kidney Transplant Patient with Chronic Hepatitis C Infection." International Journal of Nephrology 2011 (2011): 1–10. http://dx.doi.org/10.4061/2011/245823.
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Chronic Hepatitis C (HCV) infection is an important cause of morbidity and mortality in patients with end-stage renal disease. Renal transplantation confers a survival advantage in HCV-infected patients. Renal transplant candidates with serologic evidence of HCV infection should undergo a liver biopsy to assess for fibrosis and cirrhosis. Patients with Metavir fibrosis score ≤3 and compensated cirrhosis should be evaluated for interferon-based therapy. Achievement of sustained virological response (SVR) may reduce the risks for both posttransplantation hepatic and extrahepatic complications such as de novo or recurrent glomerulonephritis associated with HCV. Patients who cannot achieve SVR and have no live kidney donor may be considered for HCV-positive kidneys. Interferon should be avoided after kidney transplant except for treatment of life-threatening liver injury, such as fibrosing cholestatic hepatitis. Early detection, prevention, and treatment of complications due to chronic HCV infection may improve the outcomes of kidney transplant recipients with chronic HCV infection.
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Foda, Marwa SaidAbd Elsaed, HassanAbd Elhady Ahmed, YasseinSalahYassein Mohamed, and AhmedRagheb Tawfek. "Renal fibrosis." Menoufia Medical Journal 28, no. 2 (2015): 540. http://dx.doi.org/10.4103/1110-2098.163915.
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Zeisberg, Michael, Yohei Maeshima, Barbara Mosterman, and Raghu Kalluri. "Renal Fibrosis." American Journal of Pathology 160, no. 6 (June 2002): 2001–8. http://dx.doi.org/10.1016/s0002-9440(10)61150-9.
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Zeisberg, Michael, Gary Bonner, Yohei Maeshima, Pablo Colorado, Gerhard A. Müller, Frank Strutz, and Raghu Kalluri. "Renal Fibrosis." American Journal of Pathology 159, no. 4 (October 2001): 1313–21. http://dx.doi.org/10.1016/s0002-9440(10)62518-7.
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Cho, Min Hyun. "Renal fibrosis." Korean Journal of Pediatrics 53, no. 7 (2010): 735. http://dx.doi.org/10.3345/kjp.2010.53.7.735.
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Schnaper, H. William. "Renal fibrosis." Frontiers in Bioscience 8, no. 5 (2003): e68-86. http://dx.doi.org/10.2741/925.
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Reich, B., F. Hermann, Y. Talke, M. Rodriguez Gomez, K. Schmidbauer, N. Gobel, I. Ketelsen, et al. "Renal fibrosis." Nephrology Dialysis Transplantation 27, suppl 2 (May 1, 2012): ii44—ii45. http://dx.doi.org/10.1093/ndt/gfs198.
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Gu, Yue-Yu, Xu-Sheng Liu, Xiao-Ru Huang, Xue-Qing Yu, and Hui-Yao Lan. "TGF-β in renal fibrosis: triumphs and challenges." Future Medicinal Chemistry 12, no. 9 (May 2020): 853–66. http://dx.doi.org/10.4155/fmc-2020-0005.
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Renal fibrosis is a hallmark of chronic kidney disease. Although considerable achievements in the pathogenesis of renal fibrosis have been made, the underlying mechanisms of renal fibrosis remain largely to be explored. Now we have reached the consensus that TGF-β is a master regulator of renal fibrosis. Indeed, TGF-β regulates renal fibrosis via both canonical and noncanonical TGF-β signaling. Moreover, ongoing renal inflammation promotes fibrosis as inflammatory cells such as macrophages, conventional T cells and mucosal-associated invariant T cells may directly or indirectly contribute to renal fibrosis, which is also tightly regulated by TGF-β. However, anti-TGF-β treatment for renal fibrosis remains ineffective and nonspecific. Thus, research into mechanisms and treatment of renal fibrosis remains highly challenging.
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Ma, Hongge, Shupei Qiao, Zeli Wang, Shuai Geng, Yufang Zhao, Xiaolu Hou, Weiming Tian, Xiongbiao Chen, and Lifen Yao. "Microencapsulation of Lefty-secreting engineered cells for pulmonary fibrosis therapy in mice." American Journal of Physiology-Lung Cellular and Molecular Physiology 312, no. 5 (May 1, 2017): L741—L747. http://dx.doi.org/10.1152/ajplung.00295.2016.
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Idiopathic pulmonary fibrosis (IPF) is a progressive disease that causes unremitting deposition of extracellular matrix proteins, thus resulting in distortion of the pulmonary architecture and impaired gas exchange. Associated with high morbidity and mortality, IPF is generally refractory to current pharmacological therapies. Lefty A, a potent inhibitor of transforming growth factor-β signaling, has been shown to have promising antifibrotic ability in vitro for the treatment of renal fibrosis and other potential organ fibroses. Here, we determined whether Lefty A can attenuate bleomycin (BLM)-induced pulmonary fibrosis in vivo based on a novel therapeutic strategy where human embryonic kidney 293 (HEK293) cells are genetically engineered with the Lefty A-associated GFP gene. The engineered HEK293 cells were encapsulated in alginate microcapsules and then subcutaneously implanted in ICR mice that had 1 wk earlier been intratracheally administered BLM to induce pulmonary fibrosis. The severity of fibrosis in lung tissue was assessed using pathological morphology and collagen expression to examine the effect of Lefty A released from the microencapsulated cells. The engineered HEK293 cells with Lefty A significantly reduced the expression of connective tissue growth factor and collagen type I mRNA, lessened the morphological fibrotic effects induced by BLM, and increased the expression of matrix metalloproteinase-9. This illustrates that engineered HEK293 cells with Lefty A can attenuate pulmonary fibrosis in vivo, thus providing a novel method to treat human pulmonary fibrotic disease and other organ fibroses.
