Relevant bibliographies by topics / Kidney glomerulus Diseases

Academic literature on the topic 'Kidney glomerulus Diseases'

Author: Grafiati
Published: 4 June 2021
Last updated: 21 February 2023

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

Journal articles on the topic "Kidney glomerulus Diseases":

1

Beeman, Scott C., Min Zhang, Lina Gubhaju, Teresa Wu, John F. Bertram, David H. Frakes, Brian R. Cherry, and Kevin M. Bennett. "Measuring glomerular number and size in perfused kidneys using MRI." American Journal of Physiology-Renal Physiology 300, no. 6 (June 2011): F1454—F1457. http://dx.doi.org/10.1152/ajprenal.00044.2011.

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The goal of this work was to nondestructively measure glomerular (and thereby nephron) number in the whole kidney. Variations in the number and size of glomeruli have been linked to many renal and systemic diseases. Here, we develop a robust magnetic resonance imaging (MRI) technique based on injection of cationic ferritin (CF) to produce an accurate measurement of number and size of individual glomeruli. High-field (19 Tesla) gradient-echo MR images of perfused rat kidneys after in vivo intravenous injection of CF showed specific labeling of individual glomeruli with CF throughout the kidney. We developed a three-dimensional image-processing algorithm to count every labeled glomerulus. MRI-based counts yielded 33,786 ± 3,753 labeled glomeruli ( n = 5 kidneys). Acid maceration counting of contralateral kidneys yielded an estimate of 30,585 ± 2,053 glomeruli ( n = 6 kidneys). Disector/fractionator stereology counting yielded an estimate of 34,963 glomeruli ( n = 2). MRI-based measurement of apparent glomerular volume of labeled glomeruli was 4.89 × 10−4mm3( n = 5) compared with the average stereological measurement of 4.99 × 10−4mm3( n = 2). The MRI-based technique also yielded the intrarenal distribution of apparent glomerular volume, a measurement previously unobtainable in histology. This work makes it possible to nondestructively measure whole-kidney glomerular number and apparent glomerular volumes to study susceptibility to renal diseases and opens the door to similar in vivo measurements in animals and humans.
2

KITAMURA, MASANORI. "Renal Transfer of Genetically Engineered Cells." Journal of the American Society of Nephrology 11, suppl 2 (November 2000): S154—S158. http://dx.doi.org/10.1681/asn.v11suppl_2s154.

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Abstract. For many years, ex vivo gene transfer has been used for genetic manipulation of various organs. In the kidney, ex vivo gene transfer was reported using mesangial cells and macrophages. In rats, cultured cells injected into the renal artery are accumulated selectively in the glomerulus. With this approach, it is possible to transfer genetically engineered cells to normal and diseased glomeruli. The transfer of genetically engineered cells to glomeruli can be used for several purposes. With the use of resident glomerular cells engineered in vitro, it is possible to examine how the cells that overexpress certain genes behave differently in normal and diseased glomeruli. Both gain-of-function and loss-of-function strategies are useful for this purpose. For the latter, stable expression of antisense cDNA, ribosomes, or dominant-negative mutants is available. By transfer of engineered cells producing secretory, recombinant proteins, it is possible to modify glomerular microenvironment in vivo. Transfer of genes encoding therapeutically relevant molecules could be useful for therapeutic intervention. Transfer of engineered leukocytes to the glomerulus also allows investigation of cross talk between leukocytes and resident cells. Transfer of stimulated leukocytes is useful for investigation of the pathologic actions of infiltrating cells on glomerular structure and function. Leukocytes in which certain gene functions are selectively reinforced or deleted would be useful for elucidation of the exact functions of leukocyte-associated genes in glomerular diseases. This article summarizes current experience with the adoptive transfer of engineered cells to the glomerulus for investigation of and therapy for glomerular diseases.
3

Wang, Honglian, Jingyi Sheng, Huijun He, Xiaocui Chen, Jinhong Li, Ruizhi Tan, Li Wang, and Hui-Yao Lan. "A simple and highly purified method for isolation of glomeruli from the mouse kidney." American Journal of Physiology-Renal Physiology 317, no. 5 (November 1, 2019): F1217—F1223. http://dx.doi.org/10.1152/ajprenal.00293.2019.

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Highly purified mouse glomeruli are of great value for studying glomerulus-associated kidney diseases. Here, we developed a simple and rapid procedure for mouse glomerular isolation with large quantity and high purity based on the combination of size-selective sieving and differential adhesion techniques, which we termed the “differential adhesion method.” In this method, mouse renal cortices were minced and digested with collagenase. Glomeruli were disassociated from tubules by successive sieving through 105-, 75-, and 40-μm cell strainers. The retained glomeruli-rich preparation on the 40-μm strainer was rinsed into a cell culture dish to allow tubules to adhere quickly to the dish while leaving most glomeruli floating (termed “differential adhesion”). The floating glomerular fraction was then subjected to another wash through the 40-μm strainer followed by an additional differential adhesion step to obtain highly purified glomeruli with yields of 8,357 ± 575 and purity of 96.1 ± 1.8% from one adult C57BL/6 mouse. The purity of the isolated glomeruli was further confirmed by high expression of the podocyte marker nephrin without detectable tubular marker cadherin-16. Importantly, we also found that although both the quantity and purity of the isolated glomeruli by this and the established Dynabeads method were comparable, glomeruli isolated by the current method showed much less inflammatory stress in terms of proinflammatory cytokine expression than the Dynabeads method. In conclusion, we established a newly mouse glomerular isolation method that is simple, rapid, cost effective, and productive. It provides an advanced methodology for research into glomerulus-related kidney diseases in the mouse.
4

Yoshida, Yutaka, Masahito Miyamoto, Izumi Taguchi, Bo Xu, Ying Zhang, Eishin Yaoita, Hidehiko Fujinaka, and Tadashi Yamamoto. "Human kidney glomerulus proteome and biomarker discovery of kidney diseases." PROTEOMICS – CLINICAL APPLICATIONS 2, no. 3 (March 2008): 420–27. http://dx.doi.org/10.1002/prca.200780016.

