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The COVID-19 crisis necessitated abrupt transition to remote learning in medical schools. We aimed to assess the impact of COVID-19 on French undergraduate students and teachers, to identify practice changes, and to evaluate successes and areas for improvement of this remote learning experience. Data from 2 online questionnaires were analyzed with 509 participants among students and 189 among teachers from Sorbonne University. Responses to multiple choice, Likert response scale, and open-ended questions were evaluated. COVID-19 had negative impact on teaching continuity. Sixty-seven percent of students were in a dropout situation, and many suffered from psychological stress, leading to set up of a psychological support unit. Although most teachers (81%) and students (72%) had limited knowledge of digital resources, distance learning was quickly implemented, with a predominant use of Zoom. The analysis of several parameters revealed that students were significantly more satisfied than teachers by remote learning. Nevertheless, both students and teachers agreed to replace classical lectures by digital media and to promote in-person teaching in small interactive groups. This paper shares tips for faculty rapidly establishing remote learning. This comparative study of the students’ and teachers’ points of view underlines that new medical curricula should include more digital contents. We make recommendations regarding general university organization, equipment, and curricular development for long-term implementation of digital resources with reinforced relationships between faculty and students.
Camille Vatier; Alain Carrié; Marie-Christine Renaud; Noémie Simon-Tillaux; Alexandre Hertig; Isabelle Jéru. Lessons from the impact of COVID-19 on medical educational continuity and practices. Advances in Physiology Education 2021, 45, 390 -398.
AMA StyleCamille Vatier, Alain Carrié, Marie-Christine Renaud, Noémie Simon-Tillaux, Alexandre Hertig, Isabelle Jéru. Lessons from the impact of COVID-19 on medical educational continuity and practices. Advances in Physiology Education. 2021; 45 (2):390-398.
Chicago/Turabian StyleCamille Vatier; Alain Carrié; Marie-Christine Renaud; Noémie Simon-Tillaux; Alexandre Hertig; Isabelle Jéru. 2021. "Lessons from the impact of COVID-19 on medical educational continuity and practices." Advances in Physiology Education 45, no. 2: 390-398.
Eight years after the Kidney Disease: Improving Global Outcomes (KDIGO) universal staging of acute kidney injury (AKI) [1], <3% of the 213 new articles indexed in PubMed have alluded to it in the setting of pregnancy-related AKI (P-AKI), and of these, none has specifically studied its value. Furthermore, recent papers have continued to use obsolete definitions. Why is this?
Hadrien de Buhren; Alexandre Hertig. Staging pregnancy-related acute kidney injury according to Kidney Disease: Improving Global Outcomes guidelines: what are the barriers? Nephrology Dialysis Transplantation 2020, 1 .
AMA StyleHadrien de Buhren, Alexandre Hertig. Staging pregnancy-related acute kidney injury according to Kidney Disease: Improving Global Outcomes guidelines: what are the barriers? Nephrology Dialysis Transplantation. 2020; ():1.
Chicago/Turabian StyleHadrien de Buhren; Alexandre Hertig. 2020. "Staging pregnancy-related acute kidney injury according to Kidney Disease: Improving Global Outcomes guidelines: what are the barriers?" Nephrology Dialysis Transplantation , no. : 1.
An amendment to this paper has been published and can be accessed via a link at the top of the paper.
David Legouis; Sven-Erick Ricksten; Anna Faivre; Thomas Verissimo; Karim Gariani; Charles Verney; Pierre Galichon; Lena Berchtold; Eric Feraille; Marylise Fernandez; Sandrine Placier; Kari Koppitch; Alexandre Hertig; Pierre-Yves Martin; Maarten Naesens; Jérôme Pugin; Andrew P. McMahon; Pietro E. Cippà; Sophie De Seigneux. Author Correction: Altered proximal tubular cell glucose metabolism during acute kidney injury is associated with mortality. Nature Metabolism 2020, 1 -1.
AMA StyleDavid Legouis, Sven-Erick Ricksten, Anna Faivre, Thomas Verissimo, Karim Gariani, Charles Verney, Pierre Galichon, Lena Berchtold, Eric Feraille, Marylise Fernandez, Sandrine Placier, Kari Koppitch, Alexandre Hertig, Pierre-Yves Martin, Maarten Naesens, Jérôme Pugin, Andrew P. McMahon, Pietro E. Cippà, Sophie De Seigneux. Author Correction: Altered proximal tubular cell glucose metabolism during acute kidney injury is associated with mortality. Nature Metabolism. 2020; ():1-1.
