Academic literature on the topic 'Maladie glomérulaire'
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Journal articles on the topic "Maladie glomérulaire":
Stevanin, Mathias, Sébastien Kissling, Cécile Daccord, Samuel Rotman, Denis Comte, and Camillo Ribi. "Maladie des anticorps anti-membrane basale glomérulaire." Revue Médicale Suisse 19, no. 821 (2023): 680–85. http://dx.doi.org/10.53738/revmed.2023.19.821.680.
MALMARTEL, A. "MALADIE RENALE CHRONIQUE." EXERCER 33, no. 180 (February 1, 2022): 86–87. http://dx.doi.org/10.56746/exercer.2022.180.86.
Vergnaud, Paul, Camille Cohen, and Pierre Isnard. "Aux sources de la compréhensionde la maladie rénale chronique." médecine/sciences 39, no. 3 (March 2023): 265–70. http://dx.doi.org/10.1051/medsci/2023033.
Dabadie, A., S. Gié, S. Taque, JM Babut, and M. Roussey. "Néphropathie glomérulaire à dépôts mésangiaux d'IgA et maladie de Crohn." Archives de Pédiatrie 3, no. 9 (September 1996): 884–87. http://dx.doi.org/10.1016/0929-693x(96)87579-8.
Khelili, R., A. Kefi, M. Bouzidi, M. Hajji, A. Lotfi, C. Sassi, R. Aouadia, et al. "Maladie des anticorps anti-membrane basale glomérulaire : à propos de 37 cas." La Revue de Médecine Interne 43 (June 2022): A251—A252. http://dx.doi.org/10.1016/j.revmed.2022.03.227.
Harambat, Jérôme, and Denis Morin. "Épidémiologie des maladies rénales chroniques en pédiatrie." médecine/sciences 39, no. 3 (March 2023): 209–18. http://dx.doi.org/10.1051/medsci/2023027.
Dambaba, H., C. Kabeya Manunga, N. Jnyah, B. A. Chouhani, G. El Bardai, N. Kabbali, and T. Sqalli Houssaini. "La maladie des anticorps anti-membrane basale glomérulaire : à propos de 3 cas." Néphrologie & Thérapeutique 17, no. 5 (September 2021): 323–24. http://dx.doi.org/10.1016/j.nephro.2021.07.197.
Seret, G., A. Duveau, K. Laribi, A. Croué, J. F. Subra, and J. P. Coindre. "Microangiopathie thrombotique glomérulaire associée à une maladie de Castleman multicentrique : à propos d’un nouveau cas." Néphrologie & Thérapeutique 9, no. 5 (September 2013): 332. http://dx.doi.org/10.1016/j.nephro.2013.07.040.
Ben Kaab, B., H. Jebali, R. Kadouri, L. Ben Fatma, S. Beji, L. Raïs, R. Kheder, et al. "Néphropathie glomérulaire et cryoglobulinémie mixte au cours d’une maladie de Still : à propos d’un cas." Néphrologie & Thérapeutique 10, no. 5 (September 2014): 339–40. http://dx.doi.org/10.1016/j.nephro.2014.07.159.
Marques, C., F. Prôvot, M. Matignon, J. J. Boffa, A. Hertig, M. Touzot, X. Belenfant, et al. "Étude observationnelle multicentrique sur la maladie des anticorps anti-membrane basale glomérulaire (syndrome de Goodpasture)." La Revue de Médecine Interne 37 (June 2016): A43. http://dx.doi.org/10.1016/j.revmed.2016.04.246.
Dissertations / Theses on the topic "Maladie glomérulaire":
Huang, Jin. "Rôle de lutheran/ Basal Cell Adhesion Molecule (Lu/BCAM) dans la permsélectivité glomérulaire et l'adhérence leucocytaire au cours des néphropaties murines." Paris 7, 2013. http://www.theses.fr/2013PA077113.