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Lee, SW, AK Elfadl, MJ Chung, HM Arif Ullah, DK Yuh, SH Lee, KS Jeong, and JK Park. "Urocystitis, pyelonephritis, renal papillary necrosis and chronic tubulointerstitial disease causing chronic renal insufficiency in a Siberian tiger (Panthera tigris altaica): a case report." Veterinární Medicína 63, No. 10 (October 16, 2018): 482–87. http://dx.doi.org/10.17221/132/2017-vetmed.
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The present case report describes a case of chronic renal failure characterised by renal medullary fibrosis and renal papillary necrosis in a male Siberian tiger (Panthera tigris altaica). A 12-year-old male Siberian tiger presented with depression, anorexia and weight loss. Blood urea nitrogen (> 50.4 mmol/l) and ammonia (71.7 µmol/l) were increased, suggesting chronic renal failure and uraemia. The tiger died secondary to gastric haemorrhage. At necropsy, the kidneys had yellow lesions in the medulla and renal papillae and petechiae in the cortex. The stomach had multiple mucosal ulcers and haemorrhage. Microscopically, marked renal medullary fibrosis and renal papillary necrosis were observed with tubular atrophy, degeneration, coagulative necrosis, calcification and chronic inflammatory cell infiltration. The renal cortex showed moderate interstitial inflammation. The urinary bladder exhibited epithelial desquamation and submucosal fibrosis. The tiger was diagnosed with chronic renal failure secondary to renal papillary necrosis and medullary fibrosis.
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Eddy, Allison A. "Scraping fibrosis: UMODulating renal fibrosis." Nature Medicine 17, no. 5 (May 2011): 553–55. http://dx.doi.org/10.1038/nm0511-553.
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Jenkins, Joseph, Sergey V. Brodsky, Anjali A. Satoskar, Gyongyi Nadasdy, and Tibor Nadasdy. "The Relevance of Periglomerular Fibrosis in the Evaluation of Routine Needle Core Renal Biopsies." Archives of Pathology & Laboratory Medicine 135, no. 1 (January 1, 2011): 117–22. http://dx.doi.org/10.5858/2009-0484-oar1.1.
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Abstract Context—Renal interstitial fibrosis and, to a lesser extent, sclerotic glomeruli correlate with poor renal function. However, not all nonfunctional glomeruli are sclerotic. Many or most glomeruli with periglomerular fibrosis, while retaining blood flow, probably do not filter; therefore, they may not contribute to renal function. Objective—To examine the relationship of periglomerular fibrosis and the sum of globally sclerotic glomeruli and glomeruli with periglomerular fibrosis (GSG+PF) with interstitial fibrosis and renal function. Design—Native kidney biopsies from 177 patients with chronic renal injury were assessed for interstitial fibrosis, glomerular sclerosis, and GSG+PF. Renal biopsies with active or acute lesions were not included. The percentage of globally sclerotic glomeruli and GSG+PF was correlated with the degree of interstitial fibrosis and serum creatinine levels. Results—The percentage of GSG+PF correlates better with the degree of interstitial fibrosis and renal function than does the percentage of globally sclerotic glomeruli alone. This appears particularly true in chronic renal diseases of patients without diabetes. The number of globally sclerotic glomeruli correlates better with interstitial fibrosis and renal function than does the sum of globally and segmentally sclerotic glomeruli. Conclusions—The percentage of GSG+PF in a renal biopsy specimen provides a better estimate of chronic renal injury than does the percentage of sclerotic glomeruli alone, probably because many or most glomeruli with periglomerular fibrosis are nonfunctional. Therefore, we recommend that the number of glomeruli with periglomerular fibrosis also be provided in the renal biopsy report.
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Sun, Yu-Chao, Zhen-Zhen Qiu, Fu-Li Wen, Jin-Quan Yin, and Hao Zhou. "Revealing Potential Diagnostic Gene Biomarkers Associated with Immune Infiltration in Patients with Renal Fibrosis Based on Machine Learning Analysis." Journal of Immunology Research 2022 (April 20, 2022): 1–20. http://dx.doi.org/10.1155/2022/3027200.