Chicago/Turabian StyleDavid Legouis; Sven-Erick Ricksten; Anna Faivre; Thomas Verissimo; Karim Gariani; Charles Verney; Pierre Galichon; Lena Berchtold; Eric Feraille; Marylise Fernandez; Sandrine Placier; Kari Koppitch; Alexandre Hertig; Pierre-Yves Martin; Maarten Naesens; Jérôme Pugin; Andrew P. McMahon; Pietro E. Cippà; Sophie De Seigneux. 2020. "Author Correction: Altered proximal tubular cell glucose metabolism during acute kidney injury is associated with mortality." Nature Metabolism , no. : 1-1.
Acute kidney injury (AKI) is strongly associated with mortality, independently of its cause. The kidney contributes to up to 40% of systemic glucose production by gluconeogenesis during fasting and under stress conditions. Whether kidney gluconeogenesis is impaired during AKI and how this might influence systemic metabolism remain unknown. Here we show that glucose production and lactate clearance are impaired during human and experimental AKI by using renal arteriovenous catheterization in patients, lactate tolerance testing in mice and glucose isotope labelling in rats. Single-cell transcriptomics reveal that gluconeogenesis is impaired in proximal tubule cells during AKI. In a retrospective cohort of critically ill patients, we demonstrate that altered glucose metabolism during AKI is a major determinant of systemic glucose and lactate levels and is strongly associated with mortality. Thiamine supplementation increases lactate clearance without modifying renal function in mice with AKI, enhances glucose production by renal tubular cells ex vivo and is associated with reduced mortality and improvement of the metabolic pattern in a retrospective cohort of critically ill patients with AKI. This study highlights an unappreciated systemic role of renal glucose and lactate metabolism under stress conditions, delineates general mechanisms of AKI-associated mortality and introduces a potential intervention targeting metabolism for a highly prevalent clinical condition with limited therapeutic options.
David Legouis; Sven-Erick Ricksten; Anna Faivre; Thomas Verissimo; Karim Gariani; Charles Verney; Pierre Galichon; Lena Berchtold; Eric Feraille; Marylise Fernandez; Sandrine Placier; Kari Koppitch; Alexandre Hertig; Pierre-Yves Martin; Maarten Naesens; Jérôme Pugin; Andrew P. McMahon; Pietro E. Cippà; Sophie De Seigneux. Altered proximal tubular cell glucose metabolism during acute kidney injury is associated with mortality. Nature Metabolism 2020, 2, 732 -743.
AMA StyleDavid Legouis, Sven-Erick Ricksten, Anna Faivre, Thomas Verissimo, Karim Gariani, Charles Verney, Pierre Galichon, Lena Berchtold, Eric Feraille, Marylise Fernandez, Sandrine Placier, Kari Koppitch, Alexandre Hertig, Pierre-Yves Martin, Maarten Naesens, Jérôme Pugin, Andrew P. McMahon, Pietro E. Cippà, Sophie De Seigneux. Altered proximal tubular cell glucose metabolism during acute kidney injury is associated with mortality. Nature Metabolism. 2020; 2 (8):732-743.
Chicago/Turabian StyleDavid Legouis; Sven-Erick Ricksten; Anna Faivre; Thomas Verissimo; Karim Gariani; Charles Verney; Pierre Galichon; Lena Berchtold; Eric Feraille; Marylise Fernandez; Sandrine Placier; Kari Koppitch; Alexandre Hertig; Pierre-Yves Martin; Maarten Naesens; Jérôme Pugin; Andrew P. McMahon; Pietro E. Cippà; Sophie De Seigneux. 2020. "Altered proximal tubular cell glucose metabolism during acute kidney injury is associated with mortality." Nature Metabolism 2, no. 8: 732-743.