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5

Zhu, D., Y. Kim, M. W. Steffes, T. J. Groppoli, R. J. Butkowski, and S. M. Mauer. "Application of electron microscopic immunocytochemistry to the human kidney: distribution of type IV and type VI collagen in normal human kidney." Journal of Histochemistry & Cytochemistry 42, no. 5 (May 1994): 577–84. http://dx.doi.org/10.1177/42.5.8157929.

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We used immunogold electron microscopic (IEM) techniques with periodate-lysine-paraformaldehyde-fixed and Lowicryl-embedded or cryopreserved tissues to study the distribution of alpha 1(IV) and alpha 3(IV) chains of Types IV and VI collagen in glomerular basement membrane (GBM) and mesangial matrix of glomeruli in normal human kidneys. Monoclonal antibodies to alpha 1(IV) and alpha 3(IV) collagen chains and Type VI collagen could be detected only with cryoultramicrotomy, whereas polyclonal anti-Type IV collagen antibody was detectable in Lowicryl-embedded tissue. Ultrastructural detail was better preserved in the Lowicryl-embedded tissue. IEM labeling provided more detailed information as to the site-specific array of these extracellular matrix molecules in glomeruli than did immunofluorescent microscopy. The labeling of alpha 1(IV) collagen chain was distributed mainly along the endothelial side of glomerular basement membrane and the mesangial matrix. Mesangial GBM was relatively poorly labeled compared with that of mesangial matrix. In contrast, the alpha 3(IV) chain was detected throughout the thickness of the GBM, but there was no labeling of mesangial matrix. Type VI collagen distribution was identical to that of the alpha 1(IV) chain within the glomerulus but was also associated with interstitial collagen fibrils. This study documents and details the heterogeneous distribution of Type IV and VI collagen chains within the normal human glomerulus and provides the framework for the study of these matrix components in human glomerular diseases.
6

PATRAKKA, JAAKKO, VESA RUOTSALAINEN, ILKKA KETOLA, CHRISTER HOLMBERG, MARKKU HEIKINHEIMO, KARL TRYGGVASON, and HANNU JALANKO. "Expression of Nephrin in Pediatric Kidney Diseases." Journal of the American Society of Nephrology 12, no. 2 (February 2001): 289–96. http://dx.doi.org/10.1681/asn.v122289.

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Abstract. Nephrin is a podocyte cell adhesion protein located at the slit diaphragm area of the kidney glomerulus. Mutations in the nephrin gene (NPHS1) lead to congenital nephrosis, suggesting that nephrin is essential for the glomerular filtration barrier. This prompted this study of the expression of nephrin in acquired pediatric kidney diseases usingin situhybridization and immunohistochemistry.In situhybridization for nephrin mRNA was performed in biopsy samples from patients with proteinuria caused by minimal change nephrosis, focal segmental glomerulosclerosis, and membranous nephropathy. The expression of nephrin mRNA was evaluated by grading the signal intensity visually and by counting the number of grains in separate glomeruli. No significant difference was observed in these samples as compared with controls. Immunostaining for nephrin was performed using antibodies directed against extra- and intracellular parts of the molecule. Nephrin staining gave a linear pattern along the glomerular capillary loops. In minimal change nephrosis, focal segmental glomerulosclerosis, and membranous nephropathy, the distribution of nephrin was similar to that in controls. In proliferative forms of glomerulonephritides (Henoch-Schönlein nephritis, IgA nephropathy, postinfectious and membranoproliferative glomerulonephritis), crescents and sclerotic lesions were negative for nephrin, and mesangial proliferation led to a scattered and sparse staining pattern. The staining pattern of nephrin was compared to that of ZO-1, a component of the cytoplasmic face of the slit diaphragm. The distributions of these two proteins in capillary tufts were similar in all disease entities studied. In conclusion, immunohistochemistry andin situhybridization did not reveal major alterations in the expression of nephrin in proteinuric kidney diseases in children. Further studies are needed for more precise evaluation of the role of nephrin in these diseases.
7

SUZUKI, DAISUKE, TOSHIO MIYATA, MASAOMI NANGAKU, HIDEO TAKANO, NOBORU SAOTOME, MASAO TOYODA, YASUO MORI, et al. "Expression of Megsin mRNA, a Novel Mesangium-Predominant Gene, in the Renal Tissues of Various Glomerular Diseases." Journal of the American Society of Nephrology 10, no. 12 (December 1999): 2606–13. http://dx.doi.org/10.1681/asn.v10122606.

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Abstract. Mesangial cells play an important role in maintaining a structure and function of the glomerulus and in the pathogenesis of glomerular diseases. Recently, we discovered a new mesangium-predominant gene termed “megsin.” Megsin is a novel protein that belongs to the serine protease inhibitor (serpin) superfamily. To elucidate the pathophysiologic role of megsin in the kidney, the expression and localization of megsin mRNA in renal tissues of patients with IgA nephropathy (IgA-N), diabetic nephropathy (DN), minimal change nephrotic syndrome (MCNS), membranous nephropathy (MN), and normal human kidney (NHK) was evaluated by in situ hybridization using digoxigenin-labeled oligonucleotide. Individual cells positive for megsin mRNA were observed only in glomeruli in all renal tissues. Their localization coincided with those of mesangial cells. The percentage of positive cells for megsin mRNA in total glomerular cells was significantly greater in IgA-N than in MCNS, MN, and NHK. It was also significantly greater in DN than in MCNS and NHK. In IgA-N, the percentage of megsin mRNA-positive cells was greater in tissues from those with mesangial cell proliferation and slightly mesangial matrix expansion (periodic acid-Schiff-positive area in the total glomerulus area, <30%; cell number in mesangial matrix area, >30; assessed in cross-sections through their vascular poles) than in tissues from those with severe mesangial matrix expansion (periodic acid-Schiff-positive area in total glomerulus area, >30%; cell number in mesangial matrix area, <30). In conclusion, megsin mRNA was predominantly expressed in glomerular mesangial cells in all renal tissues. The expression of megsin mRNA was upregulated in IgA-N and DN, both of which are diseases accompanied with mesangial cell proliferation and/or mesangial matrix expansion. These data suggest a link of megsin expression to the pathogenesis of IgA-N and DN, two major causes of end-stage renal failure.
8

Rodriguez, Patricia Q., Asmundur Oddsson, Lwaki Ebarasi, Bing He, Kjell Hultenby, Annika Wernerson, Christer Betsholtz, Karl Tryggvason, and Jaakko Patrakka. "Knockdown of Tmem234 in zebrafish results in proteinuria." American Journal of Physiology-Renal Physiology 309, no. 11 (December 1, 2015): F955—F966. http://dx.doi.org/10.1152/ajprenal.00525.2014.