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Chronic kidney disease is characterized by the development of renal fibrosis. The basic mechanisms of renal fibrosis have not yet been fully investigated despite significant progress in understanding the etiology of the disease. In this work, the researchers sought to identify potential diagnostic indicators for renal fibrosis. From the GEO database, we were able to acquire two gene expression profiles with publically available data (GSE22459 and GSE76882, respectively) from human renal fibrosis and control samples. 215 renal fibrosis specimens and 124 normal specimens were examined for differentially expressed genes (DEGs). The SVM-RFE and LASSO regression models were used to discover potential markers. CIBERSORT was applied to estimate the combined cohorts’ immune cell fraction compositional trends in renal fibrosis. RT-PCR was used to examine the expression of ISG20 in renal fibrosis and healthy samples. In vitro experiments were applied to examine the function of ISG20 knockdown on the progression of renal fibrosis. In this study, we identified 24 DEGs. The result of LASSO and SVM-RFE identified nine critical genes. ROC assays confirmed the diagnostic value of the above nine genes for renal fibrosis. Immune cell infiltration analysis revealed that ISG20 and SERPINA3 were both found to be correlated with T cell follicular helper, neutrophils, T cell CD4 memory activated, eosinophils, T cell CD8, dendritic cell activated, B cell memory, monocytes, macrophage M2, plasma cells, T cell CD4 naïve, mast cell resting, B cell naïve, T cell regulatory, and NK cell activated. Finally, we observed that the expression of ISG20 and SERPINA3 was distinctly increased in renal fibrosis samples compared with normal samples. ISG20 siRNA significantly suppressed the progression of renal fibrosis in vitro. Overall, this study identified nine diagnostic biomarkers for renal fibrosis. ISG20 may be a novel therapeutic target of renal fibrosis.
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Al Habeeb, Ayman, Sara Partington, Donald Rosenthal, and Samih Salama. "Skin Thickening in a Hemodialysis Patient: A Case of Nephrogenic Fibrosing Dermopathy." Journal of Cutaneous Medicine and Surgery 13, no. 2 (March 2009): 110–14. http://dx.doi.org/10.2310/7750.2008.07085.
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Background: Nephrogenic fibrosing dermopathy (NFD), a rare fibrosing condition of the skin, occurs in patients with renal failure. Worldwide, 215 cases have been reported, but none of them are from Canada. Case Report: A 71-year-old woman with hypertensive vasculopathy and renal failure, hypothyroidism, deep vein thrombosis, and a previous abdominal aneurysm repair presented with the rapid development of indurated skin over her arms and legs. These skin changes developed 5 months after starting hemodialysis. Biopsy Results: Skin biopsies demonstrated thickened collagen bundles in the dermis with extension into the subcutaneous tissue and minimal increased mucin production. There were increased fibroblastic cells that were immunohistochemically CD34 positive. Conclusions: This patient has the clinical and pathologic features of NFD. Interestingly, this patient had a history of vein thrombosis and vascular surgery, emphasizing the possible role these features may play as instigators of fibrosis in this disease.
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Li, Chen, Yuan-Fei Liu, Chong Huang, Yan-Xia Chen, Cheng-Yun Xu, and Yan Chen. "Long noncoding RNA NEAT1 sponges miR-129 to modulate renal fibrosis by regulation of collagen type I." American Journal of Physiology-Renal Physiology 319, no. 1 (July 1, 2020): F93—F105. http://dx.doi.org/10.1152/ajprenal.00552.2019.
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The long noncoding RNA nuclear enriched abundant transcript 1 (NEAT1) has been reported to promote liver fibrosis progression. However, its molecular mechanism in renal fibrosis was not elucidated. In the present study, an in vitro model of renal fibrosis was established with HK-2 and HKC-8 cells treated with transforming growth factor-β1. C57BL/6 mice were used for the in vivo model with unilateral ureteral obstruction. Our results indicated that NEAT1 and collagen type I levels were significantly upregulated, whereas miR-129 was obviously downregulated, in the progression of renal fibrosis. Meanwhile, NEAT1 knockdown or miR-129 overexpression inhibited collagen type I deposition, the epithelial-mesenchymal transition process, and the inflammation response to suppress renal fibrosis. NEAT1 directly targeted miR-129, and miR-129 directly bound to collagen type I. Downregulation of miR-129 reversed inhibition of renal fibrosis induced by NEAT1 silencing, and upregulation of collagen type I also reversed inhibition of renal fibrosis caused by miR-129 overexpression. NEAT1 knockdown alleviated renal fibrosis in mice subjected to unilateral ureteral obstruction. In conclusion, NEAT1 sponged miR-129 to modulate the epithelial-mesenchymal transition process and inflammation response of renal fibrosis by regulation of collagen type I. Our study indicates a novel role in the regulation of renal fibrosis and provides a new potential treatment target for renal fibrosis.
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Chen, Sheng. "circ_000166/miR-296 Aggravates the Process of Diabetic Renal Fibrosis by Regulating the SGLT2 Signaling Pathway in Renal Tubular Epithelial Cells." Disease Markers 2022 (May 16, 2022): 1–10. http://dx.doi.org/10.1155/2022/6103086.