Lu/BCAM blood group glycoprotein, due to its important expression in renal endothelium, is suggested involved in facilitating accumulation of leukocyte and maintained the glomerular permselectivity. Lu/BCAM has been recognized as a receptor for two types of molecules. On one hand, it is a receptor for laminin α5 chain which constitute in particular lamininlO and 11 in the sub-endothelial matrix; on the other hand, it is a receptor for integrin α4ß1 (VLA-4) which present on the surface of leukocyte. Lu/BCAM-/-mice exposes abnormalities characterized by an irregular thickening of the glomerular basement membrane and sometimes an abnormal enlargement of foot process of podocyte. We have made two hypotheses: firstly, Lu/BCAM could promote leukocyte adhesion on endothelium via integrin α4ß1; secondly, Lu/BCAM could limit glomerular permselectivity by maintaining EC to GBM containing laminin α5 chain. To respond our first hypothesis, a passive RPGN model has been used. In this model, Lu/BCAM-/-mice attenuated glomerular accumulation of T cells and macrophages, crescent formation, and proteinuria, correlating with reduced fibrin and platelet déposition in glomeruli. Furthermore, we found pro-adhesive interaction between human monocyte α4ß1 integrin and Lu/BCAM proteins. For proving our second hypothesis, hypertension and glomerulosclerosis were induced by high salt diet (5% NaCl) and chronic infusion of Angiotensin II (l μ g/kg/min) or PBS in an osmotic mini-pump for 28 days or by administration of a NO syntheses inhibitor L-NAME in Lu-/-mice for 90 day in Lu/BCAM-/- mice and their wild-type littermates. Despite of a similar arterial tension, Lu/BCAM-/- hypertensive mice exhibited higher albuminuria. During Dextran-FITC (70K Da) diffusion test, a vascular hyper-permeability was observed in Lu/BCAM-/- carotid compared with their WT group. Furthermore, Lu/BCAM-/- mice displayed also a renal hyper-permeability during evans bleu permeability test, but this hyperpermeability was not found in the other organs such as brain, spleen and liver. In conclusion, the results indicated that: 1, Lu/BCAM-/- mice could possess a nephroprotective function in the early stage of GNRP when the leukocyte (monocyte and macrophage in particular) attached to into inflammatory glomerulus. It's function of leukocyte recruitment was possibly accomplished via VLA-4 ; 2,Lu/BCAM has no effect on systolic blood pressure but it plays a major role in glomerular permselectivity during hypertension and it has a extra reral endotherial permeability
Boucquemont, Julie. "Modèles statistiques pour l'étude de la progression de la maladie rénale chronique." Thesis, Bordeaux, 2014. http://www.theses.fr/2014BORD0411/document.
The objective of this thesis was to illustrate the benefit of using advanced statistical methods to study associations between risk factors and chrouic kidney disease (CKD) progression. In a first time, we conducted a literature review of statistical methods used to investigate risk factors of CKD progression, identified important methodological issues, and discussed solutions. In our sec ond work, we focused on survival analyses and issues with interval-censoring, which occurs when the event of interest is the progression to a specifie CKD stage, and competing risk with death. A comparison between standard survival models and the illness-death mode! for interval-censored data allowed us to illustrate the impact of modeling on the estimates of both the effects of risk factors and the probabilities of events, using data from the NephroTest cohort. Other works fo cused on analysis of longitudinal data on renal function. We illustrated the interest of linear mixed mode! in this context and presented its extension to account for sub-populations with different trajectories of renal function. We identified five classes, including one with a strong decline and one with an improvement of renal function over time. Severa! perspectives on predictions bind the two types of analyses presented in this thesis
Kaboré, Jean. "Hypertension artérielle résistante et maladie rénale chronique : déterminants et risques associés." Thesis, Université Paris-Saclay (ComUE), 2016. http://www.theses.fr/2016SACLS265/document.
