Relevant bibliographies by topics / Nephrotic syndrome

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

Academic literature on the topic 'Nephrotic syndrome'

Author: Grafiati
Published: 4 June 2021
Last updated: 15 June 2025

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Journal articles on the topic "Nephrotic syndrome"

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Jackson, Lori Williams. "Congenital Nephrotic Syndrome." Neonatal Network 26, no. 1 (2007): 47–55. http://dx.doi.org/10.1891/0730-0832.26.1.47.

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THIS COLUMN, ABOUT THE clinical management of congenital nephrotic syndrome (CNS), was prompted by an infant who presented twice within a few months of life with a diagnosis of septic arthritis. During the infant’s second admission, symptoms of acute renal failure were noted. Among the differential diagnoses was congenital nephrotic syndrome. I cared for this patient and his parents during the initial days of his diagnostic tests. In order to learn more about this potential diagnosis, I began a review of the literature. Fortunately, CNS was ruled out. The patient was found to be in failure due to nephrotoxic medications used to treat his septic arthritis. Because CNS was unfamiliar to me, I thought I would share my findings in this column.
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Sahu, Savita. "Basics of Nephrotic Syndrome." International Journal of Trend in Scientific Research and Development Volume-3, Issue-2 (2019): 591–602. http://dx.doi.org/10.31142/ijtsrd21436.

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Andolino, Tecile Prince, and Jessica Reid-Adam. "Nephrotic Syndrome." Pediatrics in Review 36, no. 3 (2015): 117–26. http://dx.doi.org/10.1542/pir.36-3-117.

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Kelsch, R. C., and A. B. Sedman. "Nephrotic Syndrome." Pediatrics in Review 14, no. 1 (1993): 30–38. http://dx.doi.org/10.1542/pir.14-1-30.

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Yao, L. P. "Nephrotic Syndrome." Pediatrics in Review 21, no. 12 (2000): 432–33. http://dx.doi.org/10.1542/pir.21-12-432.

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Yao, L. P. "Nephrotic Syndrome." Pediatrics In Review 21, no. 12 (2000): 432–33. http://dx.doi.org/10.1542/pir.21.12.432.

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Rodriguez-Ballestas, Estefania, and Jessica Reid-Adam. "Nephrotic Syndrome." Pediatrics In Review 43, no. 2 (2022): 87–99. http://dx.doi.org/10.1542/pir.2020-001230.

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Nephrotic syndrome (NS) encompasses a variety of disease processes leading to heavy proteinuria and edema. Minimal change disease (MCD) remains the most common primary cause of NS, as well as the most responsive to pharmacologic treatment with often minimal to no chronic kidney disease. Other causes of NS include focal segmental glomerulosclerosis, which follows MCD, and secondary causes, including extrarenal or systemic diseases, infections, and drugs. Although initial diagnosis relies on clinical findings as well as urine and blood chemistries, renal biopsy and genetic testing are important diagnostic tools, especially when considering non-MCD NS. Moreover, biomarkers in urine and serum have become important areas for research in this disease. NS progression and prognosis are variable and depend on etiology, with corticosteroids being the mainstay of treatment. Other alternative therapies found to be successful in inducing and maintaining remission include calcineurin inhibitors and rituximab. Disease course can range from recurrent disease relapse with or without acute kidney injury to end-stage renal disease in some cases. Given the complex pathogenesis of NS, which remains incompletely understood, complications are numerous and diverse and include infections, electrolyte abnormalities, acute kidney injury, and thrombosis. Pediatricians must be aware of the presentation, complications, and overall long-term implications of NS and its treatment.
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PRICE, P. "Nephrotic Syndrome." Archives of Disease in Childhood 77, no. 5 (1997): 463. http://dx.doi.org/10.1136/adc.77.5.463m.

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Ware, Thuvaraka. "Nephrotic syndrome." InnovAiT: Education and inspiration for general practice 13, no. 3 (2020): 159–63. http://dx.doi.org/10.1177/1755738019895050.

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Nephrotic syndrome is characterised by proteinuria, hypoalbuminaemia and oedema. The renal function is often normal and symptoms may mimic other common pathologies presenting in the community. The underlying aetiology is more heterogenous in adults compared with children, further confounding the diagnostic process and leading to delays in recognition. It is a relatively rare presentation in primary care, but the consequences of nephrotic syndrome can be significant. Complications include hyperlipidaemia, hypercoaguability, increased risk of infection and end-stage renal failure. It is, therefore, important to diagnose, investigate and manage nephrotic syndrome appropriately.
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&NA;. "NEPHROTIC SYNDROME." Journal of the American Academy of Physician Assistants 23, no. 3 (2010): 68–69. http://dx.doi.org/10.1097/01720610-201003000-00014.

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Dissertations / Theses on the topic "Nephrotic syndrome"

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Bullich, Vilanova Gemma. "Molecular study of idiopathic nephrotic syndrome." Doctoral thesis, Universitat Autònoma de Barcelona, 2016. http://hdl.handle.net/10803/385200.