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Diabetic renal fibrosis is a common cause of end-stage renal disease, and the circRNA-miRNA-mRNA network may play an important role in the progression of diabetic nephropathy- (DN-) induced renal fibrosis. In this study, the role of circ_000166/miR-296/SGLT2 in the process of DN-related renal fibrosis was studied by constructing an animal model of DN renal fibrosis via lentiviral transfection, plasmid transfection, and dual-luciferase reporting techniques. Compared with that of normal controls, the expression of circ_000166 in the kidney tissues of DN renal fibrosis mice substantially increased. Silencing circ_000166 could minimize kidney damage and decrease urine protein levels, thereby inhibiting the progression of renal fibrosis. Moreover, circ_000166 could act as the ceRNA of miR-296 and competitively bind to miR-296, leading to an increase in the expression of the SGLT2 gene regulated by miR-296. Through mutual verification via in vivo and in vitro experiments, miR-296 was overexpressed and SGLT2 was silenced. Results showed that DN renal fibrosis and cell apoptosis were considerably reduced. We postulate that circ_000166/miR-296/SGLT2 may become a new target in the progression of DN renal fibrosis, and the regulation of this pathway may be a promising strategy for clinical treatment of DN renal fibrosis.
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Pan, Bixia, Guohui Liu, Zongpei Jiang, and Dongwen Zheng. "Regulation of Renal Fibrosis by Macrophage Polarization." Cellular Physiology and Biochemistry 35, no. 3 (2015): 1062–69. http://dx.doi.org/10.1159/000373932.
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Background/Aims: Since renal fibrosis always predisposes end-stage renal disease, elucidation of the molecular mechanisms that underlie the progression of renal fibrosis may substantially improve the understanding and treatment for renal failure. Previous studies have highlighted an important counteraction between transforming growth factor β 1 (TGFβ1) and bone morphogenic protein 7 (BMP7) in the epithelial-to-mesenchymal transition (EMT) of renal tubular epithelial cells during chronic renal injury. Macrophages are also believed to play a critical role in renal fibrosis. However, the relationship between macrophages and EMT is unknown. Methods: Here, we used a mouse unilateral ureteral obstruction (UUO) model to address to these questions, and analyzed macrophage and its subpopulations purified by flow cytometry. Results: We found that the recruited macrophages are polarized to a M2 subtype after renal injury. M2 macrophages released high levels TGFβ1 to suppress BMP7 to enhance EMT-induced renal fibrosis. Depletion of M2 macrophages, but not of M1 macrophages, specifically inhibited EMT, and subsequently the renal fibrosis. Adoptive transplantation of M2 macrophages deteriorated renal fibrosis. Conclusion: Thus, our study highlights M2 macrophages as a critical target for treating renal fibrosis.
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Ramani, Kritika, Dong Zhou, Roderick Tan, Youhua Liu, Sarah Gaffen, and Partha Sarathi Biswas. "Disruption of Interleukin-17 receptor A (IL-17RA) gene in mice aggravates renal interstitial fibrosis in obstructive nephropathy." Journal of Immunology 196, no. 1_Supplement (May 1, 2016): 51.24. http://dx.doi.org/10.4049/jimmunol.196.supp.51.24.
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Abstract Renal fibrosis is the final outcome of obstructive nephropathy and a major cause of chronic renal failure. Renal fibrosis results from an imbalance between extracellular matrix (ECM) synthesis and degradation, which is regulated by multiple inflammatory mediators in the kidney. Recently, Interleukin-17 (IL-17) emerged as a key cytokine in lung and liver fibrosis. Although IL-17 producing cells were detected in the obstructed kidney, the role of IL-17 in renal fibrosis is unknown. We sought to define the contribution of IL-17 in renal fibrosis in obstructive nephropathy. Mice deficient in IL-17 receptor signaling (IL-17RA−/−) were assessed for renal fibrosis following unilateral ureteral obstruction (UUO), a well-characterized mouse model of obstructive nephropathy. We determined IL-17 receptor signaling is required for protection against renal fibrosis following UUO. IL-17RA−/− mice developed severe morphological injury and displayed increased deposition of collagen in the obstructed kidney compared to controls. We observed a significant decrease in the level of matrix degrading enzymes in the kidney of IL-17RA−/− mice, despite normal ECM synthesis, correlating with increased fibrosis. Overexpression of IL-17 increased the level of matrix degrading enzymes and protected mice from renal fibrosis. We also show that IL-17R signaling in tubular epithelial cells up regulated multiple genes of Kallikrein-kinin system, known to play a critical role in renal protection against kidney fibrosis. Our data clearly indicate a previously unappreciated role of IL-17 in renal protection against fibrosis. These results offer the opportunity for the development of potential therapies in the treatment of chronic kidney diseases.
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Zhang, Wanfen, Xiaoping Li, Yushang Tang, Cheng Chen, Ran Jing, and Tongqiang Liu. "miR-155-5p Implicates in the Pathogenesis of Renal Fibrosis via Targeting SOCS1 and SOCS6." Oxidative Medicine and Cellular Longevity 2020 (June 8, 2020): 1–11. http://dx.doi.org/10.1155/2020/6263921.