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Podocytes are highly specialized epithelial cells located at the outer aspects of the glomerular capillary tuft and critical components of the kidney filtration barrier. To maintain their unique features, podocytes express a number of proteins that are only sparsely found elsewhere in the body. In this study, we have identified four (Tmem234, Znf185, Lrrc49, and Slfn5) new highly podocyte-enriched proteins. The proteins are strongly expressed by podocytes, while other parts of the kidney show only weak or no expression. Tmem234, Slfn5, and Lrrc49 are located in foot processes, whereas Znf185 is found in both foot and major processes. Expressional studies in developing kidneys show that these proteins are first expressed at the capillary stage glomerulus, the same stage when the formation of major and foot processes begins. We identified zebrafish orthologs for Tmem234 and Znf185 genes and knocked down their expression using morpholino technology. Studies in zebrafish larvae indicate that Tmem234 is essential for the organization and functional integrity of the pronephric glomerulus filtration barrier, as inactivation of Tmem234 expression results in foot process effacement and proteinuria. In summary, we have identified four novel highly podocyte-enriched proteins and show that one of them, Tmem234, is essential for the normal filtration barrier in the zebrafish pronephric glomerulus. Identification of new molecular components of the kidney filtration barrier opens up possibilities to study their role in glomerulus biology and diseases.
9

Beck, Karl-Friedrich, and Josef Pfeilschifter. "The Pathophysiology of H2S in Renal Glomerular Diseases." Biomolecules 12, no. 2 (January 26, 2022): 207. http://dx.doi.org/10.3390/biom12020207.

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Renal glomerular diseases such as glomerulosclerosis and diabetic nephropathy often result in the loss of glomerular function and consequently end-stage renal disease. The glomerulus consists of endothelial cells, mesangial cells and glomerular epithelial cells also referred to as podocytes. A fine-tuned crosstalk between glomerular cells warrants control of growth factor synthesis and of matrix production and degradation, preserving glomerular structure and function. Hydrogen sulfide (H2S) belongs together with nitric oxide (NO) and carbon monoxide (CO) to the group of gasotransmitters. During the last three decades, these higher concentration toxic gases have been found to be produced in mammalian cells in a well-coordinated manner. Recently, it became evident that H2S and the other gasotransmitters share common targets as signalling devices that trigger mainly protective pathways. In several animal models, H2S has been demonstrated as a protective factor in the context of kidney disorders, in particular of diabetic nephropathy. Here, we focus on the synthesis and action of H2S in glomerular cells, its beneficial effects in the glomerulus and its action in the context of the other gaseous signalling molecules NO and CO.
10

Lee, Hsi-Chieh, and Ahmad Fauzan Aqil. "Combination of Transfer Learning Methods for Kidney Glomeruli Image Classification." Applied Sciences 12, no. 3 (January 20, 2022): 1040. http://dx.doi.org/10.3390/app12031040.

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The rising global incidence of chronic kidney disease necessitates the development of image categorization of renal glomeruli. COVID-19 has been shown to enter the glomerulus, a tissue structure in the kidney. This study observes the differences between focal-segmental, normal and sclerotic renal glomerular tissue diseases. The splitting and combining of allied and multivariate models was accomplished utilizing a combined technique using existing models. In this study, model combinations are created by using a high-accuracy accuracy-based model to improve other models. This research exhibits excellent accuracy and consistent classification results on the ResNet101V2 combination using a mix of transfer learning methods, with the combined model on ResNet101V2 showing an accuracy of up to 97 percent with an F1-score of 0.97, compared to other models. However, this study discovered that the anticipated time required was higher than the model employed in general, which was mitigated by the usage of high-performance computing in this study.
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Journal articles Dissertations / Theses Books

Dissertations / Theses on the topic "Kidney glomerulus Diseases":

1

Wang, Yang. "Murine adriamycin-induced nephropathy : the roles of cell-mediated immunity and CD4+ T-lymphocytes." Thesis, The University of Sydney, 2000. https://hdl.handle.net/2123/27827.

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2

Leung, Chi-kam Joseph, and 梁志錦. "The pathogenesis of IgA nephropathy: the roleof IgA molecule and the nature of IgA receptors." Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 2003. http://hub.hku.hk/bib/B29744908.

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3

Wootton, Andrew. "The glomerular basement membrane and nephritis /." Title page, contents and abstract only, 1985. http://web4.library.adelaide.edu.au/theses/09PH/09phw918.pdf.

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4

Cavaglieri, Rita de Cássia. "Terapia com células tronco derivadas do líquido amniótico humano na nefropatia crônica experimental: é possível bloquear a progresso da doença renal estabelecida?" Universidade de São Paulo, 2018. http://www.teses.usp.br/teses/disponiveis/5/5148/tde-09052018-101720/.