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Aquesta tesi és una contribució al coneixement de les bases moleculars de la síndrome nefròtica idiopàtica concretament, la nefropatia membranosa idiopàtica i la síndrome nefròtica córtico-resistent (SNCR) o glomeruloesclerosis segmentària i focal (GESF). La primera part d’aquesta tesi presenta l’associació de determinades variants genètiques tan amb el risc de desenvolupar nefropatia membranosa idiopàtica com amb el curs clínic de la malaltia, en població espanyola. Els nostres resultats mostren que determinats al·lels en els gens HLA-DQA1 i PLA2R1 estan associats amb un major risc de desenvolupar nefropatia membranosa. A més, la combinació dels al·lels de risc per a aquests dos gens resulta en un risc encara més incrementat per a desenvolupar la malaltia. Per contra, no s’ha identificat cap associació significativa entre el nombre de copies en gens FCGR3A i FCGR3B i la susceptibilitat per desenvolupar nefropatia membranosa. Per primer cop, presentem evidència de la contribució d’al·lels de risc en els gens HLA-DQA1 i PLA2R1 en la predicció de la resposta al tractament immunosupressor i l’empitjorament de la funció renal. La segona part d’aquesta tesi es centra en la millora del diagnòstic genètic de la SNCR/GESF i l’estudi de les seves bases moleculars. En primer lloc, es va demostrar la idoneïtat de les tècniques de seqüenciació massiva per al diagnòstic genètic de la SNCR/GESF. A més, es van detectar pacients amb mutacions en un gen de la SNCR/GESF conjuntament amb COL4A3. Aquests pacients presentaven un fenotip més greu suggerint que mutacions en diferents gens que convergeixen en la barrera de filtració glomerular influencien en la severitat de la malaltia. El paper causal i modificador del gen TTC21B es va examinar en una cohort de pacients amb malaltia renal quística o glomerular. Els nostres resultats indiquen que la mutació p.P209L en homozigosi no és la única mutació d’aquest gen que causa GESF. A més, variants en heterozigosis en el gen TTC21B podrien agreujar el fenotip de pacients amb malalties renals quístiques o glomerulars. Finalment, s’ha desenvolupat un panell de gens associats amb malaltia renals com a eina diagnòstica per a malalties renals hereditàries quístiques i glomerulars, permetent el diagnòstic diferencial d’aquestes malalties, així com la identificació de variants estructurals, mutacions en mosaic i patrons d’herència complexes. Aquesta aproximació s’està utilitzant actualment en el diagnòstic genètic de rutina de pacients de tot Espanya i altres països, sent un clar exemple de recerca translacional.<br>This thesis is a contribution to the knowledge of the molecular bases of idiopathic nephrotic syndrome specifically, the idiopathic membranous nephropathy and steroid-resistant nephrotic syndrome (SRNS)/ focal segmental glomerulosclerosis (FSGS). The first part of this thesis is focused in the association of genetic polymorphisms with the risk to develop idiopathic membranous nephropathy and with its clinical course in the Spanish population. Our results showed that specific alleles within HLA-DQA1 and PLA2R1 genes are associated with a higher risk of idiopathic membranous nephropathy. In addition, the combination of the risk alleles for both genes results in an increased risk of disease development. In contrast, no significant association was found between copy number variants in FCGR3A and FCGR3B genes and susceptibility to idiopathic membranous nephropathy. For the first time, we presented evidence of the contribution of the risk alleles within HLA-DQA1 and PLA2R1 genes to predict response to immunosuppressive therapy and decline in renal function. The second part of these thesis focus on the improvement of SRNS/FSGS genetic testing and the study of its molecular bases. The suitability of massive parallel sequencing for genetic diagnosis of SRNS/FSGS was demonstrated. In addition, we detected patients with mutations in an SRNS/FSGS gene together with COL4A3 that showed increased disease severity, suggesting that mutations in different genes that converge in the glomerular filtration barrier influence disease severity. The causative and modifier role of TTC21B gene was examined in our cohort of cystic and glomerular patients. Our results showed that the homozygous p.P209L is not the only causative mutation of FSGS. Furthermore, heterozygous deleterious TTC21B variants may aggravate the phenotype of patients with glomerular and cystic kidney inherited kidney diseases. Finally, a kidney-disease gene panel was developed as a diagnostic tool for cystic and glomerular inherited kidney diseases, enabling the differential diagnosis of these diseases and the identification of mosaic mutations, structural variants and complex inheritance patterns. This approach is currently used in routine genetic diagnostic of patients from all over Spain and other countries, providing a nice example of translational research.
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Koziell, A. B. "The molecular basis of childhood nephrotic syndrome." Thesis, University College London (University of London), 2007. http://discovery.ucl.ac.uk/1445264/.