In patients presenting with anti-glomerular basement membrane (GBM) disease with advanced isolated kidney involvement, the benefit of intensive therapy remains controversial due to adverse events, particularly infection. We aim to describe the burden of severe infections (SI) (requiring hospitalization or intravenous antibiotics) and identify predictive factors of SI in a large cohort of patients with anti-GBM disease. Among the 201 patients (median [IQR] age, 53 [30–71] years) included, 74 had pulmonary involvement and 127 isolated glomerulonephritis. A total of 161 SI occurred in 116 patients during the first year after diagnosis. These infections occurred during the early stage of care (median [IQR] time, 13 [8–19] days after diagnosis) with mainly pulmonary (45%), catheter-associated bacteremia (22%) and urinary tract (21%) infections. In multivariable analysis, positive ANCA (HR [95% CI] 1.62 [1.07−2.44]; p = 0.02) and age at diagnosis (HR [95% CI] 1.10 [1.00–1.21]; p = 0.047) remained independently associated with SI. Age-adjusted severe infection during the first three months was associated with an increased three-year mortality rate (HR [95% CI] 3.13 [1.24–7.88]; p = 0.01). Thus, SI is a common early complication in anti-GBM disease, particularly in the elderly and those with positive anti-neutrophil cytoplasmic antibodies (ANCA). No significant association was observed between immunosuppressive strategy and occurrence of SI.
Pauline Caillard; Cécile Vigneau; Jean-Michel Halimi; Marc Hazzan; Eric Thervet; Morgane Heitz; Laurent Juillard; Vincent Audard; Marion Rabant; Alexandre Hertig; Jean-François Subra; Vincent Vuiblet; Dominique Guerrot; Mathilde Tamain; Marie Essig; Thierry Lobbedez; Thomas Quemeneur; Jean-Michel Rebibou; Alexandre Ganea; Marie-Noëlle Peraldi; François Vrtovsnik; Maïté Daroux; Adnane Lamrani; Raïfah Makdassi; Gabriel Choukroun; Dimitri Titeca-Beauport. Severe Infection in Anti-Glomerular Basement Membrane Disease: A Retrospective Multicenter French Study. Journal of Clinical Medicine 2020, 9, 698 .
AMA StylePauline Caillard, Cécile Vigneau, Jean-Michel Halimi, Marc Hazzan, Eric Thervet, Morgane Heitz, Laurent Juillard, Vincent Audard, Marion Rabant, Alexandre Hertig, Jean-François Subra, Vincent Vuiblet, Dominique Guerrot, Mathilde Tamain, Marie Essig, Thierry Lobbedez, Thomas Quemeneur, Jean-Michel Rebibou, Alexandre Ganea, Marie-Noëlle Peraldi, François Vrtovsnik, Maïté Daroux, Adnane Lamrani, Raïfah Makdassi, Gabriel Choukroun, Dimitri Titeca-Beauport. Severe Infection in Anti-Glomerular Basement Membrane Disease: A Retrospective Multicenter French Study. Journal of Clinical Medicine. 2020; 9 (3):698.
Chicago/Turabian StylePauline Caillard; Cécile Vigneau; Jean-Michel Halimi; Marc Hazzan; Eric Thervet; Morgane Heitz; Laurent Juillard; Vincent Audard; Marion Rabant; Alexandre Hertig; Jean-François Subra; Vincent Vuiblet; Dominique Guerrot; Mathilde Tamain; Marie Essig; Thierry Lobbedez; Thomas Quemeneur; Jean-Michel Rebibou; Alexandre Ganea; Marie-Noëlle Peraldi; François Vrtovsnik; Maïté Daroux; Adnane Lamrani; Raïfah Makdassi; Gabriel Choukroun; Dimitri Titeca-Beauport. 2020. "Severe Infection in Anti-Glomerular Basement Membrane Disease: A Retrospective Multicenter French Study." Journal of Clinical Medicine 9, no. 3: 698.
The severity of human infection by one of the many Shiga toxin-producing Escherichia coli (STEC) is determined by a number of factors: the bacterial genome, the capacity of human societies to prevent foodborne epidemics, the medical condition of infected patients (in particular their hydration status, often compromised by severe diarrhea), and by our capacity to devise new therapeutic approaches, most specifically to combat the bacterial virulence factors, as opposed to our current strategies that essentially aim to palliate organ deficiencies. The last major outbreak in 2011 in Germany, which killed more than 50 people in Europe, was evidence that an effective treatment was still lacking. Herein, we review the current knowledge of STEC virulence, how societies organize the prevention of human disease, and how physicians treat (and, hopefully, will treat) its potentially fatal complications. In particular, we focus on STEC-induced hemolytic and uremic syndrome (HUS), where the intrusion of toxins inside endothelial cells results in massive cell death, activation of the coagulation within capillaries, and eventually organ failure.
