Literatura científica selecionada sobre o tema "Alport, Syndrome d' – Physiopathologie"
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Artigos de revistas sobre o assunto "Alport, Syndrome d' – Physiopathologie"
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Gerasimovska Kitanovska, Biljana, Vesna Gerasimovska, and Vesna Livrinova. "Two Pregnancies with a Different Outcome in a Patient with Alport Syndrome." Open Access Macedonian Journal of Medical Sciences 4, no. 3 (2016): 439–42. http://dx.doi.org/10.3889/oamjms.2016.073.
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BACKGROUND: Alport syndrome is a genetic disease that progresses to chronic kidney failure, with X-linked, autosomal dominant or autosomal recessive type of inheritance. Women are generally carriers of the mutation and have a milder form of the disease. During pregnancy, they have an increased risk of impaired kidney function and preeclampsia.CASE PRESENTATION: A 27-year old woman, gravida 1, para 0, in her 23rd gestational week came to the outpatient unit of the University Clinic of Nephrology for the first time because of slowly progressing proteinuria and Alport syndrome. She was admitted to the gynaecological ward in her 29th gw for proteinuria which increased from 3.8 g/day up to 20 g/day and the serum creatinine increased to 120- 150 micromol/l. She was delivered in the 30th gestational week due to obstetrical indications with a cesarian section and delivered a baby with a birth weight of 880 g. After delivery, proteinuria decreased to 2 g/d within 2 months and an angiotensin-converting enzyme inhibitor (ACEI) was started. Her second pregnancy, after 2 years, had an uneventful course and she delivered a healthy baby weighing 3000 g in the 39th week. Six months after the second delivery, her renal function remained normal and her proteinuria was 2 g/d.CONCLUSIONS: Pre-pregnancy counselling and frequent controls during pregnancy are necessary for women with Alport syndrome, as well as regular monitoring after delivery. Recent reports are more in favour of good pregnancy and nephrological outcomes in women with Alport syndrome when renal disease is not advanced.
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Sharma, Chewan Acharya, and Elijan Duwal. "Unusual refractive anomaly in Alport syndrome with lenticonus: A challenging case." Indian Journal of Ophthalmology - Case Reports 4, no. 1 (2024): 93–94. http://dx.doi.org/10.4103/ijo.ijo_2548_23.
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Herein, we report a 15-year-old male with Alport syndrome, exhibiting hemorrhagic nephritis, hearing loss, and a 1-year history of poor distance visual acuity. Slit-lamp examination revealed bilateral anterior lenticonus, with unremarkable findings in other ocular structures. Unusual reflex movements were observed during retinoscopy, characterized by distinct central and annular reflexes yielding objectively an intraeye discrepancy of 12 D. Similar to the objective findings, a pair of subjective findings for each eye was obtained and each pair resulted almost equal visual acuity. However, small pupil size veiled plus error and final prescription was myopic.
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Lubec, Barbara, and Klaus Arbeiter. "Determination of the urinary d/l trans-3-hydroxyprolineratio: A noninvasive screening test for Alport syndrome." Journal of Pediatrics 123, no. 5 (1993): 748–51. http://dx.doi.org/10.1016/s0022-3476(05)80852-2.
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Tabti, F., M. El Harrak, Z. Lahlafi, et al. "LA CARDIOMYOPATHIE NEUROGENE APRES UN ACCIDENT VASCULAIRE CEREBRAL ISCHEMIQUE: A PARTIR D UN CAS ET REVUE DE LITTERATURE." International Journal of Advanced Research 11, no. 04 (2023): 1222–28. http://dx.doi.org/10.21474/ijar01/16785.