Resistant hypertension and chronic kidney disease: Determinants and outcomesResistant hypertension defined as blood pressure above goal despite simultaneous use of 3 antihypertensive classes at optimal doses including a diuretic, is commonly associated with chronic kidney disease (CKD). Resistant hypertension prevalence and determinants, and the impact of CKD on its long term outcomes are poorly known, particularly in the elderly population.In the 3 Cities cohort, including 4262 community-dwelling elderly individuals, aged 65 years or older treated for hypertension, the prevalence of apparent treatment resistant hypertension (aTRH) – because of lack of information on optimal treatment dose – was 11.8% vs 5.2% in those with vs without CKD (defined as estimated glomerular filtration rate < 60 mL/min/1.73 m2). We showed that new-onset aTRH was more strongly related to the speed of kidney function decline than kidney function level itself, independent of other risk factors: male sex, obesity, diabetes, and history of cardiovascular disease. Compared to the reference group (with controlled hypertension and no CKD), participants with aTRH and CKD had no significantly higher risk of all-cause mortality, but had a risk of fatal or non-fatal stroke and of recurrent stroke or coronary events more than twice as high, and of coronary death more than three times higher. However, the hypothesis that CKD may worsen the prognosis of aTRH was not confirmed (no significant interaction).In the CKDREIN cohort, which included more than 3000 nephrology outpatients with moderate or severe CKD (mean age, 70 years, 60% of men), our preliminary results showed a high prevalence of aTRH, 36,7% and several potentially modifiable risk factors : poor treatment adherence, lack of diuretic use, excess salt intake and obesity.Overall, this work shows the importance of CKD in the development of aTRH and associated cardiovascular outcomes, and suggests means for prevention beyond drug therapy
Tordina, Adoum. "Le syndrome pneumo-rénal à anticorps antimembrane basale glomérulaire : syndrome de Goodpasture, à propos d'une observation." Bordeaux 2, 2000. http://www.theses.fr/2000BOR2M031.
Steinbruckner-Gaildraud, Ingrid. "Un nouveau marqueur d'évaluation de la filtration glomérulaire : la cystatine C sérique." Bordeaux 2, 2000. http://www.theses.fr/2000BOR2P040.
Kennel-De, March Anne. "Système immunitaire humoral muqueux et recirculation cellulaire dans la néphropathie A IgA." Nancy 1, 1997. http://www.theses.fr/1997NAN12162.
Doublier, Sophie. "Rôles respectifs de l'axe hormone de croissance (GH) / insulin like growth factor-I (IGF-I) et de la somatostatine dans le développement de l'inflammation et de la fibrose glomérulaires." Paris 11, 2000. http://www.theses.fr/2000PA11T009.
GH plays a role in the development of glomerulosclerosis. We addressed two questions: (1) does GH-associated kidney damage depend on GH binding to the known GH receptor?, (2) does GH act independently of IGF-1? To investigate whether GH-associated kidney damage depends on GH binding to the known GH receptor, diabetes was induced in mice in which the gene for the GH receptor/binding protein had been disrupted (GHRIBP-KO mice). GHRIBP-KO mice ppeared to be protected from diabetes-induced glomerulosclerosis. In other respects, because IGF binding proteins (IGFBP) modulate IGF actions and, bence, GH secretion, we assessed whether mice transgenic for human IGFBP-1 have altered susceptibility to glomerulosclerosis. By reducing IGF-1 bioavailability, IGFBP-1 overexpression limits potentially the negative feedback exerted by circulating IGF-1 on GH secretion and, bence, may worsen GR-dependent glomerulosclerosis. We observed an expansion of extracellular matrix area in homozygous IGFBP-1 transgenic mice at 3 months of age. This was related to a marked increase in !aminin and type IV collagen and to the appearance of type 1 collagen. These changes were not associated with glomerular hypertrophy and hypercellularity. Because nephron reduction at birth can be involved in the development of glomerulosclerosis, we then investigated the impact of IGFBP-1 overexpression on renal development, in particular on the nephron number. When only patemal allele was expressed in the transgenic mice, we observed a 20% reduction in the nephron number. When IGFBP-1 was expressed in the mother, and whatever genotypesof the fetuses were (homozygous, heterozygous or non-transgenic), an intrauterine growth retardation was present in offspring, inducing a reduction in the nephron number to the same extent. As 20% nephron reduction occured in sorne groups of mice which did not develop glomerulosclerosis in adulthood, nephron reduction does not account for the development of glomerulosclerosis in mice transgenic for IGFBP-1. Somatostatin has anti-inflammatory actions, partly by increasing glucocorticoid responsiveness in target cells. To evaluate whether this effect is mediated by up-regulating GR expression, we studied the role of somatostatin on glucocorticoid binding and signaling in macrophage cellline RAW 264. 