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Células tronco mesenquimais (CTm) apresentam potencial para tratamento da doença renal pela possibilidade de promover regeneração tecidual e recuperação funcional, possivelmente por seus efeitos parácrinos. Na última década, o líquido amniótico foi descrito como uma fonte promissora de extração e isolamento de CTm. Alguns estudos mostraram o efeito renoprotetor das CTm derivadas do líquido amniótico (CTmLA) na doença renal aguda e crônica, quando inoculadas precocemente. Entretanto, ainda não foi estudado o efeito da administração de CTmLA em modelo experimental de doença renal crônica (DRC) com a lesão já estabelecida, situação esta que reproduz melhor a apresentação clínica da doença nos pacientes. Assim, o objetivo do presente estudo foi analisar o efeito da inoculação de CTmLA na região subcapsular renal no modelo de DRC já estabelecido. As CTmLA foram obtidas de pacientes no segundo trimestre de gestação e isoladas através da sua capacidade de aderência ao plástico. A caracterização das CTm foi feita por citometria de fluxo e pela diferenciação celular in vitro. O modelo de DRC utilizado foi o de nefrectomia 5/6 (Nx) que, pela perda de massa renal, evolui com hipertensão arterial, proteinúria, glomeruloesclerose, fibrose intersticial e perda progressiva da função renal. Quinze dias após a indução do modelo, estas alterações já são marcantes e agravam-se com 30 dias. Foram realizados 2 protocolos experimentais: no protocolo I, os animais Nx com DRC estabelecida receberam dose única de CTmLA (5x105) na região subcapsular renal e foram acompanhados por 30 e 60 dias de experimento. No protocolo II, os animais Nx com DRC estabelecida receberam duas doses de CTmLA (5x105) na região subcapsular renal, no 15° e 30° dia após a nefrectomia 5/6, e foram acompanhados por 30 dias, totalizando 60 dias de experimento. Os animais foram subdivididos nos grupos: Sham, ratos submetidos à cirurgia fictícia; Sham+CTmLA, ratos submetidos à Sham que receberam CTmLA; Nx, ratos submetidos à nefrectomia 5/6; Nx+CTmLA, ratos Nx que receberam CTmLA. Para verificar a localização das CTmLA no tecido renal foi realizada a hibridização in situ para cromossomo XY. Foram realizadas análises dos parâmetros clínicos e laboratoriais, além de análise histológica, imunohistoquímica, PCR em tempo real e multiplex. Resultados: as CTmLA cultivadas mostraram grande capacidade de aderência, crescimento em colônia e de diferenciação em células osteogênicas, adipogênicas e condrogênicas. A análise por citometria mostrou-se positiva para CD29, CD44, CD90 e CD105, com uma pequena população de células de CD14, CD34, CD45 e CD117, confirmando a presença preponderante de CTm. Protocolo I: Após 30 dias, a inoculação de CTmLA, dose única, preveniu a elevação da pressão arterial, da proteinúria, da glomeruloesclerose, recuperando a expressão dos marcadores de podócitos, WT-1 e sinaptopodina. Entretanto, não houve efeito benéfico nos níveis de creatinina sérica e na fibrose intersticial, após 30 e 60 dias. O tratamento com CTmLA promoveu uma diminuição marcante do número de macrófagos e uma discreta queda dos leucócitos no infiltrado inflamatório renal, além da diminuição do número de miofibroblastos no interstício renal. Citocinas pró-inflamatórias foram encontradas em menor concentração no tecido renal dos animais que receberam CTmLA (IL-1beta, TNF-alfa, MCP-1 e RANTES). Não houve alteração significativa das citocinas Th1 e Th2, exceto por um aumento da IL-4 nos animais tratados com CTmLA. Os animais que foram acompanhados por 60 dias tiveram uma melhora da proteinúria, da glomeruloesclerose, diminuição do infiltrado de macrófagos e uma melhora da expressão de WT-1. Não foram observadas diferenças estatísticas nos parâmetros de creatinina sérica e fibrose intersticial, aos 30 e 60 dias. Protocolo II: Nos animais que receberam a segunda dose de CTmLA e foram acompanhados por 60 dias observou-se prevenção da elevação da pressão arterial e da proteinúria, além de uma marcante diminuição da fibrose intersticial. Em conclusão, o presente estudo mostrou, pela primeira vez, que a terapia com CTmLA foi capaz de induzir renoproteção nos animais com doença renal crônica estabelecida. O tratamento com CTmLA pode representar uma nova abordagem terapêutica bloqueando a progressão da doença renal crônica
Mesenchymal stem cells (mSC) represent therapeutic potential for the treatment of renal diseases, due to their ability to induce tissue regeneration and functional recovery. Human amniotic fluid stem cells (AFmSC) are a class of fetal, pluripotent stem cells, which present characteristics intermediate between embryonic and adult stem cells. These cells are characterized by the expression of mesenchymal stem cells markers. In addition, they have the ability to differentiate into lineages of all embryonic germ layers. They also show high proliferative rates, but do not induce tumor formation. Therefore, AFmSC are considered to be a very promising cell source and these characteristics have generated a great interest concerning their potential renoprotective effects. The aim of this study was to analyze the effects of AFmSC in an experimental model of chronic kidney disease, the 5/6 nephrectomy model (Nx), after the disease has been established, in order to more closely resemble the clinical settings in humans. AFmSC derived from second-trimester amniocentesis were isolated by plastic adhesion. After 4-7 passages, AFmSC characteristics were confirmed by flow cytometry and by their ability to differentiate into osteogenic, adipogenic and chondrogenic lineages. Two experimental protocols were performed: In protocol I, rats underwent 5/6 nephrectomy (Nx) or sham surgery at day 0, received at day 15 a single dose of hAFmSC (5x105 cells) injected under the renal capsule and were studied at day 30 and 60 days. In protocol II, rats underwent Nx or sham surgery, and received at days 15 and 30, two doses of hAFmSC (5x105 cells) injected under the renal capsule, and were studied at day 60. In both protocols, the animals were subdivided into four groups: Sham, rats submitted to fictitious surgery; Sham+hAFmSC, Sham rats that received hAFmSC; Nx, rats submitted to nephrectomy 5/6; Nx+hAFmSC, Nx rats receiving hAFmSC. The hAFmSC were followed in the renal tissue by in situ hybridization for XY chromosome. In all the groups, clinical and histological parameters were analyzed by immunohistochemistry and real-time PCR. Results: AFmSC cultivated demonstrated an ability to adhere to plastic, to grow in colonies and to differentiate in osteogenic, adipogenic and chondrogenic cells. Quantitative analysis of cell markers by flow cytometry showed that isolated cells were positive for CD29, CD44, CD90 and CD105, with a small population of cells positive for CD14, CD34, CD45 and CD117, confirming a preponderant presence of mSC. Protocol I: After 30 days, the single dose of hAFmSC significantly reduced the blood pressure levels, proteinuria, glomerulosclerosis and improved the expression of podocytes markers, WT-1 and synaptopodin. A marked decrease on the number of macrophages and a discrete decrease of leucocyte infiltration, as well as a reduction of interstitial myofibroblasts was observed. Treatment with hAFmSC significantly reduced some proinflammatory cytokines (IL1beta, TNF-alpha, MCP-1 and RANTES). No significant difference in Th1 or Th2 cytokines was observed, except for IL-4 increase in Nx rats treated with hAFmSC. At 60 days of follow-up, Nx rats treated with hAFmSC presented reduced proteinuria, glomerulosclerosis and macrophages besides increase in WT-1 expression. No improvements were observed on serum creatinine and of interstitial fibrosis, after 30 and 60 days. Protocol II: Inoculation of two doses of hAFmSC in Nx rats improved blood pressure levels, proteinuria and interstitial fibrosis at day 60. In conclusion, the present study demonstrated, for the first time, that hAFmSC induced renoprotection in animals with established chronic kidney disease. Treatment with hAFmSC may represent a novel therapeutic approach for blocking the progression of chronic kidney disease
5

