Relevant bibliographies by topics / Nephrotic syndrom

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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 syndrom'

Author: Grafiati
Published: 4 June 2021
Last updated: 17 February 2022

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Journal articles on the topic "Nephrotic syndrom"

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Şakarcan, Abdullah. "Idiopathic nephrotic syndrom of the childhood and its treatment." Turkiye Aile Hekimligi Dergisi 13, no. 2 (2009): 64–67. http://dx.doi.org/10.2399/tahd.09.064.

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Muls, Erik, Maryvonne Rosseneu, Roger Daneels, Mario Schurgers, and Johan Boelaert. "Lipoprotein distribution and composition in the human nephrotic syndrom." Atherosclerosis 54, no. 2 (1985): 225–37. http://dx.doi.org/10.1016/0021-9150(85)90181-9.

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Ehren, Rasmus, Marcus R. Benz, Jorg Doetsch, et al. "Initial treatment of steroid-sensitive idiopathic nephrotic syndrome in children with mycophenolate mofetilversusprednisone: protocol for a randomised, controlled, multicentre trial (INTENT study)." BMJ Open 8, no. 10 (2018): e024882. http://dx.doi.org/10.1136/bmjopen-2018-024882.

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IntroductionIdiopathic nephrotic syndrome is the most common glomerular disease in childhood with an incidence of 1.8 cases per 100 000 children in Germany. The treatment of the first episode implies two aspects: induction of remission and sustainment of remission. The recent Kidney Disease Improving Global Outcomes, American Academy of Pediatrics and German guidelines for the initial treatment of the first episode of a nephrotic syndrome recommend a 12-week course of prednisone. Despite being effective, this treatment is associated with pronounced glucocorticoid-associated toxicity due to high-dose prednisone administration over a prolonged period of time. The aim of the INTENT study (Initial treatment of steroid-sensitive idiopathic nephrotic syndrom in children with mycophenolate mofetil versus prednisone: protocol for a randomised, controlled, multicentre trial) is to show that an alternative treatment regimen with mycophenolic acid is not inferior regarding sustainment of remission, but with lower toxicity compared with treatment with glucocorticoids only.Methods and designThe study is designed as an open, randomised, controlled, multicentre trial. 340 children with a first episode of steroid-sensitive nephrotic syndrome and who achieved remission by a standard prednisone regimen will be enrolled in the trial and randomised to one of two treatment arms. The standard care group will be treated with prednisone for a total of 12 weeks; in the experimental group the treatment is switched to mycophenolate mofetil, also for a total of 12 weeks in treatment duration. The primary endpoint is the occurrence of a treated relapse within 24 months after completion of initial treatment.Ethics and disseminationEthics approval for this trial was granted by the ethics committee of the Medical Faculty of the University of Heidelberg (AFmu-554/2014). The study results will be published in accordance with the Consolidated Standards of Reporting Trials statement and the Standard Protocol Items: Recommendations for Interventional Trials guidelines. Our findings will be submitted to major international paediatric nephrology and general paediatric conferences and submitted for publication in a peer-reviewed, open-access journal.Trial registration numberDRKS0006547; EudraCT2014-001991-76; Pre-result.Date of registration30 October 2014; 24 February 2017.
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ALVES, LARYSSA PEREIRA, LETÍCIA TAVARES SELEGATTO, CAROLINA PERES BATALHA, GUSTAVO BUENO DE CAMARGO, and MARCELO VICENTE DE ANDRADE SOBRINHO. "BILATERAL ABDUCENS NERVE PALSY SECUNDARY TO INTRACRANIAL SINUSES THROMBOSIS IN A CHILD WITH NEPHROTIC SYNDROM – CASE REPORT." Vision Pan-America, The Pan-American Journal of Ophthalmology 17, no. 4 (2018): 113–16. http://dx.doi.org/10.15234/vpa.v17i4.507.