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La cardiomyopathie neurogene (CN) correspond a une sideration myocardique etendue, sans rapport avec un territoire coronarien, secondaire a une lesion neurologique et resultant dun desequilibre du systeme nerveux autonome.Le spectre danomalies cardiaques observees comprend des modifications electriques, une elevation du taux de troponine, une dysfonction ventriculaire, et des troubles de la cinetique, mimant un infarctus du myocarde mais a la coronarographie le reseau coronaire est normal ou discretement atheromateux sans stenose significative et sans aspect thrombotique.Il sagit dune cardiomyopathie auto-resolutive la prise en charge consiste a traiterle processus neurologique sous-jacent et a surveiller les complications cardiaques principalement la survenue des troubles de rythme. Nous rapportons lobservation medicale dune patiente de 73 ans ayant presente dans le cadre dun accident vasculaire cerebral ischemique des anomalies electriques, biologiques et echocardiographiques simulant le tableau dun syndrome coronarien aigu sans elevation du segment ST. Nous soulevons a travers ce cas la difficulte de distinguer la cardiomyopathie neurogene dun infarctus du myocarde en se basant uniquement sur la presentation clinique et la necessite parfois de recourir a des procedures invasives tel un catheterisme cardiaque pour exclure un Syndrome coronarien aigu (SCA).Nous aborderons enrevue lepidemiologie, la physiopathologie, les caracteristiques cliniques, lediagnostic differentiel et la prise en charge proposee de lacardiomyopathie neurogene.
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Gao, Xiaoli, Meilu Li, Kan Wang, Zengyan Li, and Cha Han. "Pregnancy in women with autosomal recessive Alport syndrome caused by novel compound heterozygous mutations of COL4A3 gene: Two cases reports." Medicine 102, no. 46 (2023): e36057. http://dx.doi.org/10.1097/md.0000000000036057.
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Rationale: Autosomal recessive Alport syndrome (ARAS) is an hereditary heterogeneous disease that poses a serious risk to pregnant women. Patient concerns: We reported 2 cases of pregnancy with progressive proteinuria. The case 1 was a 21-year-old woman with 24-h proteinuria increased from 2.03 to 11.72 g at 13 to 35 weeks of gestation, and the case 2 was a 28-year-old woman with 24-h proteinuria increased from 2.10 to 9.32 g at 8 to 36 weeks of gestation. In advanced stage of pregnancy, the fetal development was smaller than the gestational age. Diagnoses: Sanger sequencing showed that novel compound heterozygous mutations [c.1315 G>T (p.G439C) and c.4847 G>A (p.C1616Y)] of the collagen type IV alpha 3 chain (COL4A3) gene were found in the 2 cases. Renal puncture pathology confirmed the diagnosis of ARAS. Interventions: The 2 cases were treated with albumin, compounded amino acids, calcium, vitamin D, and low molecular weight heparin in addition to conventional treatment during pregnancy. Pregnancy was terminated by cesarean section at 36 to 37 weeks of gestation. After delivery, the patients were treated with Losartan for anti-proteinuric therapy for 1 year. Outcomes: The neonatal weights and Apgar scores were normal. The patients recovered well and 24-h proteinuria decreased to pre-pregnancy level. Lessons: When pregnant women present with a persistent increasing proteinuria, ARAS needs to be considered. Sanger sequencing is useful to assist in the diagnosis of ARAS. Multidisciplinary treatments from nephrologists and gynecologists are needed to ensure the safety of pregnancy and the fetus.
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Bhate, Manjushree, Divya Motwani, Somasheila I. Murthy, and Merle Fernandes. "Congenital anomalies of lens shape." Taiwan Journal of Ophthalmology 13, no. 4 (2023): 479–88. http://dx.doi.org/10.4103/tjo.tjo-d-23-00076.
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The crystalline lens is an important structure in the eye that starts to develop as early as the 22nd day of gestation, with further differentiation that continues after the induction. Congenital anomalies of the lens may involve the size, shape, and position of the lens. They may sometimes be associated with anterior segment dysgenesis or persistence of the tunica vasculosa lentis and hyperplastic vitreous and hyaloid system. Manifestations of anomalies of the lens shape are usually seen in early or late childhood however may sometimes be delayed into adulthood based on the level of visual impairment or the presence or absence of any syndromic associations. While lens coloboma has more often been reported in isolation, the more commonly implicated genes include the PAX6 gene, lenticonus in particular anterior is often part of Alport syndrome with extra-ocular manifestations in the kidneys and hearing abnormalities due to mutations in the alpha 5 chain of the Type IV collagen gene. Recognition of these manifestations and obtaining a genetic diagnosis is an important step in the management. The level of visual impairment and amblyopia dictates the outcomes in patients managed either conservatively with optical correction as well as surgically where deemed necessary. This review discusses the various anomalies of the lens shape with its related genetics and the management involved in these conditions.