Brittain, Alison Louise. "Growth Hormone (GH) and the Glomerular Podocyte." Ohio University / OhioLINK, 2019. http://rave.ohiolink.edu/etdc/view?acc_num=ohiou1554208861914841.

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6

Sousa, Mauri Félix de. ""Efeitos renais da haploinsuficiência do gene Pkd1 (Polycystic kidney disease 1) em camundongos"." Universidade de São Paulo, 2005. http://www.teses.usp.br/teses/disponiveis/5/5148/tde-21122005-163447/.

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Vários estudos mostram que na doença renal policística autossômica dominante os cistos surgem a partir de um mecanismo de "dois-golpes". A patogênese das manifestações não-císticas, contudo, é pouco compreendida. Neste estudo usamos uma linhagem de camundongos endogâmica com uma mutação nula em Pkd1, onde animais heterozigotos apresentam formação cística renal mínima até 40 semanas de idade. O clearance de inulina e o número de glomérulos foram menores em machos Pkd1+/- que Pkd1+/+, enquanto o volume glomerular médio foi maior em heterozigotos. A excreção urinária de NO2/NO3 não diferiu significantemente entre os dois grupos. Avaliamos a osmolalidade urinária máxima em machos e fêmeas Pkd1+/- and Pkd1+/+, porém não foi detectada diferença significante entre os grupos heterozigoto e selvagem. Nossos resultados oferecem evidência direta de que a haploinsuficiência de Pkd1 resulta em anormalidades anatômicas e funcionais renais e sugerem que o estado haploinsuficiente de Pkd1 possa resultar na redução do número de néfrons por diminuir a ramificação tubular renal durante a nefrogênese
Several studies show that in autosomal dominant polycystic kidney disease cysts arise through a "two-hit" mechanism. The pathogenesis of non-cystic features, however, is poorly understood. In this study we used an inbred mouse line with a null mutation of Pkd1, where heterozygotes had minimal renal cyst formation up to 40 weeks of age. Inulin clearance and the number of glomeruli were lower in Pkd1+/- than in Pkd1+/+ males, while a higher average glomerular volume was observed in heterozygotes. The urinary excretion of NO2/NO3 did not significantly differ between the two groups. Maximal urinary osmolality was evaluated in Pkd1+/- and Pkd1+/+ males and females, but no significant difference was detected between the heterozygous and the wild type groups. Our results provide direct evidence that haploinsufficiency for Pkd1 results in anatomic and functional abnormalities of the kidney and suggest that Pkd1 haploinsufficiency may result in a reduced number of nephrons by diminishing renal tubule branching during nephrogenesis
7

Baboolal, Keshwar. "The renin angiotensin system in experimental renal disease." Thesis, King's College London (University of London), 1996. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.336469.

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8

Randles, Michael. "Proteomic analyses of kidney glomerular extracellular matrix in health and disease." Thesis, University of Manchester, 2015. https://www.research.manchester.ac.uk/portal/en/theses/proteomic-analyses-of-kidney-glomerular-extracellular-matrix-in-health-and-disease(a39fe408-db06-4d80-b97b-4e0651bf7bc3).html.

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Glomerular filtration is a vital physiological process removing waste products from the circulation and this process occurs across the glomerular filtration barrier (GFB). The cells and extracellular matrix (ECM), which form this barrier, are exposed to forces during ultrafiltration and special adaptation is required to withstand these forces. Dysfunction in cellular adhesion machinery or ECM assembly within the GFB causes loss of selective glomerular filtration, however, the mechanisms governing these processes are poorly understood. To this end we sought to characterise the glomerular ECM and adhesion machinery using high throughput mass spectrometry (MS)-based proteomics. MS of human glomerular ECM identified a highly complex extracellular niche, revealing the potential involvement of novel ECM proteins in glomerular development and disease processes. Furthermore we identified that glomerular cells in culture had distinct ECM proteomes and interestingly, coculture experiments demonstrated that the ECM proteome was influenced by cellular crosstalk and had a closer resemblance to glomerular ECM in vivo. Protein network analyses of in vivo and in vitro ECM datasets revealed a common core of highly connected structural ECM proteins that may be important for glomerular ECM assembly. To understand how this ECM proteome altered in disease, we studied mice with mild glomerular dysfunction. Here, transcriptomic and proteomic analyses identified alterations in ECM composition and 3D electron microscopy revealed striking ultrastructural changes in glomerular ECM. MS-based proteomics was next applied to the analysis of glomerular podocyte adhesion complexes, leading to the discovery that the actin cytoskeletal regulators and trafficking machinery are recruited to adhesions sites in an ECM-ligand dependent manner. Furthermore, these differences functionally altered cell shape and adhesion strength. These same analyses were applied to podocyte cell-cell junctions, revealing an unexpected overlap of cell-ECM and cell-cell adhesion machinery. Overall, these findings demonstrate for the first time the complexity of the glomerular ECM and adhesion signalling complexes and reinforce the benefits of global, unbiased experimental approaches. In addition the results suggest that glomerular ECM composition, organisation and adhesion signalling are context dependent, and therefore, represent potential therapeutic targets.
9

Sheerin, Neil Stephen. "Complement in the pathogenesis of immune mediated glomerular injury." Thesis, King's College London (University of London), 2000. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.313287.

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Stitt, Erin Maureen. "The Role of Podocyte Prostaglandin E2 and Angiotensin II Receptors in Glomerular Disease." Thesis, Université d'Ottawa / University of Ottawa, 2011. http://hdl.handle.net/10393/19800.