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Childhood nephrotic syndrome results from massive leakage of protein into the urine, a low plasma albumin and oedema. Disease may be kidney-specific, occur as part of a malformation syndrome, or may complicate systemic diseases such as diabetes mellitus. Despite the apparent heterogeneity, the underlying defect is loss of the normal permselective characteristics of the glomerular filtration barrier (GFB). Clues for a molecular basis came from observation of occasional autosomal dominant or recessive inheritance, and the detection of WT1 mutations in Denys Drash syndrome (DDS), a triad of intersex, nephrotic syndrome and Wilms' tumour (Pelletier et al, 1991). The role of three glomerular genes WTl, NPHS1 and NPHS2 in the pathogenesis of glomerular protein leak was investigated. WTl mutations were not detected in non- syndromic diffuse mesangial sclerosis (DMS) and focal segmental glomerulosclerosis (FSGS), despite their association with DDS. However, subsequent analysis established that WTl mutations cause Frasier syndrome, a triad of FSGS, intersex and gonadoblastoma, by reversing the normal +(KTS)/-(KTS) WTl isoform ratio. Unfortunately, yeast 2-hybrid screens failed to ascertain any WTl protein binding partners with clear roles in glomerular function, and through which the effects of mutations might be mediated. A wide range of NPHS1 mutations was detected in Finnish type congenital nephrotic syndrome (CNF) in non-Finns, and a novel mild CNF phenotype described. NPHS2 mutations affected some CNF cases, and an overlap in the NPHS1/NPHS2 mutation spectrum was confirmed by the discovery of a unique di-genic inheritance of mutations. This modified the phenotype from CNF to congenital FSGS, providing the first evidence for a functional inter-relationship between these genes. Finally, disrupted protein-DNA binding to an area of the NPHS1 promoter containing a G->C base substitution was identified, suggesting the location of a transcription factor binding site and underscoring the importance of appropriate transcriptional control of NPHS1 for correct gene function.
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Mccaffrey, James. "Podocyte-specific glucocorticoid effects in childhood nephrotic syndrome." Thesis, University of Manchester, 2016. https://www.research.manchester.ac.uk/portal/en/theses/podocytespecific-glucocorticoid-effects-in-childhood-nephrotic-syndrome(559e1d71-6e81-46e5-84ae-7c836e4de042).html.

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Background: Nephrotic syndrome (NS) occurs when the glomerular filtration barrier becomes abnormally permeable, leading to the clinical triad of proteinuria, massive oedema, and hypoalbuminaemia. Historically, NS has been thought to result from dysregulation of the immune system, although recent evidence suggests the glomerular podocyte plays a central role in disease pathogenesis. Children with NS are generally treated with an empiric course of glucocorticoid (Gc) therapy; a class of steroids which are activating ligands for the glucocorticoid receptor (GR) transcription factor. A major factor limiting the clinical utility of these agents is the marked variation observed in response to treatment. Although Gc-therapy has been the cornerstone of NS management for several decades, the mechanism of action, and target cell, remain poorly understood. Hypothesis and aims: The central hypothesis for this thesis states that glucocorticoids act directly on the podocyte to produce clinically useful effects without involvement of the immune system. Findings: Using a wild-type human podocyte cell line, I demonstrated that the basic GR-signalling mechanism is intact in the podocyte, and that glucocorticoids produce a direct, protective effect on the podocyte without immune cell involvement, by using electrical resistance across a podocyte monolayer as a surrogate marker for barrier integrity. To understand potential mechanisms underpinning this direct effect I defined the podocyte GR cistrome (using a combination of chromatin immunoprecipitation followed by massively parallel DNA sequencing and transcriptomic analysis) as well as total cell proteomics. Subsequent gene ontology analysis revealed that Gc treatment had prominent effects on podocyte motility, and these findings were validated with live-cell imaging. To gain mechanistic insight, I investigated the role of the pro-migratory small GTPase regulator Rac1, and demonstrated that treatment with Gc reduced Rac1 activity. Furthermore, the Rac1 inhibitor EHT 1864 had a direct, protective effect on the podocyte. To create a model to study the role of podocyte GR in vivo I generated a mouse line with a podocyte-specific GR deletion. Impact: Gc exposure produces potentially clinically-relevant effects directly on the podocyte, and Gc-induced podocyte hypomobility may underlie the clinical efficacy of these agents. Future animal studies investigating the consequences of GR deletion in the podocyte and the anti-proteinuric effects of Rac1 inhibition are warranted.
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Löwenborg, Eva. "Nephrotic syndrome in children : functional, morphological and therapeutical aspects /." Stockolm, 2003. http://diss.kib.ki.se/2003/91-7349-360-0/.

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Firth, John. "Renal sodium retention in the nephrotic syndrome and other diseases." Thesis, University of Oxford, 1989. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.253149.

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Paisley, K. E. "Vascular function in human subjects with nephrotic syndrome and asymptomatic proteinuria." Thesis, University of Oxford, 2004. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.427636.