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We report a case of a child with nephrotic syndrome (NS), who presented an acute convergent strabismus, double vision and papilledema one week after a history of badly treated sinusitis. The image study revealed an extensive thrombosis of the intracranial sinuses that was treated with intravenous heparin and oral corticosteroids. Four months later, the case evolved with spontaneous resolution of the ocular deviation and no diplopia.
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Kolesnyk, M., V. Driyanska, G. Drannik, et al. "HLA-PHENOTYPE IN PATIENTS WITH GLOMERULONEPHRITIS WITH VARIOUS MORPHOLOGIC FORMS AND NEPHROTIC SYNDROM." Ukrainian Journal of Nephrology and Dialysis, no. 2(50) (April 20, 2016): 36–44. http://dx.doi.org/10.31450/ukrjnd.2(50).2016.02.

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In the work was determined the HLA-phenotype specificities in patients with different morphologic forms of chronic glomerulonephritis and nephrotic syndrome (CGN, NS) to define the additional predictors of a disease course.
 Materials and methods. There was studied the HLA-antigens distribution in the 264 CGN, NS patients and 350 healthy donors by typing the lymphocytes with the aid ofstandard microlymphocytotoxic test (Terasaki’s test). The diagnosis was confirmed morphologically using the thin needle nephrobiopsy.
 Results. It is advisable to associate CGN, NS (RR > 2) with antigens HLA- A23, 24, 28; B8, 38, 41, 44 in patients; the causal role (a > 0.1) was determined for A24, 28; B8. In proliferative GN was additionally revealed the etiologic role of B27 known as antigen associated with risk ofautoimmune diseases. In patients with various morphologic forms is advisable the association of some antigens with development of chronic renal failure (CRF) – A30, B41 in FSGS, A10 – MGN; and also hormone resistance (HR) – A19+31+32 in FSGS, B8 – MGN and MC.
 Conclusion. The revealed reliable associations ofHLA types both with CGN, NS and its separate morphologic forms with the risk of CRF and/or HR allow take into consideration the availability ofsuch antigens in phenotype ofpatients with confirmed by biopsy diagnosis as the additional diagnostic and prognostic markers.
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DESCHÊNES, GEORGES, and ALAIN DOUCET. "Collecting Duct Na+/K+-ATPase Activity Is Correlated with Urinary Sodium Excretion in Rat Nephrotic Syndromes." Journal of the American Society of Nephrology 11, no. 4 (2000): 604–15. http://dx.doi.org/10.1681/asn.v114604.

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Abstract. In puromycin aminonucleoside (PAN)-treated nephrotic rats, sodium retention is associated with increased Na+/K+-ATPase activity in the cortical collecting ducts (CCD). This study was undertaken to determine whether stimulation of Na+/K+-ATPase in the CCD is a feature of other experimental nephrotic syndromes, whether it might be responsible for renal sodium retention, and whether it is mediated by increased plasma vasopressin levels or activation of calcineurin. For this purpose, the time courses of urinary excretion of sodium and protein, sodium balance, ascites, and Na+/K+-ATPase activities in microdissected CCD were studied in rats with PAN or adriamycin nephrosis or HgCl2nephropathy. The role of vasopressin and calcineurin in PAN nephrosis were evaluated by measuring these parameters in Brattleboro rats and in rats treated with cyclosporin or tacrolimus. Despite different patterns of changes in urinary sodium and protein excretion in the three nephrotic syndrome models, there was a linear relationship between CCD Na+/K+-ATPase activities and sodium excretion in all three cases. The results also indicated that there was no correlation between proteinuria and sodium retention, but ascites was present only when proteinuria was associated with marked reduction of sodium excretion. Finally, the lack of vasopressin in Brattleboro rats or the inhibition of calcineurin by administration of either cyclosporin or tacrolimus did not prevent development of the nephrotic syndrome in PAN-treated rats or stimulation of CCD Na+/K+-ATPase. It is concluded that stimulation of Na+/K+-ATPase in the CCD of nephrotic rats might be responsible for sodium retention and that this phenomenon is independent of proteinuria and vasopressin and calcineurin activities.
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Joven, J., J. M. Simó, E. Vilella, J. Camps, E. Espinel, and C. Villabona. "Accumulation of atherogenic remnants and lipoprotein(a) in the nephrotic syndrome: relation to remission of proteinuria." Clinical Chemistry 41, no. 6 (1995): 908–13. http://dx.doi.org/10.1093/clinchem/41.6.908.

