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5 raisons identifiées
Plateau technique de référence
Assistance publique – Hôpitaux de Paris (APHP) — équipements et expertise pointus pour les cas complexes
Auteur de référence en rhumatologie
20 articles scientifiques publiés — un praticien à la pointe de la recherche
Encadrant universitaire
Forme la prochaine génération de rhumatologues (6 thèses dirigées)
Expérience confirmée
18 ans d'exercice en rhumatologie — recul clinique solide
Délais de RDV courts dans la région
336.2 rhumatos / 100 000 hab. — département bien doté
18ans d'exercice (thèse 2008)
Données ANS publiques (Licence Ouverte 2.0) · Enrichissements MonRhumato 100 % opt-in · Toute personne référencée peut demander la suppression ou la rectification.
✨ Génération du profil synthétique IA en cours…
Source : catalogue national des thèses theses.fr (ABES). Ne couvre que les doctorats / HDR — les thèses d'exercice (DES) sont archivées dans les SCD universitaires.
Régulation du métabolisme de l’urate par le récepteur AHR
2023Doctorant·e : Jérémy Zaworski
ABCC6 et biominéralisation rénale et vasculaire
2022Doctorant·e : Élise Bouderlique
Caractéristiques physico-chimiques, genèse et conséquences tissulaires des dépôts cutanés calciques
2022Doctorant·e : Hester Colboc
Lithiase rénale : de la génétique à la bactérie
2017Doctorant·e : Marine Livrozet
Rôle des calpaïnes dans le vieillissement et la réponse anti-tumorale
2016Doctorant·e : Guillaume Hanouna
Altérations osseuses dans les modèles murins de maladies rénales : Perspectives histomorphométriques et HR-pQCT
Doctorant·e : Andrea Spasiano
Source theses.fr — signal de direction d'équipe / statut PU-PH (à confirmer via le site universitaire).
Indicateurs publics agrégés sur 250 M+ d'œuvres scientifiques (OpenAlex, PubMed). Traduits ici en langage patient.
Influence scientifique
45
45 articles ont été cités au moins 45fois par d'autres chercheurs — preuve que ses travaux sont repris par la communauté médicale.
h-index
Total citations reçues
5 697
Nombre de fois où d'autres équipes ont mentionné ses publications dans leurs propres travaux.
Publications totales
294
Articles, revues et chapitres référencés dans les bases académiques internationales.
Articles influents
123
Publications ayant marqué leur domaine — chacune citée au moins 10 fois par d'autres chercheurs.
i10-index
Thématiques principales
Affiliations FR : Sorbonne Université · Assistance Publique – Hôpitaux de Paris · Centre de Recherche Saint-Antoine
Source : OpenAlex (CC0, OurResearch). Indicateurs académiques agrégés sur 250 M+ d'œuvres.
Articles déposés en accès libre sur l'archive ouverte des universités françaises (HAL) — gage d'activité de recherche en France.
Experimentally recreated workplace environments contain submicron crystalline silica particles, including ultrafine particles, which have been identified in the mediastinal lymph nodes of construction workers
2026ArticleOccupational and Environmental Medicine
Vancomycin-specific Urinary Immunostaining for Noninvasive Screening of Vancomycin-associated Cast Nephropathy
2026ArticleKidney medicine
Novel CNNM2 variant causing hypomagnesemia and early-onset calcium pyrophosphate deposition disease: A case report
2026ArticleJoint Bone Spine
Nano-Investigation of Mineralized Biological Samples Chemical Composition: Experimental Challenges, Constraints, and Considerations
2025ArticleAnalytical Chemistry
Severe hypophosphatemia induced by excessive production of FGF23 in acute hepatitis: from bedside to bench
2024ArticleClinical Kidney Journal
Comparison of normocalcemic versus hypercalcemic primary hyperparathyroidism in a hypercalciuric renal stone population
2024ArticleJournal of Clinical Endocrinology and Metabolism
Oral pyrophosphate protects Abcc6-/- mice against vascular calcification induced by chronic kidney disease
2024ArticleJournal of Molecular Medicine
Hair-straightening cosmetics containing glyoxylic acid induce crystalline nephropathy
2024ArticleKidney International
Source : HAL — archive ouverte CCSD/CNRS (couvre articles, chapitres EMC, communications congrès, thèses).
GHU APHP SUN SITE TENON
4 R DE LA CHINE, 75970 PARIS CEDEX 20
Secteur de conventionnement non disponible (médecin hospitalier ou non présent dans l'Annuaire santé CNAM des libéraux conventionnés).
Lien Doctolib = recherche Google site:doctolib.fr (le 1er résultat est presque toujours le profil correct s'il existe).
Journal of the American Society of Nephrology : JASN · 2023
Significance Statement Autophagy protects podocytes from injury in diabetic kidney disease (DKD). Restoring glomerular autophagy is a promising approach to limit DKD. This study demonstrates a novel regulatory mechanism of autophagy that blocks this critical protection of the glomerular filtration barrier. We demonstrated that TRPC6 induced in podocytes in mouse models of diabetes mediates calpain activation, thereby impairing podocyte autophagy, causing injury and accelerating DKD. Furthermore, this study provides proof of principle for druggable targets for DKD because restoration of podocyte autophagy by calpain inhibitors effectively limits glomerular destruction. Background Diabetic kidney disease is associated with impaired podocyte autophagy and subsequent podocyte injury. The regulation of podocyte autophagy is unique because it minimally uses the mTOR and AMPK pathways. Thus, the molecular mechanisms underlying the impaired autophagy in podocytes in diabetic kidney disease remain largely elusive. Methods This study investigated how the calcium channel TRPC6 and the cysteine protease calpains deleteriously affect podocyte autophagy in diabetic kidney disease in mice. We demonstrated that TRPC6 knockdown in podocytes increased the autophagic flux because of decreased cysteine protease calpain activity. Diabetic kidney disease was induced in vivo using streptozotocin with unilateral nephrectomy and the BTBRob/ob mouse models. Results Diabetes increased TRPC6 expression in podocytes in vivo with decreased podocyte autophagic flux. Transgenic overexpression of the endogenous calpain inhibitor calpastatin, as well as pharmacologic inhibition of calpain activity, normalized podocyte autophagic flux, reduced nephrin loss, and prevented the development of albuminuria in diabetic mice. In kidney biopsies from patients with diabetes, we further confirmed that TRPC6 overexpression in podocytes correlates with decreased calpastatin expression, autophagy blockade, and podocyte injury. Conclusions Overall, we discovered a new mechanism that connects TRPC6 and calpain activity to impaired podocyte autophagy, increased podocyte injury, and development of proteinuria in the context of diabetic kidney disease. Therefore, targeting TRPC6 and/or calpain to restore podocyte autophagy might be a promising therapeutic strategy for diabetic kidney disease.