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McCarthy, Hugh James. "Establishment of a comprehensive national database of Nephrotic Syndrome in childhood." Thesis, University of Bristol, 2014. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.686640.

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The principle aim of this study was to build a national cohort of children with Steroid Resistant Nephrotic Syndrome (SRNS). The secondary aims were to establish a national registry of rare renal disease in order to build the SRNS cohort. Furthermore, to phenotype and genotype the cohort and undertake development of assays that may be effective biomarkers of disease activity peritransplantation. The successful introduction of the National Registry of Rare Renal Disease, www.renalradar.org. has enabled the nephrology community in the UK to change how it approaches patients that were otherwise considered rare, isolated and difficult to manage. Patients and their families benefit directly, not only from the research but also from the on-going education of treating clinicians and by accessing patient support through the registry. This project has produced novel work in different forms: Firstly it has built a cohort of 226 paediatric patients from around the UK with SRNS, 10% of whom have congenital nephrotic syndrome. With the collection of clinical data from a mean follow-up period of 6 years, it can be shown that in this cohort, there is a 50% risk of end stage renal failure within 10years of diagnosis. In addition, 26% of transplants were complicated by recurrence of disease. Secondly, the use of massively parallel sequencing to analyse 24 genes associated with nephrotic syndrome in 108 patients identifies a definite or probable disease causing mutation in 18.5%, including in genes that would not normally be tested in this age group. It also clearly demonstrates the need to test a panel of genes, as phenotype does not accurately predict genotype. Lastly, the identification of potential biomarkers of disease in post-transplant recurrence: Both an increase in the phosphorylation of VASP (vasodilator stimulated phosphoprotein), and an increase in motility in human podocyte cell lines occur in response to human disease plasma compared to paired remission plasma from the same patients. Identifying those patients most likely to benefit from therapy and developing effective clinical agents remain the goal in SRNS, and this work will significantly aid progress towards that end.
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Guaragna, Mara Sanches 1971. "Síndrome nefrótica em crianças : avaliação molecular em uma casuística brasileira." [s.n.], 2014. http://repositorio.unicamp.br/jspui/handle/REPOSIP/317124.