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Abstract Although lipoprotein abnormalities of the nephrotic syndrome are assumed to be related to the presence of proteinuria, this topic has not been investigated extensively. We measured lipoproteins from 19 nonuremic patients during and after remission of the nephrotic syndrome in an effort to determine the extent of their putative atherogenicity. As expected, disturbances involved primarily the apoprotein B-containing lipoproteins. No patient showed serum lipoprotein(a) [Lp(a)] < 300 mg/L during the acute phase. Lp(a) concentrations correlated significantly with those of apoprotein B, and both values decreased dramatically with the remission of the nephrotic syndrome. Surprisingly, despite the resolution of proteinuria, concentrations of intermediate-density lipoproteins and Lp(a) remained above normal in hypertriglyceridemic patients, suggesting a residual effect of nephrosis in the overall lipoprotein transport. Accumulation of atherogenic remnants should be considered a characteristic of the hyperlipidemia of the nephrotic syndrome, and aggressive treatment to reduce proteinuria is mandatory.
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MAIMOUNA, M., K. T. Sandra Rabia, M. Agbor, J. Kaze Folefack, and G. Ashuntantang. "SUN-421 INSIDE THE MOUTH OF ADULTS WITH THE NEPHROTIC SYNDROM SEEN IN NEPHROLOGY OUT-PATIENT CLINICS IN YAOUNDÉ, CAMEROON." Kidney International Reports 5, no. 3 (2020): S371. http://dx.doi.org/10.1016/j.ekir.2020.02.961.

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Paik, Seung Nam, Mi Hae Sung, Kyoul Ja Cho, and Chang Ja Byun. "The Effect of Supportive Nursing Education Program on Burden and Quality of Life in Mothers of Children with Nephrotic Syndrom." Journal of Korean Academy of Nursing 29, no. 3 (1999): 721. http://dx.doi.org/10.4040/jkan.1999.29.3.721.

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Starcea, Magdalena, Mihaela Munteanu, Radu Russu, Anca Iulia Rotaru, Doina Mihaila, and Ingrith Miron. "DRUG INDUCED ACUTE TUBULAR NECROSIS – RARE CASE OF NEPHROTIC SYNDROME." Romanian Journal of Pediatrics 64, no. 4 (2015): 410–12. http://dx.doi.org/10.37897/rjp.2015.4.11.

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We presented two cases of nephrotic syndrome (NS) drug-induced with tubular nephrotoxicity, with different evolution in the context of etiologic diseases. First is 5-month-old girl admitted with NS (clinically and biological proven) and acute renal failure after another hospitalization for pneumonia. The girl was treated with ceftriaxone and gentamicin 12 days. Congenital NS suspicion was eliminated by renal biopsy who revealed renal tubular necrosis highlighting recovery phase. The development was favorable in 7 days of peritoneal dialysis. The second case was 16 years old adolescents treated 3 years with carbimazol for Basedow disease. Was presented with nephrotic syndrome not influenced by corticosteroids. Histopathology revealed toxic tubular necrosis, interstitial fibrosis, absence of glomerular injury. Nephrotoxic treatment was stopped, and, after thyroidectomy, edema were reduced, but kidney function continued to depreciate, while nephrotoxic therapy given for 3 years. Conclusions. Renal tubular necrosis clinical and laboratory expressed by nephrotic syndrome, accompanied by renal insufficiency is a rare occurrence in children; gentamicin and carbimazol can be criminalized. The suffering or impairment may be improved by removing the causative drug. Treatment failure was associated with duration of drug aggression and evolution of comorbidities.
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Dissertations / Theses on the topic "Nephrotic syndrom"

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Bonnet, Anne-Laure. "Rôles et fonctions de Vasorine, protéine osseuse, rénale et vasculaire : étude in vivo dans la formation osseuse et l'homéostasie phosphocalcique From vascular smooth muscle cells to folliculogenesis: what about vasorin?" Thesis, Sorbonne Paris Cité, 2018. http://www.theses.fr/2018USPCB161.