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Renal fibrosis is associated with the reduction in the functional renal parenchyma and in most cases progresses to end-stage kidney failure, a devastating condition that requires lifelong dialysis or kidney transplantation. However, due to the extreme complexity in the pathogenesis of renal fibrosis and our limited knowledge, therapeutic options for renal fibrosis in the clinical setting are still scarce and often ineffective. Hence, further studies on the molecular mechanisms underlying renal fibrosis are compellingly needed. Multiple miRNAs have demonstrated to participate in kidney diseases in a TGF-β dependent or independent manner, but there is very little known about miR-155-5p on renal fibrosis. In the present study, we firstly explored the expression level and functions of miR-155-5p in the setting of renal fibrosis. Our research revealed that miR-155-5p is highly expressed in kidney tissues from patients and unilateral ureteral obstruction (UUO) rat models, and miR-155-5p knockdown significantly blocks renal fibrosis both in vivo and in vitro. In mechanism, our data demonstrate that miR-155-5p promotes renal fibrosis by increasing the phosphorylated activation of STAT3 via targeting SOCS1/6. Altogether, our findings highlight a miR-155-5p/SOCS/STAT3 axis in the pathogenesis of renal fibrosis, which may provide promising therapeutic targets for clinical prevention of this disease.
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Kim, Kristin P., Caitlin E. Williams, and Christopher A. Lemmon. "Cell–Matrix Interactions in Renal Fibrosis." Kidney and Dialysis 2, no. 4 (December 7, 2022): 607–24. http://dx.doi.org/10.3390/kidneydial2040055.
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Renal fibrosis is a hallmark of end-stage chronic kidney disease. It is characterized by increased accumulation of extracellular matrix (ECM), which disrupts cellular organization and function within the kidney. Here, we review the bi-directional interactions between cells and the ECM that drive renal fibrosis. We will discuss the cells involved in renal fibrosis, changes that occur in the ECM, the interactions between renal cells and the surrounding fibrotic microenvironment, and signal transduction pathways that are misregulated as fibrosis proceeds. Understanding the underlying mechanisms of cell–ECM crosstalk will identify novel targets to better identify and treat renal fibrosis and associated renal disease.
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Cao, Yu-Han, Lin-Li Lv, Xu Zhang, Hong Hu, Li-Hong Ding, Di Yin, Ying-Zi Zhang, Hai-Feng Ni, Ping-Sheng Chen, and Bi-Cheng Liu. "Urinary vimentin mRNA as a potential novel biomarker of renal fibrosis." American Journal of Physiology-Renal Physiology 309, no. 6 (September 15, 2015): F514—F522. http://dx.doi.org/10.1152/ajprenal.00449.2014.
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Renal fibrosis is a histological outcome of chronic kidney disease (CKD) progression. However, the noninvasive detection of renal fibrosis remains a challenge. Here we constructed a renal fibrosis target mRNA array and used it to detect urinary mRNAs of CKD patients for investigating potential noninvasive biomarkers of renal fibrosis. We collected urine samples from 39 biopsy-proven CKD patients and 11 healthy controls in the training set. Urinary mRNA profiles of 86 genes showed a total of 21 mRNAs that were differentially expressed between CKD patients and controls ( P < 0.05), and vimentin (VIM) mRNA demonstrated the highest change fold of 9.99 in CKD vs. controls with robust correlations with decline of renal function and severity of tubulointerstitial fibrosis. Additionally, VIM mRNA further differentiated patients with moderate-to-severe fibrosis from none-to-mild fibrosis group with an area of the curve of 0.796 ( P = 0.008). A verification of VIM mRNA in the urine of an additional 96 patients and 20 controls showed that VIM is not only well correlated with renal function parameters but also correlated with proteinuria and renal fibrosis scores. Multiple logistic regression and receiver-operating characteristics analysis further showed that urine VIM mRNA is the best predictive parameter of renal fibrosis compared with estimated glomerular filtration rate, serum creatinine, and blood urea nitrogen. In addition, there is no improved predictive performance for the composite biomarkers to predict renal fibrosis severity compared with a single gene of VIM. Overall, urinary VIM mRNA might serve as a novel independent noninvasive biomarker to monitor the progression of kidney fibrosis.
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Colon, Selene, Haiyan Luan, Yan Liu, Cameron Meyer, Leslie Gewin, and Gautam Bhave. "Peroxidasin and eosinophil peroxidase, but not myeloperoxidase, contribute to renal fibrosis in the murine unilateral ureteral obstruction model." American Journal of Physiology-Renal Physiology 316, no. 2 (February 1, 2019): F360—F371. http://dx.doi.org/10.1152/ajprenal.00291.2018.
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Renal fibrosis is the pathological hallmark of chronic kidney disease (CKD) and manifests as glomerulosclerosis and tubulointerstitial fibrosis. Reactive oxygen species contribute significantly to renal inflammation and fibrosis, but most research has focused on superoxide and hydrogen peroxide (H2O2). The animal heme peroxidases myeloperoxidase (MPO), eosinophil peroxidase (EPX), and peroxidasin (PXDN) uniquely metabolize H2O2 into highly reactive and destructive hypohalous acids, such as hypobromous and hypochlorous acid. However, the role of these peroxidases and their downstream hypohalous acids in the pathogenesis of renal fibrosis is unclear. Our study defines the contribution of MPO, EPX, and PXDN to renal inflammation and tubulointerstitial fibrosis in the murine unilateral ureteral obstruction (UUO) model. Using a nonspecific inhibitor of animal heme peroxidases and peroxidase-specific knockout mice, we find that loss of EPX or PXDN, but not MPO, reduces renal fibrosis. Furthermore, we demonstrate that eosinophils, the source of EPX, accumulate in the renal interstitium after UUO. These findings point to EPX and PXDN as potential therapeutic targets for renal fibrosis and CKD and suggest that eosinophils modulate the response to renal injury.