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The incidence of chronic kidney disease (CKD) is increasing. CKD is characterized by a gradual decrease in renal function leading to end stage renal disease (ESRD). Damage to the glomerular podocytes, is one of the first hallmarks of CKD. We hypothesized that podocyte prostaglandin E2 (PGE2) receptors contribute to the progression of glomerular injury in models of CKD. To test this hypothesis, transgenic mice were generated with either podocyte-specific overexpression or deletion of the PGE2 EP4 receptor (EP4pod+and EP4pod-/- respectively). Mice were next tested in the 5/6 nephrectomy (5/6 Nx) or angiotensin II (Ang II) models of CKD. These studies revealed increased proteinuria and decreased survival for EP4pod+ mice while EP4pod-/- mice were protected against the development of glomerular injury. Furthermore, our findings were supported by in vitro studies using cultured mouse podocytes where an adhesion defect was uncovered for cells overexpressing the EP4 receptor. Additionally, our investigations have demonstrated a novel synergy between angiotensin II AT1 receptors and prostaglandin E2 EP4 receptors. This was revealed by in vitro studies using isolated mouse glomeruli. There we were able to show that Ang II stimulation leads to increased expression of cyclooxygenase 2 (COX-2), the enzyme responsible for synthesis of PGE2, in a p38 mitogen activated protein kinase (MAPK) dependent fashion. Moreover increased PGE2 synthesis was measured in response to Ang II stimulation. We confirmed the presence of this synergy in our cultured mouse podocytes and showed an adhesion defect in response to Ang II stimulation which was COX-2 and EP4 dependent. These findings suggest that Ang II AT1 receptors and PGE2 EP4 receptors act in concert to exacerbate glomerulopathies. Studies using mice with either podocyte-specific overexpression of a dominant negative p38 MAPK or mice with global deletion of the EP1 receptor did not provide conclusive results as to their respective signaling involvement in podocyte injury. Altogether our findings provide novel insight for podocyte PGE2 EP4 and Ang II AT1 receptor signaling in models of CKD. These studies provide novel avenues for pursuing therapeutic interventions for individuals with progressive kidney disease.
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Books on the topic "Kidney glomerulus Diseases":

1

Rotter, Wolfgang. Color atlas of kidney biopsy: Pathology of glomerular diseases. New York: Liss, 1985.

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Prabhakar, Sharma S. An update on glomerulopathies: Clinical and treatment aspects. Rijeka, Croatia: InTech, 2011.

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Prabhakar, Sharma S. An update on glomerulopathies: Etiology and pathogenesis. Rijeka, Croatia: InTech, 2011.

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Wardle, E. N. Glomerulopathies: Cell biology and immunology. Australia: Harwood Academic Press, 1996.

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Valaitis, Jonas. Renal glomerular diseases: Atlas of electron microscopy with histopathological bases and immunofluorescence findings : presention of 110 cases of patients undergoing kidney biopsies. Chicago: ACSP Press, 2002.

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Churg, Jacob. Renal disease: Classification and atlas of glomerular diseases. 2nd ed. New York: Igaku-Shoin, 1995.

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Dickersin, G. Richard. Diagnostic electron microscopy: A text/atlas. New York: Igaku-Shoin, 1988.

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Membranes, International Symposium on Renal Basement. Progress in basement membrane research: Renal and related aspects in health and disease : proceedings. London: J. Libbey, 1988.

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Elger, M. The vascular pole of the renal glomerulus of rat. Berlin: Springer, 1998.

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International Symposium on Renal Basement Membranes (4th 1987 Paris, France). Progress in basement membrane research: Renal and related aspects in health and disease : proceedings of the IVth International Symposium on Renal Basement Membranes and Related Research held in Paris, 21-25 July 1987. London: Libbey, 1988.

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Book chapters on the topic "Kidney glomerulus Diseases":

1

Gould, Edward R., and Anna Marie Burgner. "Glomerular Disease." In The Kidney, 175–97. New York, NY: Springer New York, 2016. http://dx.doi.org/10.1007/978-1-4939-3286-3_12.

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Glassock, Richard J. "Other Glomerular Diseases." In Core Concepts in Parenchymal Kidney Disease, 285–89. New York, NY: Springer New York, 2013. http://dx.doi.org/10.1007/978-1-4614-8166-9_19.

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Grünfeld, Jean-Pierre, Guillaume Bobrie, Jean-Michel Pochet, and Micheline Levy. "Inheritance of Glomerular Diseases." In Inheritance of Kidney and Urinary Tract Diseases, 67–87. Boston, MA: Springer US, 1990. http://dx.doi.org/10.1007/978-1-4613-1603-9_3.

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Jabor, Antonín, Janka Franeková, and Lenka Hošková. "Estimation of Glomerular Filtration Rate." In Biomarkers in Kidney Disease, 1143–73. Dordrecht: Springer Netherlands, 2016. http://dx.doi.org/10.1007/978-94-007-7699-9_33.

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Jabor, Antonín, Janka Franeková, and Lenka Hošková. "Estimation of Glomerular Filtration Rate." In Biomarkers in Kidney Disease, 1–32. Dordrecht: Springer Netherlands, 2015. http://dx.doi.org/10.1007/978-94-007-7743-9_33-1.

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Smyth, Andrew, and Vesna D. Garovic. "Glomerular Disease in Pregnancy." In Core Concepts in Parenchymal Kidney Disease, 315–28. New York, NY: Springer New York, 2013. http://dx.doi.org/10.1007/978-1-4614-8166-9_22.

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Uppal, Nupur N., Divya Monga, and Hitesh H. Shah. "Glomerular Disease After Kidney Transplantation." In Glomerulonephritis, 787–808. Cham: Springer International Publishing, 2019. http://dx.doi.org/10.1007/978-3-319-49379-4_48.

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Uppal, Nupur N., Divya Monga, and Hitesh H. Shah. "Glomerular Disease After Kidney Transplantation." In Glomerulonephritis, 1–22. Cham: Springer International Publishing, 2017. http://dx.doi.org/10.1007/978-3-319-27334-1_48-1.