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La Vasorine (Vasn) est une protéine transmembranaire de type I initialement étudiée dans le contexte du développement. Vasn a été également mise en évidence chez la souris adulte où elle est fortement exprimée dans les gros vaisseaux, les os et les reins mais le rôle de Vasn est aujourd'hui inconnu. De nombreuses pathologies osseuses, rénales et vasculaires restent encore inexpliquées, et bien qu'à ce jour aucun variant de Vasn n'ait été associé à une pathologie humaine, il est nécessaire d'identifier des marqueurs précoces de ces pathologies ainsi que les voies moléculaires/protéines défaillantes. L'objectif de ce travail est de comprendre les principaux rôles et fonctions de Vasn à travers plusieurs modèles animaux ; les souris Vasn knock-out (KO) constitutives et les souris Vasn KO inductibles (Cassette Cre-Lox inductible). Les analyses ont montré que les souris Vasn KO développent un phénotype non viable, entrainant un décès précoce autour de 24 jours post-natal. Ces souris sont de petite taille, atteintes d'un syndrome néphrotique sévère s'installant à J14 et ont une microarchitecture osseuse anormale par rapport aux souris Wild-type (WT). Des anomalies majeures rénales ont été observées, notamment au sein des podocytes glomérulaires, avec la perte de leurs pédicelles et une absence de diaphragme de fente. Ces altérations expliquent l'accumulation des protéines retrouvées dans les tubules et l'urine. Ce syndrome néphrotique évolue vers une insuffisance rénale sévère. Les souris Vasn KO ont par ailleurs un os trabéculaire fémoral osteopénique, lié au moins en partie à une activité ostéoclastique augmentée. De plus, la média des gros vaisseaux est fortement altérée, se traduisant par une désorganisation des fibres élastiques et des cellules musculaires lisses hypertrophiques, voir totalement absentes de certaines zones. Les souris adultes Vasn KO inductibles présentent un phénotype comparable au souris Vasn KO. Un décès précoce survient autour de 24 jours après la délétion du gène. Le syndrome néphrotique sévère s'installe rapidement entre J15 et J17 post induction, caractérise par une protéinurie majeure et la présence d'une importante quantité d'ascite intrapéritonéal. La microarchitecture osseuse est étonnamment anormale par rapport aux souris contrôles, et cela est lié au moins en partie à une activité ostéoclastique augmentée. La rapidité de la mise en place de l'ostéopénie des souris Vasn KO inductible suggère un rôle direct de Vasn dans le remaniement osseux. A l'issu de ce travail, les répercussions de la perte Vasorine dans des modèles murins adultes ont été décrites, et plusieurs pistes fonctionnelles explorées. L'implication de Vasorine dans le dialogue os/rein est confirmée et son analyse sera poursuivie<br>Vasorin (Vasn) is a type I transmembrane protein initially studied in the context of development. Vasn has also been localized in adult mice where it is highly expressed in large vessels, bones and kidneys. The main(s) role(s) of Vasn is/are actually unknown. Many bone, renal and vascular pathologies are still unexplained, and even if to date no Vasn variant has been associated with a human pathology, it is necessary to identify early markers of these pathologies as well as the molecular pathways / defective proteins. The objective of this work is to understand the main roles and functions of Vasn through several animal models; Vasn knockout (KO) mice and inducible Vasn KO mice (Cre-Lox inducible cassette). Analyzes showed that Vasn KO mice develop a non-viable phenotype, resulting in an early death around 24 days postnatal. In general, they are smaller, with severe nephrotic syndrome taking place from day 14 and have abnormal bone microarchitecture compared to Wild-Type (WT) mice. Major renal abnormalities were observed in the podocytes, with the loss of their pedicels and the absence of a slit diaphragm, which explain the accumulation of proteins found in the tubules and urine. This nephrotic syndrome progresses to severe renal failure. Vasn KO mice have an osteopenic femoral trabecular bone that is at least partly linked to increased osteoclastic activity. In addition, the media of large vessels is strongly altered, resulting in disorganization of elastic fibers and smooth muscle cells are hypertrophic or completely absent from certain areas. The inducible Vasn KO mice have a phenotype comparable to the Vasn KO mouse. An early death occurs around 24 days after deletion of the gene. Severe nephrotic syndrome is rapidly established between D15 and D17 postinduction, characterized by major proteinuria and the presence of intraperitoneal ascite. Bone microarchitecture is surprisingly abnormal compared to control mice, linked at least in part to increased osteoclastic activity. In vitro experiments of primary cell cultures taken from Vasn KO mice compared to cells taken from WT mice validated Vasn expression in podocytes, osteoclasts and smooth muscle cells. The rapid onset of osteopenia in inducible Vasn KO mice suggests a direct role for Vasn in bone remodeling. At the end of this work, the repercussions of the Vasorin loss in adult mouse models were described, and several functional tracks are explored. The involvement of Vasorin in the bone / kidney dialogue is confirmed and its analysis will be continued
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Vachin, Pauline. "Etude des dysfonctions lymphocitaires T dans le syndrome néphrotique idiopathique." Thesis, Paris Est, 2018. http://www.theses.fr/2018PESC0044/document.