Adrien Joseph; Aurélie Cointe; Patricia Mariani Kurkdjian; Cédric Rafat; Alexandre Hertig. Shiga Toxin-Associated Hemolytic Uremic Syndrome: A Narrative Review. Toxins 2020, 12, 67 .
AMA StyleAdrien Joseph, Aurélie Cointe, Patricia Mariani Kurkdjian, Cédric Rafat, Alexandre Hertig. Shiga Toxin-Associated Hemolytic Uremic Syndrome: A Narrative Review. Toxins. 2020; 12 (2):67.
Chicago/Turabian StyleAdrien Joseph; Aurélie Cointe; Patricia Mariani Kurkdjian; Cédric Rafat; Alexandre Hertig. 2020. "Shiga Toxin-Associated Hemolytic Uremic Syndrome: A Narrative Review." Toxins 12, no. 2: 67.
Stéphane Mitrovic; Alexandre Hertig; Bruno Fautrel. Reply to the Letter: ‘Thrombotic microangiopathy in adult-onset Still’s disease: the story is just beginning’. Expert Review of Clinical Immunology 2019, 15, 1125 -1126.
AMA StyleStéphane Mitrovic, Alexandre Hertig, Bruno Fautrel. Reply to the Letter: ‘Thrombotic microangiopathy in adult-onset Still’s disease: the story is just beginning’. Expert Review of Clinical Immunology. 2019; 15 (11):1125-1126.
Chicago/Turabian StyleStéphane Mitrovic; Alexandre Hertig; Bruno Fautrel. 2019. "Reply to the Letter: ‘Thrombotic microangiopathy in adult-onset Still’s disease: the story is just beginning’." Expert Review of Clinical Immunology 15, no. 11: 1125-1126.
Patricia Villie; Guillaume Lefevre; Romain Arrestier; Alexandra Rousseau; Nadia Berkane; Alexandre Hertig. ELABELA concentration is not decreased in maternal plasma before the onset of preeclampsia. American Journal of Obstetrics and Gynecology 2019, 220, 284 -285.
AMA StylePatricia Villie, Guillaume Lefevre, Romain Arrestier, Alexandra Rousseau, Nadia Berkane, Alexandre Hertig. ELABELA concentration is not decreased in maternal plasma before the onset of preeclampsia. American Journal of Obstetrics and Gynecology. 2019; 220 (3):284-285.
Chicago/Turabian StylePatricia Villie; Guillaume Lefevre; Romain Arrestier; Alexandra Rousseau; Nadia Berkane; Alexandre Hertig. 2019. "ELABELA concentration is not decreased in maternal plasma before the onset of preeclampsia." American Journal of Obstetrics and Gynecology 220, no. 3: 284-285.
Severe preeclampsia may require the delivery of the placenta to avoid life-threatening complications for the mother. Before 26 weeks of gestation, this often results in perinatal death. A decrease in soluble fms-like tyrosine kinase 1 (sFlt1), an anti-angiogenic factor central to the pathophysiology of the maternal syndrome, has been reported after LDL- apheresis. The present study tested whether LDL-apheresis could be used to allow women with early and severe preeclampsia to reach a gestational age where the baby had a viable chance of survival. A phase II prospective study. Adult women were included if they had very early (< 26 weeks of gestation) preeclampsia without severe (<5th percentile) intra-uterine growth retardation. Treatment consisted of two weekly sessions (90 minutes each) of LDL-apheresis of whole blood. The primary endpoint was the status of the baby (dead or living) at 6 months post-delivery. Sample size and stopping rules were calculated assuming a desired success rate of at least 90%. The study was interrupted for safety reasons after the inclusion of two patients: both developed secondary uncontrolled hypertension and blurred vision during the first week of treatment. The first neonate, born at 25 + 3 weeks of gestation, died of sepsis at day 5; the second, born at 26 + 2 weeks of gestation, is still alive and well. In these two patients, the impact of apheresis sessions on sFlt1 concentrations was inconsistent. LDL-apheresis did not result in the prolongation of pregnancy in this phase II trial. Further studies will be needed to delineate the appropriate contours of this therapeutic strategy.