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Chavez, Efren, Juanly Rodriguez, Yelena Drexler, and Alessia Fornoni. "Novel Therapies for Alport Syndrome." Frontiers in Medicine 9 (April 25, 2022). http://dx.doi.org/10.3389/fmed.2022.848389.
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Alport syndrome (AS) is a hereditary kidney disease associated with proteinuria, hematuria and progressive kidney failure. It is characterized by a defective glomerular basement membrane caused by mutations in type IV collagen genes COL4A3/A4/A5 which result in defective type IV collagen α3, α4, or α5 chains, respectively. Alport syndrome has three different patterns of inheritance: X-linked, autosomal and digenic. In a study of CKD of unknown etiology type IV collagen gene mutations accounted for the majority of the cases of hereditary glomerulopathies which suggests that AS is often underrecognized. The natural history and prognosis in patients with AS is variable and is determined by genetics and environmental factors. At present, no preventive or curative therapies exist for AS. Current treatment includes the use of renin-angiotensin-aldosterone system inhibitors which slow progression of kidney disease and prolong life expectancy. Ramipril was found in retrospective studies to delay the onset of ESKD and was recently demonstrated to be safe and effective in children and adolescents, supporting that early initiation of Renin Angiotensin Aldosterone System (RAAS) blockade is very important. Mineralocorticoid receptor blockers might be favorable for patients who develop “aldosterone breakthrough.” While the DAPA-CKD trial suggests a beneficial effect of SGLT2 inhibitors in CKD of non-metabolic origin, only a handful of patients had Alport in this cohort, and therefore conclusions can't be extrapolated for the treatment of AS with SGLT2 inhibitors. Advances in our understanding on the pathogenesis of Alport syndrome has culminated in the development of innovative therapeutic approaches that are currently under investigation. We will provide a brief overview of novel therapeutic targets to prevent progression of kidney disease in AS. Our review will include bardoxolone methyl, an oral NRf2 activator; lademirsen, an anti-miRNA-21 molecule; sparsentan, dual endothelin type A receptor (ETAR) and angiotensin 1 receptor inhibitor; atrasentan, oral selective ETAR inhibitor; lipid-modifying agents, including cholesterol efflux transporter ATP-binding cassette A1 (ABCA1) inducers, discoidin domain receptor 1 (DDR1) inhibitors and osteopontin blocking agents; the antimalarial drug hydroxychloroquine; the antiglycemic drug metformin and the active vitamin D analog paricalcitol. Future genomic therapeutic strategies such as chaperone therapy, genome editing and stem cell therapy will also be discussed.
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Alexandre HERTIG. "Prééclampsie : la piste d’ un défaut de la stéroïdogenèse." REPRODUCTION HUMAINE ET HORMONES 26, no. 02 (2013). http://dx.doi.org/10.54695/rhh.26.02.4271.
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Alors que la physiopathologie du syndrome maternel de préeclampsie est beaucoup mieux comprise,celle de son versant placentaire, qui est le primummovens du syndrome, reste mystérieuse. Les outilsmodernes et spécifiques de mesure des stéroïdescomme la spectrométrie de masse après chromatographie gazeuse, ont cependant permis de détecterune diminution de la synthèse de l’œstradiol dansle sang des femmes accouchant dans un contextede préeclampsie. Ce défaut semble consécutif à undéfaut d’aromatisation des androgènes fœtaux etmaternels par le placenta. Ici, nous faisons l’hypothèse que ce défaut est précoce et joue un rôle causal dans les anomalies de la pseudovasculogénèseplacentaire qui caractérisent mais aussi induisent lapréeclampsie.
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Carrillo, Isabel Galan, Serena Gatius, and Ana Cristina Rodenas Galvez. "#6359 DAPAGLIFLOZIN TREATMENT IN AUTOSOMAL DOMINANT ALPORT SYNDROME (ADAS)." Nephrology Dialysis Transplantation 38, Supplement_1 (2023). http://dx.doi.org/10.1093/ndt/gfad063c_6359.