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Rayner, Hugh C., Mark E. Thomas, and David V. Milford. "Measuring Kidney Function: How to Use Laboratory Tests to Measure Glomerular Filtration Rate." In Understanding Kidney Diseases, 11–28. Cham: Springer International Publishing, 2020. http://dx.doi.org/10.1007/978-3-030-43027-6_2.

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O�Donnell, M. P., Z. A. Massy, C. Guijarro, B. L. Kasiske, Y. Kim, and W. F. Keane. "Isoprenoids, Ras and Proliferative Glomerular Disease." In Lipids and the Kidney, 219–27. Basel: KARGER, 1997. http://dx.doi.org/10.1159/000059840.

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Conference papers on the topic "Kidney glomerulus Diseases":

1

Slesareva, E. V., R. V. Ureneva, S. M. Slesarev, and O. V. Lyapeykova. "The pathomorphology of the renal cortex depending of arterial hypertension duration course." In VIII Vserossijskaja konferencija s mezhdunarodnym uchastiem «Mediko-fiziologicheskie problemy jekologii cheloveka». Publishing center of Ulyanovsk State University, 2021. http://dx.doi.org/10.34014/mpphe.2021-180-183.

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The kidneys autopsy material of persons with arterial hypertension in different duration was examined. Morphometry of the renal corpuscle area and cortical and juxtamedullary nephrons vascular glomeruli was performed. There were 4 groups - a control group (with a normal blood pressure level), and groups with arterial hypertension - the initial stage (group 2), arterial hypertension for 5-10 years (group 3), long-term arterial hypertension - more than 10 years (group 4). It was found that cortical nephrons are distinguished by earlier and more pronounced hyperplasia of the vascular glomerulus, they are more rapidly exposed to sclerosis, which appears in the 5-10th year of the course of the disease. The hyperplasia of the vascular glomerulus components is progressively increasing in juxtaglomerular nephrons, they are less susceptible to sclerosis processes. Key words: arterial hypertension, juxtaglomerular apparatus, juxtamedullary nephrons, vascular glomerulus.
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Никитенко, О. П., Т. В. Стоева, М. В. Федин, and А. И. Гоженко. "ЭТИОЛОГИЯ И ОСОБЕННОСТИ ТЕЧЕНИЯ ХБП У ДЕТЕЙ ПРИ ПАТОЛОГИИ МОЧЕВЫДЕЛИТЕЛЬНОЙ СИСТЕМЫ." In International Trends in Science and Technology. RS Global Sp. z O.O., 2021. http://dx.doi.org/10.31435/rsglobal_conf/28022021/7434.

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This article presents data on the development of (chronickidney disease) CKD in children.In particular, with the pathology of the urinary system in children of different age groups.We analyzed the main clinical characteristics and laboratory parameters in children with pathology of the urinary system.The main parameters of the functional state of the kidneys were considered, the glomerular filtration rate (GFR) was calculated using the CKD EPI formula.The chronic pathology of the urinary systemin children was also analyzed.The course of CKD in children with various clinical nosological forms of kidney pathology was studied.
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Hunt, Sarah, Yoav Segal, Kevin D. Dorfman, and Victor H. Barocas. "A Model of Glomerular Mesangial Transport in Health and Disease." In ASME 2013 Summer Bioengineering Conference. American Society of Mechanical Engineers, 2013. http://dx.doi.org/10.1115/sbc2013-14712.

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Transport in the kidney is critically important in normal function and in disease. Solute transport occurs in many locations within the kidney, including convection within the capillaries, filtration across the basement membrane, and convection/diffusion within the mesangium (Figure 1). Models of transport in the kidney have traditionally focused on ultrafiltration [1], which is the predominant pathway for fluid and solutes passing into the urinary space. However, the mesangium is often the site of the first symptoms in disease [2], suggesting that mesangial transport is significant, at least in some cases.
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Nieto-Chaupis, Huber. "Nephrine-Albumin Interaction and the Spontaneous Apparition of Series Capacitors in the Renal Glomerulus as Indicator of Kidney Disease." In 2021 IEEE/ACIS 22nd International Conference on Software Engineering, Artificial Intelligence, Networking and Parallel/Distributed Computing (SNPD). IEEE, 2021. http://dx.doi.org/10.1109/snpd51163.2021.9704915.

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Gasparotto, M., M. Gatto, RA Sinico, G. Moroni, L. Iaccarino, and A. Doria. "PO.5.98 Glomerular activity at second kidney biopsy predicts of end-stage kidney disease in a large multi-centric cohort of patients with active lupus nephritis." In 13th European Lupus Meeting, Stockholm (October 5–8, 2022). Lupus Foundation of America, 2022. http://dx.doi.org/10.1136/lupus-2022-elm2022.123.

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Xun, Liu, Wu Xiaoming, Li Ningshan, and Lou Tanqi. "Application of radial basis function neural network to estimate glomerular filtration rate in Chinese patients with chronic kidney disease." In 2010 International Conference on Computer Application and System Modeling (ICCASM 2010). IEEE, 2010. http://dx.doi.org/10.1109/iccasm.2010.5622616.

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Bilancieri, Giovanna Benichel, Gabriela Beck Dos Santos, Letícia Umetsu Yaginuma, Eliazar Da Silva Santos Júnior, and Eliane Cardozo Silva. "VANTAGENS E DESVANTAGENS NA UTILIZAÇÃO DO QUESTIONÁRIO SCORED PARA TRIAGEM DE DOENÇA RENAL CRÔNICA EM PACIENTES NA ATENÇÃO BÁSICA: UMA REVISÃO DE LITERATURA." In I Congresso Brasileiro de Saúde Pública On-line: Uma abordagem Multiprofissional. Revista Multidisciplinar em Saúde, 2021. http://dx.doi.org/10.51161/rems/2989.