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Orientador: Maricilda Palandi de Mello<br>Tese (doutorado) - Universidade Estadual de Campinas, Instituto de Biologia<br>Made available in DSpace on 2018-08-25T05:17:39Z (GMT). No. of bitstreams: 1 Guaragna_MaraSanches_D.pdf: 3317402 bytes, checksum: 18a0edd0d0e225eed7d57b65d9bea76b (MD5) Previous issue date: 2014<br>Resumo: A Síndrome Nefrótica (SN) é a principal doença renal na infância, sendo caracterizada por proteinuria, edema, hipoalbuminuria e hiperlipidemia. Usualmente é classificada de acordo com a idade em que se apresenta em Congênita (SNC), quando se manifesta intraútero ou durante os primeiros três meses de vida, Infantil durante o primeiro ano de vida, na Infância, entre o primeiro ano até os 12 anos de idade e Juvenil, entre os 12 e os 18 anos de idade, aproximadamente. De acordo com a resposta ao tratamento com corticoesteróides os pacientes podem ser divididos em córtico-resistentes (CR), córtico-sensíveis (CS) ou córtico-sensíveis com recidiva frequente (CS,RF). Uma disfunção na barreira de filtração glomerular leva às manifestações clínicas decorrentes da síndrome, tais como proteinúria maciça na urina. Mutações em diversos genes vêm sendo correlacionadas com a SN em crianças. No entanto, os genes mais estudados e responsáveis pela maioria dos casos são os genes NPHS1, NPHS2 e WT1. Os objetivos deste trabalho foram identificar e verificar a distribuição de mutações nestes três genes em uma casuística brasileira com SN ou proteinúria isolada e avaliar cada alteração identificada utilizando diversas predições in silico, com o intuito de se esclarecer suas respectivas funções biológicas. Para isto foi realizada a análise molecular de 150 crianças e adolescentes, sendo três não aparentados com SNC e os demais 147 com SN Infantil, SN na infância, SN juvenil e proteinúria isolada, dos quais 134 eram não aparentados. Além destes 150 pacientes, também foram analisados os materiais de biópsias renais fixadas em bloco de parafina de sete pacientes que já foram a óbito com SNC. Para verificar a segregação alélica nas famílias, para os casos nos quais foram identificadas alterações, a análise molecular dos pais foi realizada, quando possível. Um grupo controle de indivíduos saudáveis foi incluído para se avaliar a frequência de alterações não depositadas em bancos de dados. No estudo do gene NPHS1 para os casos com SNC identificamos mutações missense, frameshift e em região de splicing nos três pacientes encaminhados no período da tese e em um dos materiais proveniente de biópsia renal. Assim, um total de quatro pacientes com SNC apresentaram mutações que se correlacionam com o grave quadro clínico apresentado. Para os pacientes com SN infantil, SN infância/juvenil e proteinúria isolada, foram triados o gene NPHS2 e os éxons 8-9 do gene WT1. No estudo do gene NPHS2 foram identificadas duas alterações em heterozigose nos padrões de herança autossômica recessiva em 2,7% (4/147), todos CR, enquanto que apenas uma alteração em heterozigose simples foi identificada em 9,5% (14/147) em casos de SN com apresentação menos grave e tardia. Em três dos 14 pacientes com uma alteração no gene NPHS2, alterações no gene NPHS1 foram também identificadas, todas já descritas como polimorfismos frequentes na população em geral. Para o gene WT1, com herança autossômica dominante, foram identificadas mutações em heterozigose simples em 2,04% (3/147). A avaliação da frequência e distribuição de mutações nestes genes em crianças com SN é inédita no Brasil e traz um direcionamento para a análise molecular de grupos específicos das crianças com SN. Além disto, este trabalho contribui para o estabelecimento das bases moleculares da doença na população brasileira, o que tem uma repercussão importante na conduta dos pacientes, uma vez que, nos que apresentam mutações, pode-se considerar o transplante renal a partir de doador vivo, pois para estes considera-se um risco menor de recidiva de glomérulo esclerose focal e segmentar após transplante do que para pacientes sem mutações<br>Abstract: Nephrotic syndrome (NS) is the main kidney disease in children. It is characterized by proteinuria, edema, hypoalbuminemia and hyperlipidemia. Acccording to the age of the diagnosis, it is usually classified as Congenital (CNS) when it manifests in utero or during the first three months of life, Infantile when the event occurs during the first year of life, in Childhood when symptoms occur between one year and 12 years and Juvenile, with onset between 12 and 18 years old. NS is traditionally separated on the basis of the response to standard steroid treatment as steroid-resistant (SRNS), steroid-sensitive (SSNS) or steroid sensitive with frequent relapses. A dysfunction in the glomerular filtration barrier leads to the characteristic clinical manisfestations of the syndrome such as massive loss of essential proteins in the urine. Mutations in different genes have been associated with NS in children. However, the most studied genes are NPHS1, NPHS2 and WT1, which are responsible for the great majority of the cases. The aims of this study were to identify and verify mutation distributions in those three genes in a Brazilian cohort with NS or isolated proteinuria and to characterize each identified variation by using different in silico prediction programs in order to understand its biological functions. For that, we performed molecular analyses of 150 children and adolescents, being three unrelated children with CNS and the remaining 147 with Infantile, Childhood, Juvenile NS and isolated proteinuria, being 134 unrelated. Besides those 150 patients, paraffin-embebbed renal biopsies of seven patients who had died from CNS have been also analysed. To verify allelic segregation in the family, molecular analyses were also held, whenever possible, for parents of patients in whom mutations were identified. A healthy control group was included in the study to evaluate the frequency of alterations that were absent in the databanks. In the NPHS1 study for CNS cases, we identified missense, frameshift and splicing mutations in the three patients included during the thesis project and in the paraffin-embedded renal biopsy tissue of a patient who had died of CNS. Therefore a total of four CNS cases bore mutations that are associated with the disease. NPHS2 gene and exons 8-9 of WT1 were screened for the 147 patients with infantile NS, childhood/juvenile NS and isolated proteinuria. In the NPHS2 study, two heterozygous alterations compatible to an autossomal recessive inheritance have been identified in 2,7% (4/147), all of the cases were SRNS; whereas, only one heterozygous alteration was identified in 9,5% (14/147), such cases had a less severe and late onset form of NS. Three out of those 14 patients presented sequence variations also in NPHS1 gene, but they have been described as neutral polymorphisms. For the WT1 gene whose mutations present a dominant pattern of inheritance, heterozygous alterations have been identified in 2,04% (3/147). This is the first study focusing frequency evaluation and mutation distribution in Brazilian children with NS and provides a guidance to the molecular analysis of specific case groups of SN. Moreover, this work contributes to the establishment of the molecular bases of this disease in the Brazilian population, what reflects mainly in the conduction of patients, since those bearing mutations can be considered for receiving a kidney from a living donor, because for them it is considered a lower risk of recurrent focal segmental glomerulosclerosis after kidney transplant than for patients without mutations<br>Doutorado<br>Genetica Animal e Evolução<br>Doutora em Genética e Biologia Molecular
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Cotta, Doné Stefania. "Nephrin - intracellular trafficking and podocyte maturation /." Stockholm, 2007. http://diss.kib.ki.se/2007/978-91-7357-411-2/.

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Nieuwhof, Christina Maria Gertrudis. "Idiopathic glomerular disease a prospective study of chronic haematuria and nephrotic syndrome /." [Maastricht : Maastricht : Universiteit Maastricht] ; University Library, Maastricht University [Host], 1999. http://arno.unimaas.nl/show.cgi?fid=8567.

