Relevant bibliographies by topics / Podocytes in urine

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  2. Dissertations / Theses
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Academic literature on the topic 'Podocytes in urine'

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

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Journal articles on the topic "Podocytes in urine"

1

Kimura, Moritsugu, Masao Toyoda, Nobumichi Saito, et al. "A Liquid-Based Cytology System, without the Use of Cytocentrifugation, for Detection of Podocytes in Urine Samples of Patients with Diabetic Nephropathy." Journal of Diabetes Research 2019 (February 17, 2019): 1–7. http://dx.doi.org/10.1155/2019/9475637.

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Objective. Podocytes have highly differentiated functions and are extremely difficult to grow; thus, damage of podocytes is associated with glomerular dysfunction. Desquamated podocytes can be detected in urine of patients with severe renal impairment. Unlike the rapidly progressive glomerular damage in glomerulonephritis, only a few desquamated podocytes are usually detected in diabetic nephropathy (DN). It is not clear whether the low podocyte count in DN is due to limitation of the conventional method or true pathological feature. The aim of this study was to compare the conventional method
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Chebotareva, N. V., I. N. Bobkova, and L. V. Lysenko. "The role of podocytes dysfunction in chronic glomerulonephritis progression." Terapevticheskii arkhiv 90, no. 6 (2018): 92–97. http://dx.doi.org/10.26442/terarkh201890692-97.

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In the review, the mechanisms of podocytes damage underlying the development of proteinuria and progression of glomerulosclerosis in chronic glomerulonephritis are discussed in detail. The results of experimental and clinical studies are presented. Under the different immune and non-immune factors the podocytes form a stereotyped response to damage consisting in the reorganization of the actin cytoskeleton, foot process effacement, the detachment of podocytes from the glomerular basement membrane, and the appearance of specific podocyte proteins and whole cells (podocyturia) in the urine. Mass
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Sakairi, Toru, Yoshifusa Abe, Hiroshi Kajiyama, et al. "Conditionally immortalized human podocyte cell lines established from urine." American Journal of Physiology-Renal Physiology 298, no. 3 (2010): F557—F567. http://dx.doi.org/10.1152/ajprenal.00509.2009.

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Evidence suggests that loss of podocytes into urine contributes to development of glomerular diseases; shed podocytes are frequently viable and proliferate in culture conditions. To determine the phenotypic characteristics of viable urinary cells derived from human subjects, we established long-term urinary cell culture from two patients with focal segmental glomerulosclerosis and two healthy volunteers, via transformation with the thermosensitive SV40 large T antigen (U19tsA58) together with human telomerase (hTERT). Characterization of arbitrarily selected two clonal cell lines from each hum
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Kostovska, Irena, Katerina Tosheska Trajkovska, Svetlana Cekovska, Goce Spasovski, and Danica Labudovic. "Nephrin and Podocalyxin - New Podocyte Proteins for Early Detection of Secondary Nephropathies." BANTAO Journal 14, no. 1 (2016): 11–16. http://dx.doi.org/10.1515/bj-2016-0003.

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AbstractIn the last two decades a great progress was observed in understanding of podocytes, their specific structure and function identifying many specific podocyte proteins, such as nephrin and podocalyxin. Podocytes form the final barrier to plasma proteins leakage. Nephrin as a main component of the filtration diaphragm forms a physical barrier while podocalyxin as sialoglycoprotein forms an electrostatic barrier. Podocyte damage, i.e. podocytopathies and their loss through urine-podocyturia, are crucial in pathogenesis and progression of nephropathies with proteinuria as main clinical man
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Liu, Ying, Shan Li, Weiwei Rong, et al. "Podocyte-Released Migrasomes in Urine Serve as an Indicator for Early Podocyte Injury." Kidney Diseases 6, no. 6 (2020): 422–33. http://dx.doi.org/10.1159/000511504.

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<b><i>Background:</i></b> Levels of urinary microvesicles, which are increased during various kidney injuries, have diagnostic potential for renal diseases. However, the significance of urinary microvesicles as a renal disease indicator is dampened by the difficulty to ascertain their cell source. <b><i>Objectives:</i></b> The aim of this study was to demonstrate that podocytes can release migrasomes, a unique class of microvesicle with size ranging between 400 and 2,000 nm, and the urine level of migrasomes may serve as novel non-invasive biomar
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Vogelmann, Stefanie U., W. James Nelson, Bryan D. Myers, and Kevin V. Lemley. "Urinary excretion of viable podocytes in health and renal disease." American Journal of Physiology-Renal Physiology 285, no. 1 (2003): F40—F48. http://dx.doi.org/10.1152/ajprenal.00404.2002.