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Sugiura, Hidekazu, Takumi Yoshida, Shunji Shiohira, Junko Kohei, Michihiro Mitobe, Hiroshi Kurosu, Makoto Kuro-o, Kosaku Nitta, and Ken Tsuchiya. "Reduced Klotho expression level in kidney aggravates renal interstitial fibrosis." American Journal of Physiology-Renal Physiology 302, no. 10 (May 15, 2012): F1252—F1264. http://dx.doi.org/10.1152/ajprenal.00294.2011.
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Renal expression of the klotho gene is markedly suppressed in chronic kidney disease (CKD). Since renal fibrosis is the final common pathology of CKD, we tested whether decreased Klotho expression is a cause and/or a result of renal fibrosis in mice and cultured renal cell lines. We induced renal fibrosis by unilateral ureteral obstruction (UUO) in mice with reduced Klotho expression ( kl/+ mice) and compared them with wild-type mice. The UUO kidneys from kl/+ mice expressed significantly higher levels of fibrosis markers such as α-smooth muscle actin (α-SMA), fibronectin, and transforming growth factor-β1 (TGF-β1) than those from wild-type mice. In addition, in cultured renal fibroblast cells (NRK49F), the levels of α-SMA and PAI1 expression were significantly suppressed by addition of recombinant Klotho protein to the medium. The similar effects were observed by a TGF-β1 receptor inhibitor (ALK5 inhibitor). These observations suggest that low renal Klotho expression enhances TGF-β1 activity and is a cause of renal fibrosis. On the other hand, TGF-β1 reduced Klotho expression in renal cultured epithelial cells (inner medullary collecting duct and human renal proximal tubular epithelium), suggesting that low renal Klotho expression is a result of renal fibrosis. Taken together, renal fibrosis can trigger a deterioration spiral of Klotho expression, which may be involved in the pathophysiology of CKD progression.
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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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Farris, Alton B., and Robert B. Colvin. "Renal interstitial fibrosis." Current Opinion in Nephrology and Hypertension 21, no. 3 (May 2012): 289–300. http://dx.doi.org/10.1097/mnh.0b013e3283521cfa.
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Ding, Hao, Lei Jiang, Jing Xu, Feng Bai, Yang Zhou, Qi Yuan, Jing Luo, Ke Zen, and Junwei Yang. "Inhibiting aerobic glycolysis suppresses renal interstitial fibroblast activation and renal fibrosis." American Journal of Physiology-Renal Physiology 313, no. 3 (September 1, 2017): F561—F575. http://dx.doi.org/10.1152/ajprenal.00036.2017.
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Chronic kidney diseases generally lead to renal fibrosis. Despite great progress having been made in identifying molecular mediators of fibrosis, the mechanism that governs renal fibrosis remains unclear, and so far no effective therapeutic antifibrosis strategy is available. Here we demonstrated that a switch of metabolism from oxidative phosphorylation to aerobic glycolysis (Warburg effect) in renal fibroblasts was the primary feature of fibroblast activation during renal fibrosis and that suppressing renal fibroblast aerobic glycolysis could significantly reduce renal fibrosis. Both gene and protein assay showed that the expression of glycolysis enzymes was upregulated in mouse kidneys with unilateral ureter obstruction (UUO) surgery or in transforming growth factor-β1 (TGF-β1)-treated renal interstitial fibroblasts. Aerobic glycolysis flux, indicated by glucose uptake and lactate production, was increased in mouse kidney with UUO nephropathy or TGF-β1-treated renal interstitial fibroblasts and positively correlated with fibrosis process. In line with this, we found that increasing aerobic glycolysis can remarkably induce myofibroblast activation while aerobic glycolysis inhibitors shikonin and 2-deoxyglucose attenuate UUO-induced mouse renal fibrosis and TGF-β1-stimulated myofibroblast activation. Furthermore, mechanistic study indicated that shikonin inhibits renal aerobic glycolysis via reducing phosphorylation of pyruvate kinase type M2, a rate-limiting glycolytic enzyme associated with cell reliance on aerobic glycolysis. In conclusion, our findings demonstrate the critical role of aerobic glycolysis in renal fibrosis and support treatment with aerobic glycolysis inhibitors as a potential antifibrotic strategy.
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Sun, Donglin, Jing Guo, Weifei Liang, Yangxiao Chen, Xiangqiu Chen, and Li Wang. "Anlotinib Alleviates Renal Fibrosis via Inhibition of the ERK and AKT Signaling Pathways." Oxidative Medicine and Cellular Longevity 2023 (February 18, 2023): 1–11. http://dx.doi.org/10.1155/2023/1686804.