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La pathogénie du syndrome néphrotique idiopathique est inconnue, mais de nombreux arguments clinques et expérimentaux favorisent l’hypothèse d’une pathogénie dys-immunitaire à expression immunologique et rénale, au cours de laquelle on observerait une altération des lymphocytes T. Cependant, le mécanisme exact reste encore mal connu. Récemment, le Rituximab, un anticorps dirigé contre l’antigène CD20, a montré une efficacité à induire une rémission à moyen et long terme suggérant l’implication d’une dysfonction des lymphocytes B et/ou un défaut de coopération T-B. Notre laboratoire a isolé un nouveau gène C-MIP dont l’expression est induite dans certaines sous-populations lymphocytaires T et B, ainsi que dans les podocytes de patients atteints de SNI en phase de poussée mais quasiment indétectable chez les sujets sains.Dans ces travaux, ancillaires au PHRC NEPHRUTIX, nous avons étudié les perturbations lymphocytaires T, avant, au moment de la rechute et en période de rémission au cours de syndrome néphrotique à lésions glomérulaires minimes et l’effet du traitement par le Rituximab. Dans cette étude, nous avons mis en évidence que la rechute était associée à un effondrement des lymphocytes T régulateurs, une baisse profonde de l’interleukine-2 ainsi qu’à une surexpression significative de C-MIP, précédant la survenue de la rechute. Ces modifications se restaurent en rémission. Enfin, la rémission obtenue dans le bras Rituximab, entraîne une diminution des lymphocytes T folliculaires (Tfh), des iNKT et des cellules double-négatives DN-TCR Vα24, suggérant que le SNLGM implique un défaut des réponses immunitaires innées et adaptatives, qui peut être stabilisé par un traitement par Rituximab.Afin d’étudier le rôle de C-MIP, nous avons généré des souris transgéniques sur-exprimant ce gène dans les lymphocytes T matures périphériques. Cette surexpression est à l’origine d’un phénotype lymphocytaire altéré marqué par une accumulation de lymphocytes T naïfs, un effondrement des cytokines activatrices de type Th1 et Th2 et une accumulation des formes inactives des Src kinases. Ces résultats suggèrent que C-MIP, en inhibant les Src kinases, est un régulateur négatif de l’activation T impliqué dans la signalisation proximale et pourrait être impliqué dans l’hypo-réactivité lymphocytaire T observée chez les patients atteints de SNLGM actif<br>The pathogenesis of minimal-change nephrotic syndrom (MCNS) is unknown, but, supported by many clinical and experimental arguments, it was suggested that MCNS is a dys-immune disorder with immunogical and renal expression, during which T-cell alteration would be observed. However, the exact mechanism remains unknown. Recently, Rituximab, a B-cell depleting agent, is effctive in inducing mid- and long-term remission suggesting involvement of B-cell dysfunction and/or lack of T-B cooperation. Our laboratory identified a new gene: C-MIP. We have shown that C-MIP abundance is increased in some T and B lymphocyte subpopulations, as well as in podocytes of MCNS patients during relapse phase but undetectable in healthy subjects.In this work, ancillary to the NEPHRUTIX PHRC, we studied T-cell disturbances before and during the relapse or during the remission time in MCNS and the effect of Rituximab therapy. In this study, we found that relapses were associated with significant decrease in regulatory T cell and interleukin-2 expression, while C-MIP abundance was significantly increased. These changes are restored during remission time. Finally, remission after Rituximab therapy leads to a decrease in follicular T cells (Tfh), iNKT and double-negative (CD4- CD8-) T cells expressing the invariant Vα24 chain, suggesting that MCNS involves a disorder of innate and adaptative immune response, which can be stabilized by Rituximab treatment.In order to study the C-MIP role, we generated transgenic mice overexpressing this gene in the peripheral mature T-cells. This overexpression leads to an altered lymphocyte phenotype with an accumulation of naive T lymphocytes, a significant decrease of Th1 and Th2 activating cytokines and accumulation of inactive Src kinases. These results suggest that, by inhibiting Src kinases, C-MIP is a negative regulator of activation T involved in proximal signalling and may be responsable of the lymphocyte T hypo-reactivity observed in patients with active MCNS
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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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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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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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Books on the topic "Nephrotic syndrom"