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Books on the topic "Nephrotic syndrome"

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Stewart, Cameron J., and Glassock Richard J, eds. The Nephrotic syndrome. Dekker, 1988.

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National Kidney and Urologic Diseases Information Clearinghouse (U.S.), ed. Childhood nephrotic syndrome. National Institute of Diabetes and Digestive and Kidney Diseases, National Institutes of Health, 2000.

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1946-, Smith Michael C., ed. Proteinuria and the nephrotic syndrome. Year Book Medical Publishers, 1986.

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Meyrier, A. Optimal use of Sandimmun in nephrotic syndrome. Springer, 1992.

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Meyrier, A., P. Niaudet, and J. Brodehl. Optimal Use of Sandimmun® in Nephrotic Syndrome. Springer Berlin Heidelberg, 1992. http://dx.doi.org/10.1007/978-3-642-77310-5.

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Parker, James N. The official parent's sourcebook on childhood nephrotic syndrome. Icon Health Publications, 2002.

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Hulton, Sally-Anne. Immunological aspects of the nephrotic syndrome in childhood. University of Birmingham, 1995.

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Kaneko, Kazunari, ed. Molecular Mechanisms in the Pathogenesis of Idiopathic Nephrotic Syndrome. Springer Japan, 2016. http://dx.doi.org/10.1007/978-4-431-55270-3.

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Siesel, Nancy. A Puffy Face. Nancy Siesel, 2019.

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Lomu, Jonah. Jonah: My story. Hachette New Zealand, 2013.

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Book chapters on the topic "Nephrotic syndrome"

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Meyrier, A., P. Niaudet, and J. Brodehl. "Idiopathic nephrotic syndrome (nephrosis)." In Optimal Use of Sandimmun® in Nephrotic Syndrome. Springer Berlin Heidelberg, 1992. http://dx.doi.org/10.1007/978-3-642-77310-5_3.

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Ananthakrishnan, Shubha, Jane Y. Yeun, and George A. Kaysen. "Nephrotic Syndrome." In Nutrition in Kidney Disease. Springer International Publishing, 2020. http://dx.doi.org/10.1007/978-3-030-44858-5_24.

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Gilbert, Patricia. "Nephrotic syndrome." In The A-Z Reference Book of Syndromes and Inherited Disorders. Springer US, 1996. http://dx.doi.org/10.1007/978-1-4899-6918-7_53.

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Passerini, Patrizia, and Claudio Ponticelli. "Nephrotic Syndrome." In Suki and Massry’s THERAPY OF RENAL DISEASES AND RELATED DISORDERS. Springer US, 1998. http://dx.doi.org/10.1007/978-1-4757-6632-5_23.

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Kelsey, Janet. "Nephrotic Syndrome." In Care Planning in Children and Young People's Nursing. John Wiley & Sons, Ltd,., 2013. http://dx.doi.org/10.1002/9781118785324.ch30.

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Pressler, Barrak. "Nephrotic Syndrome." In Nephrology and Urology of Small Animals. John Wiley & Sons, Ltd., 2014. http://dx.doi.org/10.1002/9781118785546.ch44.

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Groggel, Gerald C., and Wayne A. Border. "Nephrotic Syndrome." In Therapy of Renal Diseases and Related Disorders. Springer US, 1991. http://dx.doi.org/10.1007/978-1-4613-0689-4_20.

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Byerly, Stephanie I. "Nephrotic Syndrome." In Consults in Obstetric Anesthesiology. Springer International Publishing, 2018. http://dx.doi.org/10.1007/978-3-319-59680-8_110.

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Brunkhorst, Reinhard. "Nephrotic Syndrome." In Urology at a Glance. Springer Berlin Heidelberg, 2014. http://dx.doi.org/10.1007/978-3-642-54859-8_35.

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Dinesh, Kumar, Jane Y. Yeun, and George A. Kaysen. "Nephrotic Syndrome." In Nutrition in Kidney Disease. Humana Press, 2013. http://dx.doi.org/10.1007/978-1-62703-685-6_20.

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Conference papers on the topic "Nephrotic syndrome"

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Munteanu, Teodora, and Cornel Olimpiu Aldea. "P136 Challenging infantile nephrotic syndrome." In 8th Europaediatrics Congress jointly held with, The 13th National Congress of Romanian Pediatrics Society, 7–10 June 2017, Palace of Parliament, Romania, Paediatrics building bridges across Europe. BMJ Publishing Group Ltd and Royal College of Paediatrics and Child Health, 2017. http://dx.doi.org/10.1136/archdischild-2017-313273.224.

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Ciciu, Elena. "ALPORT SYNDROME: A CHALLENGING CAUSE OF NEPHROTIC SYNDROME DURING LATE PREGNANCY." In 6th SWS International Scientific Conference on Social Sciences ISCSS 2019. STEF92 Technology, 2019. http://dx.doi.org/10.5593/sws.iscss.2019.3/s12.050.

