Academic literature on the topic 'Lésions tubulaires'
Create a spot-on reference in APA, MLA, Chicago, Harvard, and other styles
Consult the lists of relevant articles, books, theses, conference reports, and other scholarly sources on the topic 'Lésions tubulaires.'
Next to every source in the list of references, there is an 'Add to bibliography' button. Press on it, and we will generate automatically the bibliographic reference to the chosen work in the citation style you need: APA, MLA, Harvard, Chicago, Vancouver, etc.
You can also download the full text of the academic publication as pdf and read online its abstract whenever available in the metadata.
Journal articles on the topic "Lésions tubulaires":
Luque, Y. "Toxicité rénale des immunoglobulines intraveineuses." Médecine Intensive Réanimation 27, no. 4 (July 2018): 324–30. http://dx.doi.org/10.3166/rea-2018-0059.
Audard, V., S. Moutereau, A. Habibi, M. Khellaf, P. Grimbert, Y. Levy, S. Loric, et al. "Lésions tubulaires infra-cliniques au cours des crises vaso-occlusives drépanocytaires." Néphrologie & Thérapeutique 10, no. 5 (September 2014): 357. http://dx.doi.org/10.1016/j.nephro.2014.07.204.
Girshovich, A., C. Vinsonneau, J. Perez, S. Vandermeersch, S. Placier, E. Letavernier, L. Baud, and J. P. Haymann. "Effet protecteur du FGF7 dans un modèle d’insuffisance rénale aiguë ischémique : prévention des lésions tubulaires et accélération de la régénération." Néphrologie & Thérapeutique 8, no. 5 (September 2012): 289–90. http://dx.doi.org/10.1016/j.nephro.2012.07.347.
Kormann, R., N. Prakoura, S. Placier, S. Vandermeersch, M. C. Verpont, J. C. Dussaule, C. Chadjichristos, and C. Chatziantoniou. "La délétion du gène de la periostine augmente les lésions tubulaires, réduit l’infiltrat inflammatoire macrophagique, et augmente la fibrose rénale dans le modèle murin d’ischémie-reperfusion rénale." Néphrologie & Thérapeutique 14, no. 5 (September 2018): 268. http://dx.doi.org/10.1016/j.nephro.2018.07.045.
Ogunleye, A. O., A. T. P. Ajuwape, A. I. Adetosoye, and O. G. Ohore. "Pathogénicité de Salmonella Paratyphi A chez des poulettes." Revue d’élevage et de médecine vétérinaire des pays tropicaux 59, no. 1-4 (January 1, 2006): 5. http://dx.doi.org/10.19182/remvt.9954.
Gabarre, Paul, Guillaume Dumas, and Lara Zafrani. "Insuffisance rénale aiguë chez les patients COVID-19 en soins intensifs." Médecine Intensive Réanimation 30, Hors-série 1 (June 16, 2021): 43–52. http://dx.doi.org/10.37051/mir-00069.
Marchiset, Antoine, and Matthieu Jamme. "Répercussions rénales au cours du SDRA." Médecine Intensive Réanimation 33, no. 2 (June 7, 2024): 205–16. http://dx.doi.org/10.37051/mir-00220.
Iyeghe-Erakpotobor, G. T., J. O. Omirinde, A. E. Enaohwo, and P. P. Barje. "Semen Characteristics and Testiculo-Epididymal Histology of Red Sokoto Bucks Fed Whole Cottonseed and Cottonseed Cake." Nigerian Journal of Animal Production 49, no. 5 (May 26, 2023): 75–86. http://dx.doi.org/10.51791/njap.v49i5.3766.
Dissertations / Theses on the topic "Lésions tubulaires":
Dewitte, Antoine. "Plaquettes sanguines et insuffisance rénale aiguë : rôle du couple CD154/CD40 dans la constitution des lésions tubulaires." Thesis, Bordeaux, 2017. http://www.theses.fr/2017BORD0906.
Acute kidney injury (AKI) is a common complication in critically ill patients and is associated with increased morbidity and mortality. Sepsis is the most common cause of AKI. The understanding of sepsis pathophysiology and its complications has progressed significantly in recent years but has not yet been translated into significant therapeutic advances in clinical practice. The traditional paradigm that sepsis-induced AKI is linked to renal hypoperfusion has been challenged by recent evidences showing that renal blood flow is not universally impaired during sepsis,and that AKI can develop in the presence of normal or even increased renal bloodflow. Sepsis is characterized by profound alterations of the immune response and adisproportionate inflammatory response. Inflammation and microcirculatorydysfunction are now considered as fundamental pathophysiological mechanisms atthe origin of renal injuries. Beyond haemostasis, the contribution of platelets ininflammation, tissue integrity and defence against infections has considerablywidened the spectrum of their role and made them potential physiopathologicalactors in sepsis. Platelets fulfil most of these functions through the expression ofmembrane-bound or soluble mediators. Among them, CD154 holds a peculiarposition, as platelets represent a major source of CD154 and as CD154 is a centralregulator of inflammation. Here, we provide an overview of these recentpathophysiological advances and discuss the platelets and CD154 contribution tomicrocirculatory alterations in multi-organ dysfunction in sepsis. We investigated thepro-inflammatory role of CD154 under hypoxic conditions in the renal tubularepithelium as recent data highlight the importance of hypoxia in the inflammatoryreaction. We studied the control of interleukin (IL)-6 production, a key cytokineinvolved in inflammation, by CD154 in oxygen deprivation conditions using a kidneytubular epithelial (TEC) cell line model. We also studied a murine model of kidneyinjury after ischemia/reperfusion, a model that was applied in CD154 and CD40deficient mice. We found that CD154 is a potent inducer of IL-6 secretion by TEC inhypoxia and that CD154-deficient mice regenerate earlier the tubular epithelium afterischemia/reperfusion injury. These findings may provide potential avenues for septicAKI management and therapy
Pillebout, Evangéline. "Progression des lésions rénales après réduction néphronique : rôle de la prolifération tubulaire et de l'angiogenèse." Paris 7, 2003. http://www.theses.fr/2003PA077177.