1

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

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

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Jonah: My story. Hodder Moa Beckett, 2004.

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Herrington, William G., Aron Chakera, and Christopher A. O’Callaghan. Nephrotic syndrome. Edited by Patrick Davey and David Sprigings. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780199568741.003.0161.

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Nephrotic syndrome is a clinical syndrome of heavy proteinuria (greater than 3.5 g per 24 hours), oedema, and hypoalbuminaemia, which is associated with hyperlipidaemia and a procoagulant state. Causes of nephrotic syndrome are traditionally classified by their histopathological descriptions. In most cases, the histological picture can have a primary (idiopathic) or secondary cause. Minimal change, membranous nephropathy, and focal segmental glomerulosclerosis account for over 60% of cases. Diabetic nephropathy and renal amyloidosis are common secondary causes of nephrotic syndrome. Nephrotic-range proteinuria will show up as at least 3+ protein on urinalysis. The diagnosis is confirmed by a urinary protein-to-creatinine ratio over 300 mg/mmol, and hypalbuminaemia. In adults, renal biopsy is the diagnostic test. This chapter addresses the causes, diagnosis, and management of nephrotic syndrome in adults.
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Rajakrishna, Premil, Stewart Cameron, and Neil Turner. Nephrotic syndrome. Edited by Neil Turner. Oxford University Press, 2015. http://dx.doi.org/10.1093/med/9780199592548.003.0052.

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Nephrotic syndrome is the constellation of manifestations seen in patients with such severe proteinuria that serum albumin falls below normal levels. Its severity and the risk of complications are graded by the severity of the protein loss. The risks of some complications begin to rise at levels of proteinuria below those conventionally associated with nephrotic syndrome. The main manifestation, oedema, is characterized by avid sodium retention and managed by sodium restriction and diuretics. A pronounced thrombotic tendency is particularly apparent within the first 6 months of diagnosis and in patients with the most severe proteinuria. Venous thromboembolism may be a presenting feature. Prophylactic full anticoagulation may be considered for those at highest risk. Hyperlipidaemia is severe and justifies lipid-lowering therapy in patients with sustained nephrotic syndrome. There is a marked increased risk of bacterial infection, particularly from Streptococcus pneumoniae. The causes of nephrotic syndrome are diseases affecting the podocyte, either directly or through an effect on glomerular matrix (e.g. through scarring). Identification of a cause is important for management and often requires a renal biopsy.
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Book chapters on the topic "Nephrotic syndrom"

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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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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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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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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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Froehlich, Stephan J., Carlo A. Lackerbauer, Guenter Rudolph, et al. "Nephrotic Syndrome." In Encyclopedia of Molecular Mechanisms of Disease. Springer Berlin Heidelberg, 2009. http://dx.doi.org/10.1007/978-3-540-29676-8_1256.

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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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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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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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Conference papers on the topic "Nephrotic syndrom"

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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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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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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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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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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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"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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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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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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Reports on the topic "Nephrotic syndrom"

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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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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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