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Angelova, Sirma. "Oral-Hygiene Condition in Children with Nephrotic Syndrome." In The 6th Human and Social Sciences at the Common Conference. Publishing Society, 2018. http://dx.doi.org/10.18638/hassacc.2018.6.1.268.

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Jasrotia, A., A. Jabri, Y. Radhakrishnan, and A. Cucci. "Nephrotic Syndrome - A Rare Presentation of Necrotizing Sarcoidosis." In American Thoracic Society 2019 International Conference, May 17-22, 2019 - Dallas, TX. American Thoracic Society, 2019. http://dx.doi.org/10.1164/ajrccm-conference.2019.199.1_meetingabstracts.a4570.

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Gadelha-Parente, T., M. Gouault-Heilmann, G. Rostoker, et al. "TOTAL AND FREE PROTEIN S IN NEPHROTIC SYNDROME." In XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1644296.

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25 consecutive patients (15M, 10F ; mean age 30 years) with nephrotic syndrome (NS) of different grade were studied. Control group consisted in 18 healthy adult volunteers. Total protein S antigen (TPS:Ag) and free protein S antigen (FPS:Ag) after precipitation of C4-BP-bound protein S by PEG 3-5 % final concentration were measured by Laurell's technique. PS:Ag was also searched in concentrated urine of 9 patients by ELISA method, more sensitive than the Laurell's technique. In the same plasma samples we measured C4-BP, Protein C Ag and AT III biological activity (all reagents from D.Stago). Serum albumin level, proteinuria, proteinuria selectivity index, triglycerides, cholesterol levels were recorded. TPS:Ag was found elevated in NS (1.30±0.3 U/ml) in comparison with control group (1.09±0.32 U/ml) and the difference was statistically significant (p&lt;0.05). The mean values of FPS:Ag observed in patients and controls were not statistically different, but if we consider 95 % confidence limits (0.99-1-35 U/ml), 16 pts had normal or elevated FPS:Ag level, whereas 9 had decreased FPS:Ag level. A positive correlation was found between TPS:Ag and FPS:Ag in control group (r=0.66 ; p&lt; 0.001) and in patients with NS (r=0.4l, p&lt;0.05). C4-BP was significantly (p&lt;0.01) increased in nephrotic patients ( 1.37 ± 0.36 U/ml) in comparison with control group (1.04±0.27 U/ml). A negative correlation was found between FPS:Ag and C4-BP levels in control group (r = −0.57, P&lt; 0.01) but not in nephrotic patients. A positive correlation was found between FPS:Ag and albumin level and between FPS:Ag and cholesterol level. No correlation was found between TPS:Ag or FPS:Ag and proteinuria, proteinuria selectivity index, AT III and protein C levels. Traces of PS were found in urine (0. to 2.5 U/day) in 9 patients tested. 2/25 pts suffered thromboembolic events : one had a very low level of FPS:Ag in addition to a decreased level of AT III. The other one had normal FPS:Ag and AT III level but a borderline Protein C level. In conclusion. An acquired FPS:Ag deficiency was observed in 9/25 pts with NS despite an increased level of TPS:Ag. In this small series of patients the acquired FPS deficiency does not seem to be related either to an urinary loss of FPS or to an increased binding to C4-BP, as suggested by some authors.
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Son, R., D. Hwang, AH Jung, et al. "5PSQ-082 Cyclophosphamide therapy in children with nephrotic syndrome." In Abstract Book, 23rd EAHP Congress, 21st–23rd March 2018, Gothenburg, Sweden. British Medical Journal Publishing Group, 2018. http://dx.doi.org/10.1136/ejhpharm-2018-eahpconf.436.

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E.V, Plotnikova, Borisova M.A, Belova E.G, and Borisov V.S. "P322 Treatment optimisation of steroid-resistant paediatric nephrotic syndrome." In 8th Europaediatrics Congress jointly held with, The 13th National Congress of Romanian Pediatrics Society, 7–10 June 2017, Palace of Parliament, Romania, Paediatrics building bridges across Europe. BMJ Publishing Group Ltd and Royal College of Paediatrics and Child Health, 2017. http://dx.doi.org/10.1136/archdischild-2017-313273.410.

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Picard, P., J. Y. Borg, M. Vasse, et al. "BIOLOGICAL PRETHROMBOTIC MARKERS AND COAGULATION INHIBITORS IN NEPHROTIC SYNDROME." In XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1643051.