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Abstract Background and Aims Alport Syndrome (AS; ORPHA 63) is one of the most frequent hereditary kidney diseases (HKD). Its autosomal dominant form due to COL4A3-4 heterozygous mutations is being increasingly diagnosed thanks to the generalization of genetic studies. Since there is no curative treatment for the disease, management is based on drugs that slow its progression, mainly RAAS inhibitors. The SGLT2 inhibitor Dapagliflozin has demonstrated to slow chronic kidney disease (CKD) progression by decreasing proteinuria, however very few ADAS patients were included in its clinical trial. Our aim is to analyze whether dapagliflozin is associated with a decrease in proteinuria in ADAS patients. Method In this prospective observational study, we analyzed 12 ADAS patients that started dapagliflozin due to proteinuria in spite of maximum tolerated RAAS inhibitor treatment and eGFR > 25 ml/min/1.73 m2. We analyzed diabetes and hypertension presence (and its control), weight changes, possible adverse effects and laboratory variables before and after treatment initiation (Cr, eGFR, K, uric acid, albuminuria, proteinuria). Results During a mean follow-up period of 7±4 months, we observed 12 patients, 5 (41.7%) male, 61±10 years old. 2 (33.3%) had type 4 diabetes, 2 (16.7%) had impaired fasting glucose (IFG), 11 had hypertension diagnosis, 1 patient had obesity (BMI 36) and other 7 were overweight (mean BMI 28±2). 9 patients had the higher dose of an RAASi, the other three couldn’t achieved it because of hypotension events. 3 patients also took an antagonist of mineralocorticoid. Only one had another diuretic prescription (furosemide 40 mg/d). Mean proteinuria prior to Dapagliflozin initiation was 1.0±0.4 gr/d, protein-to-creatinine ratio (UPCR) 1275±635 mg/g and albumin-to-creatinine ratio (ACR) 784±418 mg/g. 10 out of the 12 patients had some grade of decrease in their proteinuria, with a mean decrease of 416±183 mg/g of UPCR (p = 0,046) and a mean decrease of 292±178 mg/g of ACR (p = 0,020). Looking only at patients without diabetes, they had a lesser degree of estimated glucosuria than diabetes patients, but maintained the improvement in proteinuria quite similar to the overall group (mean ACR improvement 244±95 mg/g). All patients had optimal blood pressure control, and there were no significant body weight losses. Mean eGFR previous to SGLT2i initiation was 50±22 ml/min/1.73 m2, and after 45±19 ml/min/1.73 m2 (p = 0,008), with a mean fall of 8±8%. There were no differences in potassium levels (p = 0,079) and a decrease of uric acid levels (6.7±1.3 mg/dl vs 6.0±1.4 mg/dl, p = 0,016). The two patients who didn’t achieve an improvement in their proteinuria were not diabetic patients and had optimal blood pressure control, one of them had a weight gain of two kilograms, and the other had no weight changes. They had a similar eGFR fall to the overall group. Possible adverse events were monitored, although we didn’t find any of them: no urine tract infections, hyperpotassemia, acute kidney injury, dehydration. No patient required treatment suspension. Two of them required a withdrawal in their other diabetes medications and the one on furosemide tried a lesser dose but had to increase it again. Conclusion Slower progression drugs are the main treatment of ADAS nowadays. Dapagliflozin had demonstrated its beneficial effects in other proteinuric CKD, but it hasn’t been well studied in ADAS. In our sample, it seems to achieve a proteinuria improvement without significant adverse effects and known bearable eGFR fall. Large studies must be considered to determine its beneficial use in a long-time basis.
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Firat, Emilia Anouk Margo, Eva Miriam Buhl, Nassim Bouteldja, et al. "PDGF-D is dispensable for the development and progression of murine Alport syndrome." American Journal of Pathology, February 2024. http://dx.doi.org/10.1016/j.ajpath.2023.12.009.
Texto completo da fonteTeses / dissertações sobre o assunto "Alport, Syndrome d' – Physiopathologie"
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Larrue, Romain. "Déterminants moléculaires et cellulaires des maladies rénales chroniques et de leurs complications." Electronic Thesis or Diss., Université de Lille (2022-....), 2024. http://www.theses.fr/2024ULILS026.