Journal of the American Society of Nephrology : JASN · 2022
Significance Statement The pathophysiology of AKI during tumor lysis syndrome (TLS) is not fully understood. We aimed to decipher crystal-dependent and crystal-independent mechanisms of TLS-induced AKI. Analyzing urine and blood from patients with TLS provided data on crystal-independent mechanisms of the pathogenesis of AKI during TLS. We also explored mechanisms of TLS-induced AKI in vitro and in vivo in a murine model of TLS (syngeneic mice with acute myeloid leukemia receiving chemotherapy). We found that extracellular histones released in huge amounts during TLS profoundly alter the endothelium. Nonanticoagulant heparin mitigated AKI in this model. Background The pathophysiology of AKI during tumor lysis syndrome (TLS) is not well understood due to the paucity of data. We aimed to decipher crystal-dependent and crystal-independent mechanisms of TLS-induced AKI. Methods Crystalluria, plasma cytokine levels, and extracellular histones levels were measured in two cohorts of patients with TLS. We developed a model of TLS in syngeneic mice with acute myeloid leukemia, and analyzed ultrastructural changes in kidneys and endothelial permeability using intravital confocal microscopy. In parallel, we studied the endothelial toxicity of extracellular histones in vitro. Results The study provides the first evidence that previously described crystal-dependent mechanisms are insufficient to explain TLS-induced AKI. Extracellular histones that are released in huge amounts during TLS caused profound endothelial alterations in the mouse model. The mechanisms of histone-mediated damage implicates endothelial cell activation mediated by Toll-like receptor 4. Heparin inhibits extracellular histones and mitigates endothelial dysfunction during TLS. Conclusion This study sheds new light on the pathophysiology of TLS-induced AKI and suggests that extracellular histones may constitute a novel target for therapeutic intervention in TLS when endothelial dysfunction occurs.
Kidney international reports · 2023
Source PubMed · Recherche par auteur (homonymes possibles, vérifier l'affiliation).
Occupational and environmental medicine · 2026 · Journal Article
Bazin D, Bressot C, Colboc H, Meunier L, et al.
Kidney medicine · 2026 · Journal Article
Rafat C, Tang E, Zavorski J, Rozenblat D, et al.
World journal of urology · 2025 · Published Erratum
Somani B, Emiliani E, Knoll T, Mandrile G, et al.
Journal of clinical medicine · 2025 · Journal Article
Sita LL, Mboliasa PI, Sumaili EK, Frochot V, et al.
Nephrology, dialysis, transplantation : official publication of the European Dialysis and Transplant Association - European Renal Association · 2025 · Journal Article
Pagniez MS, Lombardi Y, Fages V, Larrue R, et al.
World journal of urology · 2025 · Journal Article
Somani B, Emiliani E, Knoll T, Mandrile G, et al.
Journal of molecular medicine (Berlin, Germany) · 2024 · Journal Article
Bouderlique E, Kervadec J, Tang E, Zaworski J, et al.
Kidney international reports · 2024 · Published Erratum
Letavernier E, Schwoehrer M, Livrozet M, Saint-Jacques C, et al.
The New England journal of medicine · 2024 · Letter
Robert T, Tang E, Kervadec J, Zaworski J, et al.
Journal of the American Society of Nephrology : JASN · 2023 · Journal Article
Salemkour Y, Yildiz D, Dionet L, 't Hart DC, et al.
Journal of the American Society of Nephrology : JASN · 2022 · Journal Article
Arnaud M, Loiselle M, Vaganay C, Pons S, et al.
Kidney international reports · 2022 · Case Reports
Letavernier E, Schwoehrer M, Livrozet M, Saint-Jacques C, et al.
Joint bone spine · 2026 · Journal Article
Robert C, Perrot L, Zelus A, Letavernier E, et al.
Scientific reports · 2024 · Journal Article
Azencot R, Saint-Jacques C, Haymann JP, Frochot V, et al.
Arthritis care & research · 2026 · Journal Article
Richette P, Walter-Petrich A, Nguyen QD, Resche-Rigon M, et al.
Rheumatology (Oxford, England) · 2023 · Journal Article
Bardin T, Ducrot YM, Nguyen Q, Letavernier E, et al.
Kidney international · 2025 · Journal Article
Vodovar D, Mousseaux C, Daudon M, Jamme M, et al.
Clinical kidney journal · 2024 · Journal Article
Dang J, Chevalier K, Letavernier E, Tissandier C, et al.
Kidney international reports · 2023 · Journal Article
Doreille A, Lombardi Y, Dancer M, Lamri R, et al.
Clinical kidney journal · 2024 · Journal Article
Pszczolinski R, Acquaviva C, Berrahal I, Biebuyck N, et al.