7. Somatostatin promoted a time- and dose-dependent increase in [3H] dexamethasone binding. Cell exposure to 10 nM somatostatin for 18 h promoted a 2-fold increase in the number of GR sites per cell without significant modification of the affinity. Analysis of GR heterocomplex components demonstrated that somatostatin increased the level of GR-associated heat shock protein (Hsp) 90, by limiting its calpain-dependent cleavage. Somatostatin exerts its function through binding to a family of five G protein-coupled receptors (sst1 to sst5). We then tried to identify somatostatin receptors involved in the anti-inflammatory activity of somatostatin in macrophages. By reverse transcriptase polymerase chain reaction, the mRNA for the receptor subtypes sst1, sst2 and sst3 could be detected in RAW 264. 7 macrophages. Binding assays on macrophages of mice in which the gene for the sst2 had been disrupted and of control mice showed a specifie somatostatin binding which did not involved sst2
Huynh, Cong Evelyne. "Le rôle émergeant des microtubules dans la physiopathologie des podocytopathies héréditaires." Thesis, Sorbonne Paris Cité, 2015. http://www.theses.fr/2015PA05T028.
The genetic study of familial forms of nephrotic syndrome or proteinuria with focal segmental glomerulosclerosis has permitted the identification of 30 causal genes, mainly expressed in the podocyte, which is the principal actor of the glomerular filtration barrier (GFB). Among those genes, approximately ten encode actin cytoskeleton regulators and components, thus highlighting the dramatic role of the podocyte architecture and plasticity in the function of the GFB. During the last decade, all the accumulating results, has made a new category of disease called hereditary podocytopathies. The aim of my thesis project was to characterize the effect of mutations in three candidate genes (TTC21B, WDR73, WDR73), identified by whole exome sequencing in isolated or syndromic podocytopathies. In the first part of my project, we found a homozygous missense mutation (p.P209L) in TTC21B, which encodes a ciliary gene named Intraflagellar transport protein IFT139. This protein ensures the trafficking of components from the tip to the base of the primary cilium, which is an organelle present on most mammalian epithelial cells. These results were unexpected because until now, the existence of the primary cilium was unknown. Our work demonstrates the presence of the primary cilium in the human immature podocyte that disappears once podocytes have differentiated. We also showed that IFT139 localized at the basal body and then relocalized along the complex microtubule network of differenciated cells. We showed that the hypomorphic mutation p.P209L causes minor ciliary defects in undifferentiated cells that are not responsible for the glomerular phenotype. Indeed, the glomerular lesions are rather due to drastic damage in actin and, microtubular dysregulation, found in differentiated podocytes. The second part of my thesis aimed to characterize the effects of truncating mutations identified in the WDR73 gene, found in two families. WDR73 is the first gene identified in Galloway Mowat syndrome by whole exome sequencing combined with homozygous mapping. This rare disease is defined by the association of microcephaly with nephrotic syndrome. In this study, the phenotypes of patients with WDR73 mutations are homogenous concerning neurological features, and are heterogeneous with regards to the renal defects. Thus, WDR73 mutations are responsible for a subset of particular patients affected with Galloway-Mowat syndrome. The WDR73 gene encodes WDR73, a WD-40 containing protein of unknown function. Our studies demonstrated that this protein is expressed in both neurons and podocytes in human tissues. We demonstrated that in undifferentiated cells, WDR73 is weakly expressed in the cytosol, while strong expression and relocalization to the spindle pole, microtubule asters and in the cleavage furrow occur during mitosis. Patient fibroblasts and WDR73-depleted podocytes displayed defects in nuclear morphology, which was associated with a decrease in cell survival in patient fibroblasts. Furthermore, we showed that patient fibroblasts and differentiated WDR73-depleted podocytes harbored an atypical morphology associated with a disorganized microtubule network, suggesting microtubule polymerization defects. Our functional studies demonstrated that WDR73 is crucial in both cell survival and microtubule polymerization in neurons and podocytes. The final part of my PhD work focused on the characterization of a missense mutation in the TRIM3 gene R28W identified by whole exome sequencing in a non consanguineous family with autosomal dominant focal segmental glomerulosclerosis. TRIM3 encodes TRIM3, an E3 ubiquitin-ligase that plays a role in transferrin endosomal recycling, and in microtubule trafficking via KIF21B, one of its known partners. Interestingly, the polymorphism V801M in ACTN4 co-segrates with the disease. Furthermore, mutations in this gene were already incriminated in autosomal dominant cases of HSF. (...)