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The loss of glomerular visceral epithelial cells (podocytes) has been associated with the development of glomerular sclerosis and loss of renal function. Viability of podocytes recovered from urine of subjects with glomerular disease and of healthy controls was investigated by propidium iodide exclusion and TUNEL staining. Podocyte loss was quantified by cytospin. The growth behavior in culture of urinary cells and their expression of specific markers were examined. The majority of urinary podocytes are viable, although apoptosis occurs in about one-half of the cells. Patients with active glom
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Matsusaka, Taiji, Kazuto Kobayashi, Valentina Kon, Ira Pastan, Agnes B. Fogo, and Iekuni Ichikawa. "Glomerular sclerosis is prevented during urinary tract obstruction due to podocyte protection." American Journal of Physiology-Renal Physiology 300, no. 3 (2011): F792—F800. http://dx.doi.org/10.1152/ajprenal.00570.2010.

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Urine outflow obstruction activates a variety of profibrotic factors, including the intrarenal renin-angiotensin system. However, the obstruction also nullifies the transmural hydraulic pressure difference across the glomerular capillary wall, an established inducer of glomerulosclerosis. In the present study, we investigated whether, and by what mechanism, urine outflow obstruction affects the process of progressive glomerulosclerosis. For this purpose, we tested the effect of unilateral ureteral obstruction (UUO) of 7 days duration in two distinct mouse models of glomerulosclerosis. In the h
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8

Raij, Leopoldo, Runxia Tian, Jenny S. Wong, John C. He, and Kirk N. Campbell. "Podocyte injury: the role of proteinuria, urinary plasminogen, and oxidative stress." American Journal of Physiology-Renal Physiology 311, no. 6 (2016): F1308—F1317. http://dx.doi.org/10.1152/ajprenal.00162.2016.

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Podocytes are the key target for injury in proteinuric glomerular diseases that result in podocyte loss, progressive focal segmental glomerular sclerosis (FSGS), and renal failure. Current evidence suggests that the initiation of podocyte injury and associated proteinuria can be separated from factors that drive and maintain these pathogenic processes leading to FSGS. In nephrotic urine aberrant glomerular filtration of plasminogen (Plg) is activated to the biologically active serine protease plasmin by urokinase-type plasminogen activator (uPA). In vivo inhibition of uPA mitigates Plg activat
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Peco-Antic, Amira, and Bilsana Mulic. "Podocytopathies." Srpski arhiv za celokupno lekarstvo 148, no. 9-10 (2020): 631–36. http://dx.doi.org/10.2298/sarh181226067p.

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Podocytopathies include a wide spectrum of primary or secondary glomerular diseases that are the consequence of the podocyte injuries. The damage of podocytes can occur due to congenital or acquired disorders of podocyte transcriptional regulators, altered components of the slit diaphragm complex, abnormal assembly, or function of the actin-based cytoskeleton, dysfunction of membranes or cytoplasmic proteins, and mitochondrial injury. Podocytes reactions to injurious stimulus include FP effacement, apoptosis, and loss of podocyte, developmental arrest associated by mild proliferative activity,
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Schordan, Sandra, Olaf Grisk, Eric Schordan, et al. "OPN deficiency results in severe glomerulosclerosis in uninephrectomized mice." American Journal of Physiology-Renal Physiology 304, no. 12 (2013): F1458—F1470. http://dx.doi.org/10.1152/ajprenal.00615.2012.

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Osteopontin (OPN) expression has been reported to be elevated in experimental models of renal injury such as arterial hypertension or diabetic nephropathy finally leading to focal segmental glomerulosclerosis (FSGS). FSGS is characterized by glomerular matrix deposition and loss or damage of podocytes that represent the main constituents of the glomerular filtration barrier. To evaluate the role of OPN in the kidney we investigated WT and OPN knockout mice (OPN−/−) without treatment, after uninephrectomy (UNX), as well as after UNX and desoxycorticosterone acetate (DOCA)-salt treatment with re
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Dissertations / Theses on the topic "Podocytes in urine"

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Nascimento, Jonathan Fraportti do. "Expressão gênica de proteínas do podócito na urina de pacientes diabéticos normo, micro ou macroalbuminúricos e em pré diabeticos." reponame:Biblioteca Digital de Teses e Dissertações da UFRGS, 2012. http://hdl.handle.net/10183/142953.