Bassam Haddad; Guillaume Lefèvre; Alexandra Rousseau; Thomas Robert; Samir Saheb; Cedric Rafat; Marie Bornes; Camille Petit-Hoang; Frédéric Richard; Edouard Lecarpentier; Vassilis Tsatsaris; Jean Guibourdenche; Anthony Corchia; Eric Rondeau; Tabassome Simon; Alexandre Hertig. LDL-apheresis to decrease sFlt-1 during early severe preeclampsia: Report of two cases from a discontinued phase II trial. European Journal of Obstetrics & Gynecology and Reproductive Biology 2018, 231, 70 -74.
AMA StyleBassam Haddad, Guillaume Lefèvre, Alexandra Rousseau, Thomas Robert, Samir Saheb, Cedric Rafat, Marie Bornes, Camille Petit-Hoang, Frédéric Richard, Edouard Lecarpentier, Vassilis Tsatsaris, Jean Guibourdenche, Anthony Corchia, Eric Rondeau, Tabassome Simon, Alexandre Hertig. LDL-apheresis to decrease sFlt-1 during early severe preeclampsia: Report of two cases from a discontinued phase II trial. European Journal of Obstetrics & Gynecology and Reproductive Biology. 2018; 231 ():70-74.
Chicago/Turabian StyleBassam Haddad; Guillaume Lefèvre; Alexandra Rousseau; Thomas Robert; Samir Saheb; Cedric Rafat; Marie Bornes; Camille Petit-Hoang; Frédéric Richard; Edouard Lecarpentier; Vassilis Tsatsaris; Jean Guibourdenche; Anthony Corchia; Eric Rondeau; Tabassome Simon; Alexandre Hertig. 2018. "LDL-apheresis to decrease sFlt-1 during early severe preeclampsia: Report of two cases from a discontinued phase II trial." European Journal of Obstetrics & Gynecology and Reproductive Biology 231, no. : 70-74.
Preeclampsia appears to be characterized by specific steroidogenesis dysregulation long before PE diagnosis, highlighting potential new biomarkers of PE.
Nadia Berkane; Philippe Liere; Guillaume Lefevre; Nadia Alfaidy; Roland Abi Nahed; Jessica Vincent; Jean-Paul Oudinet; Antoine Pianos; Annie Cambourg; Patrick Rozenberg; Pierre Galichon; Alexandra Rousseau; Tabassome Simon; Michael Schumacher; Nathalie Chabbert-Buffet; Alexandre Hertig. Abnormal steroidogenesis and aromatase activity in preeclampsia. Placenta 2018, 69, 40 -49.
AMA StyleNadia Berkane, Philippe Liere, Guillaume Lefevre, Nadia Alfaidy, Roland Abi Nahed, Jessica Vincent, Jean-Paul Oudinet, Antoine Pianos, Annie Cambourg, Patrick Rozenberg, Pierre Galichon, Alexandra Rousseau, Tabassome Simon, Michael Schumacher, Nathalie Chabbert-Buffet, Alexandre Hertig. Abnormal steroidogenesis and aromatase activity in preeclampsia. Placenta. 2018; 69 ():40-49.
Chicago/Turabian StyleNadia Berkane; Philippe Liere; Guillaume Lefevre; Nadia Alfaidy; Roland Abi Nahed; Jessica Vincent; Jean-Paul Oudinet; Antoine Pianos; Annie Cambourg; Patrick Rozenberg; Pierre Galichon; Alexandra Rousseau; Tabassome Simon; Michael Schumacher; Nathalie Chabbert-Buffet; Alexandre Hertig. 2018. "Abnormal steroidogenesis and aromatase activity in preeclampsia." Placenta 69, no. : 40-49.
Atypical haemolytic and uraemic syndrome (aHUS) is a rare condition that rapidly compromises renal function, often in a matter of days. Although the majority of patients affected by aHUS have a genetic mutation in the alternate complement pathway [1, 2], most cases are sporadic (mutation unknown at the first flare), thus important decisions must be made in the absence of information regarding exact mechanisms of endothelial injury. In order to take appropriate action, four issues should be considered immediately (see Figure 1): (i) the patient’s background; (ii) the cause of the flare; (iii) the symptoms, particularly hypertension and (iv) whether and how the complement cascade should be stopped, and...
Alexandre Hertig. Atypical haemolytic and uraemic syndrome: how can we protect the kidneys? Nephrology Dialysis Transplantation 2018, 33, 1708 -1711.