Vieux, Rachel. "Déterminants de la fonction rénale d'enfants nés grands prématurés dans leur environnement néonatal et dans l'enfance." Thesis, Nancy 1, 2011. http://www.theses.fr/2011NAN10095/document.
Background: Physiological development of renal may be altered in preterm infants by environmental factors. Their imprinting could persist beyond the neonatal period. Objectives: 1) to determine reference values of glomerular filtration rate (GFR) during the first month of life in preterm newborns, 2) to determine the impact of perinatal factors and of the drugs often prescribed on their renal function, 3) to determine the effect of the perinatal imprinting, and of the growth and height catch-up, on their renal function in early childhood. Sample: Multicentre cohort of children born very preterm at 27-31 weeks of gestation, with a measure of their renal function during the neonatal period, and at 4 years of age. Results: 1) 275 infants included. Median reference GFR value (mL/min/1.73m²) was: 7.9 on day7 to 37.9 on day 28. 2) GFR was significantly reduced on day 7 in ibuprofen-infused infants in comparison to Controls: 12.8±6.2 vs. 18.1±12.1 ml/min/1.73 m², p < 0.001. This decrease persisted throughout the first month of life, and tubular function was also altered. Among all antenatal drugs and drugs administered during the first week of life, alone ibuprofen was significantly associated with a GFR < median reference value on day 7. 3) Height >= -1 SD in early childhood was associated with a high albuminuria in 119 four year-old preterm-born children. Conclusion: i) These GFR reference values are to be used in clinical research, ii) Neonatal therapeutic environment impairs renal function and delays its maturation, iii) The height at age four is an independent risk factor of high albuminuria in preterm-born children
Tynkevich, Elena. "Muscle Wasting in Non-end Stage Chronic Kidney Disease : Determinants and Outcomes." Thesis, Paris 11, 2014. http://www.theses.fr/2014PA11T086.
Mainly described in patients on dialysis, muscle wasting has received little attention in early stage chronic kidney disease (CKD). We used 24-hour creatininuria to assess determinants of low muscle mass and its putative associations with CKD outcomes, using data from the NephroTest cohort, including 1429 non-dialysis patients with CKD stages 1 to 5. Kidney function was assessed with both measured (mGFR, by 51Cr-EDTA renal clearance) and estimated glomerular filtration rate (eGFR, by CKD-EPI equation). End-stage renal disease (ESRD) and pre-ESRD death were the main studied outcomes. The mean baseline creatininuria decreased from 15.3±3.1 to 12.1±3.3 mmol/24 h in men and from 9.6±1.9 to 7.6±2.5 in women, when mGFR fell from ≥ 60 to < 15 mL/min/1.73 m2. Other determinants of low creatininuria were an older age, diabetes, a lower body mass index, a lower level of proteinuria or protein intake. A fast annual decline in mGFR of 5 mL/min/1.73 m2 was linked with a 2-fold decrease in creatininuria, independent of changes in protein intake and other determinants of muscle mass. Over a median follow-up of 3.6 years, 229 patients developed ESRD and 113 patients died before ESRD. After adjustment for confounders, patients with low muscle mass showed a significantly higher risk for pre-ESRD death (HR 1.6, 95% CI 0.88-2.9), but a lower risk for ESRD (HR 0.60, 95% CI 0.39-0.91). The latter was reversed (HR 1.5, 95% CI 1.01-2.4) when mGFR was replaced by eGFR. Decrease in 24-hour creatininuria may appear early in CKD patients, is related to pre-ESRD death. The lower risk for ESRD may reflect later dialysis start due to overestimation of true GFR by eGFR in patients with low muscle mass