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La maladie rénale chronique est définie indépendamment de sa cause, par la présence,pendant plus de 3 mois, de marqueurs d’atteinte rénale ou d’une baisse du débit de filtration glomérulaire estimé (DFG estimé) au-dessous de 60 ml/min/1,73 m². Elle est associée à un risque accru de progression vers l’insuffisance rénale chronique terminale et à une diminution de la survie des patients. Les options thérapeutiques restent limitées et reposent essentiellement sur la dialyse et la transplantation rénale.Le projet de thèse proposé vise à identifier de nouveaux déterminants moléculaires et cellulaires associés à la maladie rénale chronique et ses complications en s’appuyant sur différentes entités cliniques. D’une part, la recherche de facteurs génétiques impliqués dans la pathogenèse de certaines néphropathies héréditaires telles que la néphronophtise ou le syndrome d’Alport a été appréhendée par des techniques analytiques innovantes telles que le séquençage à haut débit. D’autre part, l’implication d’un microARN, miR-21, a été évalué dans un modèle murin de néphropathie secondaire où les lésions rénales sont induites par l’exposition à un agent anticancéreux, le cisplatine.Nos résultats ont permis l’identification de nouveaux variants génétiques jouant un rôle causal dans le syndrome d’Alport et la néphronophtise à l’aide d’une stratégie analytique permettant le séquençage complet du génome. Par ailleurs, nos données suggèrent également que miR-21 aurait un rôle néphroprotecteur et que sa modulation pharmacologique permettrait d’éviter la survenue d’une insuffisance rénale chronique chez le patient recevant des chimiothérapies à base de dérivés du platine.Au total, les résultats obtenus dans ce travail devraient permettre de mieux comprendre la physiopathologie de la maladie rénale chronique et pourrait aboutir à plus ou moins long terme à de nouvelles options thérapeutiques<br>Chronic Kidney Disease (CKD) is defined, regardless of its primary cause, by the presence, for more than 3 months, of markers of kidney damage or a decrease in estimated glomerular filtration rate below 60 ml/min/1.73 m². CKD is associated with an increased risk of progression to end-stage renal disease as well as decreased patient survival. Therapeutic options remain limited and rely primarily on dialysis and renal transplantation.This thesis project aims at identifying novel molecular and cellular determinants associated with CKD and its complications based on different clinical entities. On the one hand, the search for genetic factors involved in the pathogenesis of certain hereditary nephropathies such as nephronophthisis or Alport syndrome has been addressed using innovative analytical techniques such as high-throughput sequencing. On the other hand, the involvement of a particular microRNA, miR-21, was evaluated in a mouse model of secondary nephropathy where kidney damage is induced by exposure to an anticancer agent, cisplatin. Our results allowed the identification of new genetic variants playing a causal role in Alport syndrome and nephronophthisis using an analytical strategy enabling complete genome sequencing. Furthermore, our data also suggest that miR-21 has a nephroprotective role and that its pharmacological modulation may prevent the occurrence of chronic renal failure in patients receiving chemotherapy including platinum derivatives. Overall, the results obtained in this work provide a better understanding of the pathophysiology of chronic kidney disease and could lead to new therapeutic options in the more or less long term
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Albert, Isabelle. "Inférence bayesienne par les methodes de Monte Carlo par chaînes de Markov et arbres de régression pour l'analyse statistique des données corrélées." Paris 11, 1998. http://www.theses.fr/1998PA11T020.