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Introdução: A lesão do podócito exerce um papel crítico na nefropatia diabética (ND) e é um fator preditivo de albuminúria patológica e progressão da doença. Neste estudo foi avaliada a expressão gênica de proteínas associadas ao podócito na urina de pacientes diabéticos em diferentes estágios da ND e em indivíduos com pré diabetes. Material e Métodos: Foram estudados 67 pacientes diabéticos com normo (n=34), micro (n=14) ou macroalbuminúria (n=19), dezenove indivíduos pré diabéticos e 15 controles saudáveis. O RNAm de nefrina, podocina, podocalixina, sinaptopodina, Transient Receptor Potentia
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Kratochvílová, Markéta. "Oxidační a karbonylový stres u onemocnění ledvin." Doctoral thesis, 2016. http://www.nusl.cz/ntk/nusl-348959.

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Aims: 1. Determination of AGEs (Advanced Glycation End products) in patients with various types of nephropathy. 2. Association AGEs with nutritional parameters and anemia. 3. Influence of renal parameters on sRAGE (soluble form of Receptor for Advanced Glycation End products) levels. 4. Technics and proceeding methods of the podocytes cultivation. 5. Determination of urine podocytes. Methods: We determined fluorescent AGEs by spectrofluorometry, sRAGE by Enzyme-Linked ImmunoSorbent Assay (ELISA). Podocytes were passaged and identified immunocytochemically. Podocytes in urine were specified by
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"Urinary gene expression as a marker of glomerular podocyte injury and disturbance of renin-angiotensin system in patients with diabetic nephropathy." Thesis, 2008. http://library.cuhk.edu.hk/record=b6074579.

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Diabetic nephropathy (DN) is one of the leading causes of end stage renal disease (ESRD) in western world and has a trend to spread in developing countries. Pathogenesis of DN is not fully elucidated. Studies of recent years showed that podocyte loss and activation of the rennin-angiotensin system (RAS), especially intra-renal RAS, played important roles in this process. Although renal biopsy is currently the most common way used to determine the expression pattern of podocyte and RAS associated molecules in DN, this invasive procedure has its own risk and is not practical for serial monitorin
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Books on the topic "Podocytes in urine"

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Hughes, Jeremy. Proteinuria as a direct cause of progression. Edited by David J. Goldsmith. Oxford University Press, 2015. http://dx.doi.org/10.1093/med/9780199592548.003.0137.

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Proximal tubular cells reabsorb any filtered proteins during health via cell surface receptors such as megalin and cubulin so that very low levels of protein are present in the excreted urine. Significant proteinuria is a common finding in patients with many renal diseases. Proteinuria is a marker of glomerular damage and podocyte loss and injury in particular. The degree of proteinuria at presentation or during the course of the disease correlates with long-term outcome in many renal diseases. Proteinuria per se may be nephrotoxic and thus directly relevant to the progression of renal disease
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Book chapters on the topic "Podocytes in urine"

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Moreno-Gómez-Toledano, Rafael, María I. Arenas, Sandra Sánchez-Esteban, Alberto Cook, Marta Saura, and Ricardo J. Bosch. "Critical Analysis of Human Exposure to Bisphenol a and its Novel Implications on Renal, Cardiovascular and Hypertensive Diseases." In Hot Topics in Endocrinology and Metabolism [Working Title]. IntechOpen, 2021. http://dx.doi.org/10.5772/intechopen.96309.

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Bisphenol A (BPA), an endocrine disruptor involved in synthesizing numerous types of plastics, is detected in almost the entire population’s urine. The present work aims to estimate daily exposure to BPA by systematically reviewing all articles with original data related to urinary BPA concentration. This approach is based on human pharmacokinetic models, which have shown that 100% of BPA (free and metabolized form) is eliminated only in a few hours through urine. Several extensive population studies and experimental data have recently proven a significant association between urinary excretion of BPA and albuminuria, associated with renal damage. Our team’s previous work has shown that low-dose BPA can promote a cytotoxic effect on renal mouse podocytes. Moreover, BPA administration in mice promotes kidney damage and hypertension. Furthermore, preliminary studies in human renal cells in culture (podocytes) strongly suggest that BPA might also promote kidney damage. Overall, the present review analyzed BPA exposure data from mammalian cell studies, experimental animal models, and several human populations. Studying principal cohorts calculated the exposures to BPA globally, showing a high BPA exposure suggesting the need to decrease BPA exposure more effectively, emphasizing groups with higher sensitivity as kidney disease patients.
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