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Purpose. We examined whether anlotinib can attenuate folic acid-induced and unilateral ureteral obstruction-induced renal fibrosis and explored the underlying antifibrotic mechanism. Materials and Methods. We have evaluated the effects of anlotinib on folic acid-induced and unilateral ureteral obstruction-induced renal fibrosis in mice through in vivo experiments of unilateral ureteral obstruction or folic acid-induced interstitial fibrosis and in vitro models of transforming growth factor-β1 induced HK-2 human renal proximal tubule cells. Serum renal function parameters and inflammatory cytokine levels were measured, and histological changes of renal injury and fibrosis were analyzed by HE staining and immunohistochemistry. Immunohistochemistry and Western blotting were used to determine the mechanism of action of anlotinib in ameliorating renal fibrosis. Results. Anlotinib improved proteinuria and reduced renal impairment in folic acid-induced mouse models of renal fibrosis. Anlotinib reduced tubular injury, deposition of tubular extracellular matrix, and expression of alpha-smooth muscle actin, transforming growth factor-β1, and cytosolic inflammatory factors compared with controls. Conclusions. Anlotinib ameliorated renal function, improved extracellular matrix deposition, reduced protein levels of epithelial-mesenchymal transition markers, and decreased cellular inflammatory factors. Anlotinib reduced renal injury and fibrosis by inhibiting the transforming growth factor-β1 signaling pathway through AKT and ERK channels.
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Cao, Yuhan, Yuwei Wang, Yinhua Liu, Xinjian Zhu, Guifa Zhang, Sufen Wang, Xiaomei Chen, Daoqin Liu, and Cong Fu. "Decreased Expression of Urinary Mammalian Target of Rapamycin mRNA Is Related to Chronic Renal Fibrosis in IgAN." Disease Markers 2019 (August 14, 2019): 1–10. http://dx.doi.org/10.1155/2019/2424751.
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Background. Renal fibrosis is a common outcome of all pathological types of chronic kidney disease (CKD). However, the noninvasive detection of renal fibrosis remains a challenge. Methods. We collected urine samples from 154 biopsy-proven IgA nephropathy (IgAN) patients and 61 healthy controls. The expression of mTOR was measured and the correlation with renal function parameter and pathological indicators. The receiver operating characteristic (ROC) curve for the diagnosis of IgAN and renal fibrosis was calculated. Results. The urinary mammalian target of rapamycin (mTOR) expression was decreased in IgAN patients. The expression of mTOR was correlated with serum creatinine, blood urea nitrogen, estimated glomerular filtration rate, 24 h proteinuria, and cystatin C. Further, the urinary mTOR expression was significantly decreased in severe renal fibrosis patients compared with mild or moderate renal fibrosis patients. Urinary mTOR expression was correlated with score of tubulointerstitial fibrosis (TIF) and score of glomerular sclerosis. The ROC curve showed that mTOR can diagnose IgAN at a cut-off value of 0.930 with the sensitivity of 90.2% and specificity of 73.8% and renal fibrosis at a cut-off value of 0.301 with the sensitivity of 71.7% and specificity of 64.8%. Conclusion. Urinary mTOR mRNA expression was a potential biomarker for diagnosis of IgAN and renal fibrosis in IgAN patients.
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Bülow, Roman David, and Peter Boor. "Extracellular Matrix in Kidney Fibrosis: More Than Just a Scaffold." Journal of Histochemistry & Cytochemistry 67, no. 9 (May 22, 2019): 643–61. http://dx.doi.org/10.1369/0022155419849388.
Full textAbstract:
Kidney fibrosis is the common histological end-point of progressive, chronic kidney diseases (CKDs) regardless of the underlying etiology. The hallmark of renal fibrosis, similar to all other organs, is pathological deposition of extracellular matrix (ECM). Renal ECM is a complex network of collagens, elastin, and several glycoproteins and proteoglycans forming basal membranes and interstitial space. Several ECM functions beyond providing a scaffold and organ stability are being increasingly recognized, for example, in inflammation. ECM composition is determined by the function of each of the histological compartments of the kidney, that is, glomeruli, tubulo-interstitium, and vessels. Renal ECM is a dynamic structure undergoing remodeling, particularly during fibrosis. From a clinical perspective, ECM proteins are directly involved in several rare renal diseases and indirectly in CKD progression during renal fibrosis. ECM proteins could serve as specific non-invasive biomarkers of fibrosis and scaffolds in regenerative medicine. The gold standard and currently only specific means to measure renal fibrosis is renal biopsy, but new diagnostic approaches are appearing. Here, we discuss the localization, function, and remodeling of major renal ECM components in healthy and diseased, fibrotic kidneys and the potential use of ECM in diagnostics of renal fibrosis and in tissue engineering.
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Sun, Qinxue, Maike Baues, Barbara M. Klinkhammer, Josef Ehling, Sonja Djudjaj, Natascha I. Drude, Christoph Daniel, et al. "Elastin imaging enables noninvasive staging and treatment monitoring of kidney fibrosis." Science Translational Medicine 11, no. 486 (April 3, 2019): eaat4865. http://dx.doi.org/10.1126/scitranslmed.aat4865.