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Introdução: A doença renal crônica (DRC) é um grave problema de saúde pública, com alta prevalência, de 3 a 6 milhões de brasileiros, e mortalidade, de 15,7 por 100 mil ao ano. O rastreamento precoce em pacientes com comorbidades que predispõem à DRC, é infrequente no sistema único de saúde, resultando no diagnóstico tardio e prejuízos ao paciente. Pretendendo rastrear a DRC em fase inicial, foi elaborado o questionário SCORED, do inglês Screening for Occult Renal Disease. Constituído por 11 perguntas referentes a dados demográficos e clínicos, com pontuação de 0 a 12, sendo considerado paciente de alto risco para desenvolvimento de DRC aqueles com pontuação maior ou igual a 4. Objetivo: O presente estudo busca levantar as vantagens e desvantagens da utilização do questionário SCORED em pacientes da atenção primária à saúde. Materiais e métodos: Revisão baseada em artigos publicados no período de 2007 a 2021, nas plataformas LILACS e PubMed, a partir dos termos “Screening for Occult Renal Diseases” (15 e 5 artigos, respectivamente) e “SCORED and chronic kidney disease” (10 e 8 artigos, respectivamente). Posteriormente, foram excluídos os artigos incoerentes com o tema proposto e selecionados 9 trabalhos para a composição da revisão de literatura. Resultados: O método SCORED proporciona benefícios ao paciente, melhorando a qualidade de vida, acesso facilitado a medicamentos de alto custo e redução da mortalidade. A fácil aplicabilidade em contextos de assistência à saúde, meios de comunicação e a autoaplicação, somado ao baixo-custo, podem auxiliar a reduzir os gastos com tratamentos e terapia renal substitutiva. Todavia, o SCORED limita os fatores envolvidos na gênese da DRC, e considera o histórico médico autorrelatado, gerando alta sensibilidade e baixa especificidade. Ademais, necessita de confirmação por dosagem de creatinina sérica e taxa de filtração glomerular, que em idosos pode ser reduzida, devido ao declínio fisiológico. Conclusão: O questionário auxilia no diagnóstico precoce de DRC, sendo de fácil aplicação e custos baixos. Apesar disso, deve-se realizar o atendimento médico completo e exames complementares. Portanto, deve-se conscientizar que esse método de triagem carece de rastreio de outros quadros, como a doença renal policística autossômica dominante e glomerulonefrite.
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Nowinski, Adam, Anna Czyzak-Gradkowska, Damian Korzybski, Luiza Jonczak, Przemyslaw Bielen, Robert Plywaczewski, and Pawel Sliwinski. "Obstructive sleep apnea and the risk of chronic kidney disease – glomerular filtration rate estimations based on serum cystatin C and creatinine concentrations." In Annual Congress 2015. European Respiratory Society, 2015. http://dx.doi.org/10.1183/13993003.congress-2015.pa2329.

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Hamed, Marwa Ibrahim, Salma Al-Dakhakhny, Hassaan Rathore, and Mohamed Izham Mohamed Ibrahim. "Reno-Protective Effects of Angiotensin Receptor Blockers in Hypertensive Rodent Models: A systematic review." In Qatar University Annual Research Forum & Exhibition. Qatar University Press, 2021. http://dx.doi.org/10.29117/quarfe.2021.0126.

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Background and objective: Essential hypertension is a leading risk factor for chronic kidney disease, yet there is no conclusive evidence that lowering blood pressure alone improves renal outcome measures. Angiotensin-II receptor blockers (ARBs) proposed to have renal-protective effects independent of their antihypertensive effect. This systematic review of animal studies aims to collect available information from the published literature about the ARBs' consequences in murine models and analyze it in a structured way to provide a pre-clinical baseline for future analysis of similar clinical investigations. Methods: Following the PRISMA checklist, we conducted a systematic review for quasi non-randomized controlled studies using PubMed, Embase, Science-Direct, SCOPUS, and Google Scholar to determine the effects of ARBs on kidney functions. Eligible articles report the ARBs' effect on proteinuria, albuminuria, and glomerular filtration rate in murine models of hypertension. Outcomes were present as Mean ± Standard Error of Mean (SEM) with 95% confidence intervals (CIs). Results: This preliminary analysis includes ten out of 56 total eligible articles after quality assessment, reporting twelve renal outcome measures. Two studies showed improvement in CrCl versus one study showing no difference. Four out of five studies showed a reduction in proteinuria compared to the control group. All three studies showed a significant reduction in albuminuria compared to control and other antihypertensives. A study Evaluating BUN showed no difference. Nine outcomes supported the reno-protective effect of ARBs on different hypertensive models with various ARBs and different follow-up durations. Low dose valsartan 10mg/kg was showing no significant effect across two different studies. Conclusion: Preliminary results are encouraging. ARBs contribute to improvement in renal biomarkers in different hypertensive models regardless of their BP-lowering effect.
10

Gyoneva, Lazarina, Mohammad F. Hadi, Yoav Segal, Kevin D. Dorfman, and Victor H. Barocas. "Role of Lateral Interactions in Type IV Collagen Network Mechanics." In ASME 2013 Summer Bioengineering Conference. American Society of Mechanical Engineers, 2013. http://dx.doi.org/10.1115/sbc2013-14625.

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The basement membrane is a specialized part of the extra-cellular matrix. It is usually characterized as a scaffold for epithelial cells but in some tissues it serves other, mechanical, roles [1]. The mechanical properties of the basement membrane are mainly determined by one of its main constituents — type IV collagen. Unlike the well-known fibrous type I collagen, collagen IV assembles into planar networks (Fig. 1) [2]. The α 1(IV) and α 2(IV) collagen IV chains assemble into the so-called major chain network, present in all basement membranes. The α 3(IV), α 4(IV), α 5(IV) collagen IV chains form the minor chain network which is found only in the adult basement membranes of the kidney glomerular capillaries (GBM), ocular lens (LBM), cochlea, and the testes [3]. The minor chains have a higher number of cysteine residues, allowing them to form a higher number of lateral interactions. In the minor chain network, the greater potential to interact laterally manifests in the formation of super-coils, which are rarely observed in the major chain network [4]. Increasing the number of cross-links in a polymeric material is known to increase material stiffness; therefore, it is believed that the minor chain network confers basement membranes with additional strength and stability [5]. In the hereditary disease Alport syndrome, a mutation causes the absence of the minor chain network. The GBM and LBM of Alport patients appear weakened and unable to meet their mechanical demands, further supporting this theory [6]. The objective of this study was to evaluate the importance of cross-linking in the minor chains for the mechanical properties of type IV collagen networks, specifically in the GBM and LBM where the absence of the minor chains has an observed mechanical effect.

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