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L’analyse statistique des données corrélées permet l'étude des schémas d'échantillonnage comportan une structure de groupe. Les modèles marginaux et à effets mixtes, qui constituent des extensions des modèles linéaires généralisés, ont été proposés dans ce contexte pour prendre en compte la non indépendance des observations. Nous considérons deux approches : une inférence bayésienne des modèles à effets mixtes par les méthodes de Monte Carlo par chaînes de Markov (MCMC) et une méthode de régression arborescente (CART) pour l'analyse des données censurées corrélées. La première partie est consacrée à l'étude de l’approche bayésienne par les méthodes MCMC. Les principes de l'inférence bayésienne, des méthodes MCMC et leurs apports lors des étapes-clés d'une analyse de régression (estimation, comparaison, adéquation des modèles et étude de prédiction) sont étudiés. Cette méthode d'estimation est utilisée pour l'étude des accidents allergiques survenant au cours d'échanges plasmatiques. Nous proposons dans la seconde partie une nouvelle méthode de type CART pour l'analyse des données censurées corrélées. Cette méthode utilise des tests du log-rank robustes à une spécification inadéquate de la structure de corrélation des données, et un critère BIC corrigé pour le choix de l'arbre final. La méthode développée a été étudiée par simulation et appliquée à des données réelles concernant une maladie génétique, le Syndrome d'Alport.
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Oulès, Bénédicte. "Impact physiologique du transfert de calcium entre le réticulum endoplasmique (RE) et la mitochondrie : rôle de l'isoforme SERCAI tronquée (S1T) dans le stress du RE et la maladie d'Alzheimer." Paris 5, 2010. http://www.theses.fr/2009PA05T063.
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Le transfret de calcium (Ca2+) entre le réticulum endoplasmique (RE) et la mitochondrie est médié par des sites de contact dynamiques. Nous avons montré que l'isoforme tronquée de la SERCA1 (S1T) ignitie et amplifie la voie pro-apoptotique du stress du RE. De plus, elle détermine une fuite localisée du Ca2+ au niveau des sites de contacts RE-mitochondrie induisant l'apoptose. Nous avons également montré que S1T est surexprimée dans la maladie d'Alzheimer. Parallèlement, l'Aβ s'accumule au niveau des sites de contact RE-mitochondrie. Par ailleurs, l'analyse de la signalisation calcique subcellulaire nous a permis de démontrer une dérégulation majeure de celle-ci. Enfin, nous avons révélé que le Ca2+ contrôle les processus bioénergétiques altérés dans la maladie de Leigh due au déficit du complexe II de la chaîne respiratoire mitochondriale. Nos résultats ont mis en évidence l'impact du transfert du Ca2+ entre le RE et la mitochondrie dans les pathologies du RE et de la mitochondrie<br>Calcium (Ca2+) transfer between endoplasmic reticulum (ER) and mitochondria is mediated through dynamic contacts sites. We showed that the truncated isoform of SERCA1 (S1T) initiates and simplifies the proapoptotic pathway of the ER stress signaling. In addition, owing to its localization at the ER-mitochondria contacts sites, it determines a localized ER Ca2+ leak towards the mitochondria leading to mitochondrial apoptosis. We also demonstrated that S1T is overexpressed in Alzheimer's disease. In parallel, Aβ accumulates in ER-mitochondria contact sites. In addition, an extensive analysis of subcellular Ca2+ signaling allowed us to demonstrate its drastic deregulation. Lastly, we have revealed that Ca2+ control bioenergetics pathways in Leigh's disease related to mitochondrial respiratory chain complex II deficiency. Our results showed the impact of Ca2+ transfer from ER to mitochondria-related pathologies
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Luchs, Klaus. "Veränderung der Nierenfunktion, des Proteoms und des Phosphorylierungsstatus der Proteine bei Alport-Mäusen unter Mycophenolat-Mofetil." Doctoral thesis, 2016. http://hdl.handle.net/11858/00-1735-0000-002B-7C50-D.
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Ninichuk, Volha [Verfasser]. "The role of chemokine receptor CCR1-dependent macrophage recruitment for the progression of chronic kidney disease in murine Alport syndrome or type 2 diabetes / vorgelegt von Volha Ninichuk." 2008. http://d-nb.info/987945971/34.
Texto completo da fonteLivros sobre o assunto "Alport, Syndrome d' – Physiopathologie"
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Takao, Kumazawa, Kruger Lawrence, and Mizumura Kazue, eds. The polymodal receptor: A gateway to pathological pain. Elsevier, 1996.
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(Editor), T. Kumazawa, L. Kruger (Editor), and K. Mizumura (Editor), eds. The Polymodal Receptor - A Gateway to Pathological Pain (Progress in Brain Research). Elsevier Science, 1996.
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