Full textAbstract:
Fibrosis is the common endpoint and currently the best predictor of progression of chronic kidney diseases (CKDs). Despite several drawbacks, biopsies remain the only available means to specifically assess the extent of renal fibrosis. Here, we show that molecular imaging of the extracellular matrix protein elastin allows for noninvasive staging and longitudinal monitoring of renal fibrosis. Elastin was hardly expressed in healthy mouse, rat, and human kidneys, whereas it was highly up-regulated in cortical, medullar, and perivascular regions in progressive CKD. Compared to a clinically relevant control contrast agent, the elastin-specific magnetic resonance imaging agent ESMA specifically detected elastin expression in multiple mouse models of renal fibrosis and also in fibrotic human kidneys. Elastin imaging allowed for repetitive and reproducible assessment of renal fibrosis, and it enabled longitudinal monitoring of therapeutic interventions, accurately capturing anti-fibrotic therapy effects. Last, in a model of reversible renal injury, elastin imaging detected ensuing fibrosis not identifiable via routine assessment of kidney function. Elastin imaging thus has the potential to become a noninvasive, specific imaging method to assess renal fibrosis.
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Sang, Yizhen, Kenji Tsuji, Kazuhiko Fukushima, Kensaku Takahashi, Shinji Kitamura, and Jun Wada. "Semaporin3A inhibitor ameliorates renal fibrosis through the regulation of JNK signaling." American Journal of Physiology-Renal Physiology 321, no. 6 (December 1, 2021): F740—F756. http://dx.doi.org/10.1152/ajprenal.00234.2021.
Full textAbstract:
Renal fibrosis is the common pathological pathway in the progression of renal diseases. This study, using a unilateral ureteral obstruction (UUO) mouse model, indicated increased semaphorin3A (SEMA3A) signaling in renal tubular cells as well as fibroblast cells under UUO surgery, and SEMA3A inhibitor ameliorated UUO-induced renal fibrosis through the regulation of JNK signaling. The study proposes the potential therapeutic option of SEMA3A inhibitor to treat renal fibrosis.
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Yoon, Yeo Min, Gyeongyun Go, Chul Won Yun, Ji Ho Lim, Jun Hee Lee, and Sang Hun Lee. "Melatonin Suppresses Renal Cortical Fibrosis by Inhibiting Cytoskeleton Reorganization and Mitochondrial Dysfunction through Regulation of miR-4516." International Journal of Molecular Sciences 21, no. 15 (July 27, 2020): 5323. http://dx.doi.org/10.3390/ijms21155323.
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Renal fibrosis, a major risk factor for kidney failure, can lead to chronic kidney disease (CKD) and is caused by cytoskeleton reorganization and mitochondrial dysfunction. In this study, we investigated the potential of melatonin treatment to reduce renal fibrosis by recovering the cytoskeleton reorganization and mitochondrial dysfunction. We found that miR-4516 expression was downregulated in the renal cortex of CKD mice and P-cresol-treated TH1 cells. Decreased miR-4516 expression stimulated cytoskeleton reorganization and mitochondrial dysfunction, and induced renal fibrosis. Melatonin treatment suppressed fibrosis by inhibiting cytoskeleton reorganization and restoring mitochondrial function via increased miR-4516 expression. More specifically, melatonin treatment increased miR-4516 expression while decreasing ITGA9 expression, thereby inhibiting cytoskeleton reorganization. In addition, increased expression of miR-4516 by melatonin treatment reduced ROS formation and restored mitochondrial function. These findings suggest that melatonin may be a promising treatment for patients with CKD having renal fibrosis. Moreover, regulation of miR-4516 expression may be a novel strategy for the treatment of renal fibrosis.
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Chen, Meiling, Yihang Yu, Tao Mi, Qitong Guo, Bin Xiang, Xiaomao Tian, Liming Jin, et al. "MK-2206 Alleviates Renal Fibrosis by Suppressing the Akt/mTOR Signaling Pathway In Vivo and In Vitro." Cells 11, no. 21 (November 5, 2022): 3505. http://dx.doi.org/10.3390/cells11213505.
Full textAbstract:
Renal fibrosis is a common pathological feature of various kidney diseases, leading to irreversible renal failure and end-stage renal disease. However, there are still no effective treatments to reverse renal fibrosis. This study aimed to explore the potential mechanism of a targeted drug for fibrosis. Here, unilateral ureteral obstruction (UUO)-treated mice and a TGF-β1-treated human renal tubular epithelial cell line (HK-2 cells) were used as models of renal fibrosis. Based on the changes of mRNA in UUO kidneys detected by transcriptome sequencing, MK-2206, an Akt inhibitor, was predicted as a potential drug to alleviate renal fibrosis through bioinformatics. We dissolved UUO mice with MK-2206 by gastric gavage and cultured TGF-β-induced HK-2 cells with MK-2206. Histopathological examinations were performed after MK-2206 intervention, and the degree of renal fibrosis, as well as the expression of Akt/mTOR pathway-related proteins, were evaluated by immunohistochemical staining, immunofluorescence staining, and Western blot. The results showed that MK-2206 significantly improved the pathological structure of the kidney. Furthermore, MK-2206 intervention effectively inhibited UUO- and TGF-β1-induced epithelial-mesenchymal transition, fibroblast activation, and extracellular matrix deposition. Mechanistically, MK-2206 treatment attenuated the activation of the Akt/mTOR signaling pathway. Taken together, our study revealed for the first time that MK-2206 is a promising drug for the improvement of renal fibrosis.