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Nephrotic syndrome (NS) has long been recognized as a clinical prethrombotic state, because of severe thrombo-embolic complications. But underlying mechanisms are still poorly defined. In 56 untreated nephrotic adult patients (most of them without renal failure), we investigate in vivo coagulation activation by measuring 0 plasmatic specific fibrin degradation products (FbDP) (immuno-enzymological assay using a monoclonal anti D-neo antibody) and (2) the ratio of factor VII coagulant activity (V11c) to factor VII:Anti gen (VII;Ag) tested by an ELISA method. We examined coagulation inhibitors in plasmas and urines (antithrombin III—AT III, heparin cofactor II-HC II by amidolytic and laurell methods; protein C-PC by an ELISA assay ;free and bound protein S—PS:Ag by laurell assays). In few patients we also determinecjfribronectin and t-PA inhibitor.Results in plasma are submitted and expressed as mean ± DS and compared (t test) with controls (C) without nephropathySignificantly elevated activated factor VII and FbDP levels show an “in vivo activation” of coagulation in NS. Plasmatic fibronectin, HC II, PC:frg, and tPA-I levels are alsp significantly elevated and roughly paralleled fibrinogen (6,25 ± 2,9 g/1) and other acute-phase proteins measurements. Significant amounts of AT 111:Ag were present in about half tested urines, but in a degraded form with low or absent heparin cofactor activity. Mean plasmatic AT III concentration was in normal range, but three of the 4 patients with a thrombotic disease had the lowest values of AT III and the highest fibrinogen levels.We could demonstrate a biological prethrombotic state in NS and suggest the way of identifying patients with high risk of thrombosis.
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"Expression of glycogen synthase kinase 3β in nephrotic syndrome". У Bioinformatics of Genome Regulation and Structure/ Systems Biology. institute of cytology and genetics siberian branch of the russian academy of science, Novosibirsk State University, 2020. http://dx.doi.org/10.18699/bgrs/sb-2020-343.

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Mysliwiec, M., D. Alderson, L. Poller, and P. Ackrill. "PROTEIN C AND OTHER CLOTTING STUDIES IN MEMBRANOUS AND NON-MEMBRANOUS GLOMERULONEPHRITIS." In XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1644310.

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The occurrence of thrombosis in the nephrotic syn drome has long been known. Thrombotic complications are predominantly associated with membranous glomerulonephritis (MG). The aim of the present work was to study whether the tendency of nephrotic patients with MG to thrombotic episodes could be attributed to a hypercoagulable state. Thirty consecutive patients with the nephrotic syndrome were studied. Of these 17 suffered from MG and 13 had other forms of glomerulonephritis. The control group consisted of 10 healthy volunteers. In addition to standard coagulation assays, we studied: soluble fibrin monomer complexes (FM test, Boehringer), fibrin monomer polymerization, factor VIII:C, factor VIII:vWF, anti thrombin III (AT III) and alpha2 antiplasmin (alpha2AP) using chromogenie substrates; the levels of AT III and alpha2 AP were measured immunologically; beta thromboglobulin (BTG), platelet factor 4 and fibrinopeptide A (FPA) using radioimmunoassay kits; protein C was studied functionally and immunologically. There was a significant shortening of the prothrombin time and activated partial thromboplastin time, increase in alpha9 AP, factor V111:vWF, FPA and BTG in nephrotic patients associated with in or eases in both functional and imminclogical protein C levels and impairment of fibrin polymerization. FM test was negative in all but one of the patients. None of the coagulation tests showed a significant difference in the two nephrotic groups. High protein C and impaired polymerization may be considered as mechanisms counteracting disclosed hypercoagulability in the nephrotic syndrome.
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Reports on the topic "Nephrotic syndrome"

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Ou, Yuanshu. Effect of Chinese medicine prescription on nephrotic syndrome: A protocol for systematic review and meta-analysis. INPLASY - International Platform of Registered Systematic Review Protocols, 2020. http://dx.doi.org/10.37766/inplasy2020.4.0181.

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Zhang, LiBo, GuangZhen Liu, and YanChuang Liang. Meta analysis of traditional Chinese medicine combined with cyclophosphamide in the treatment of adult refractory nephrotic syndrome. International Platform of Registered Systematic Review and Meta-analysis Protocols, 2020. http://dx.doi.org/10.37766/inplasy2020.5.0020.

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Yu, Hangxing, Miaoru Han, Wei Lin, et al. Efficacy of Chinese Herbal Injections for the Treatment of Primary Nephrotic Syndrome: A Bayesian Network Meta-Analysis of Randomized Controlled Trials. INPLASY - International Platform of Registered Systematic Review and Meta-analysis Protocols, 2020. http://dx.doi.org/10.37766/inplasy2020.8.0091.

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Luo, Ningxin, Xiaoyu Shen, and Li Zhao. The aim of this meta-analysis of randomized controlled trials is to evaluate the efficacy and safety of rituximab for frequently relapsing nephrotic syndrome in children. INPLASY - International Platform of Registered Systematic Review and Meta-analysis Protocols, 2021. http://dx.doi.org/10.37766/inplasy2021.11.0099.

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Length of steroid course for childhood nephrotic syndrome makes little difference to later recurrences. National Institute for Health Research, 2019. http://dx.doi.org/10.3310/signal-000812.

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