AMA StyleAlexandre Hertig. Atypical haemolytic and uraemic syndrome: how can we protect the kidneys? Nephrology Dialysis Transplantation. 2018; 33 (10):1708-1711.
Chicago/Turabian StyleAlexandre Hertig. 2018. "Atypical haemolytic and uraemic syndrome: how can we protect the kidneys?" Nephrology Dialysis Transplantation 33, no. 10: 1708-1711.
Background/Aims: Fatty acid oxidation (FAO), the main source of energy produced by tubular epithelial cells in the kidney, was found to be defective in tubulo-interstitial samples dissected out in kidney biopsies from patients with chronic kidney disease (CKD). Experimental data indicated that this decrease was a strong determinant of renal fibrogenesis, hence a focus for therapeutic interventions. Nevertheless, whether persistently differentiated renal tubules, surviving in a pro-fibrotic environment, also suffer from a decrease in FAO, is currently unknown. Methods: To address this question, we isolated proximal tubules captured ex vivo on the basis of the expression of an intact brush border antigen (Prominin-1) in C57BL6/J mice subjected to a controlled, two-hit model of renal fibrosis (reversible ischemic acute kidney injury (AKI) or sham surgery, followed by angiotensin 2 administration). A transcriptomic high throughput sequencing was performed on total mRNA from these cells, and on whole kidneys. Results: In contrast to mice subjected to sham surgery, mice with a history of AKI displayed histologically more renal fibrosis when exposed to angiotensin 2. High throughput RNA sequencing, principal component analysis and clustering showed marked consistency within experimental groups. As expected, FAO transcripts were decreased in whole fibrotic kidneys. Surprisingly, however, up- rather than down-regulation of metabolic pathways (oxidative phosphorylation, fatty acid metabolism, glycolysis, and PPAR signalling pathway) was a hallmark of the differentiated tubules captured from fibrotic kidneys. Immunofluorescence co-staining analysis confirmed that the expression of FAO enzymes was dependent of tubular trophicity. Conclusions: These data suggest that in differentiated proximal tubules energetic hyperactivity is promoted concurrently with organ fibrogenesis.
Aurélien Bataille; Pierre Galichon; Nadjim Chelghoum; Badreddine Mohand Oumoussa; Marie-Julia Ziliotis; Iman Sadia; Sophie Vandermeersch; Noémie Simon-Tillaux; David Legouis; Raphael Cohen; Yi-Chun Xu-Dubois; Morgane Commereuc; Éric Rondeau; Stéphane Le Crom; Alexandre Hertig. Increased Fatty Acid Oxidation in Differentiated Proximal Tubular Cells Surviving a Reversible Episode of Acute Kidney Injury. Cellular Physiology and Biochemistry 2018, 47, 1338 -1351.
AMA StyleAurélien Bataille, Pierre Galichon, Nadjim Chelghoum, Badreddine Mohand Oumoussa, Marie-Julia Ziliotis, Iman Sadia, Sophie Vandermeersch, Noémie Simon-Tillaux, David Legouis, Raphael Cohen, Yi-Chun Xu-Dubois, Morgane Commereuc, Éric Rondeau, Stéphane Le Crom, Alexandre Hertig. Increased Fatty Acid Oxidation in Differentiated Proximal Tubular Cells Surviving a Reversible Episode of Acute Kidney Injury. Cellular Physiology and Biochemistry. 2018; 47 (4):1338-1351.
Chicago/Turabian StyleAurélien Bataille; Pierre Galichon; Nadjim Chelghoum; Badreddine Mohand Oumoussa; Marie-Julia Ziliotis; Iman Sadia; Sophie Vandermeersch; Noémie Simon-Tillaux; David Legouis; Raphael Cohen; Yi-Chun Xu-Dubois; Morgane Commereuc; Éric Rondeau; Stéphane Le Crom; Alexandre Hertig. 2018. "Increased Fatty Acid Oxidation in Differentiated Proximal Tubular Cells Surviving a Reversible Episode of Acute Kidney Injury." Cellular Physiology and Biochemistry 47, no. 4: 1338-1351.
Sickle cell trait is not completely benign, and some renal complications can occur. The baseline rate of admission for gross hematuria in normal males carrying the sickle cell trait is 2%. A 35-year-old non-smoking African man experienced a 2-week history of painless, profuse and persistent gross hematuria. Laboratory tests showed normal renal function, hematuria and mild proteinuria. Abdominal ultrasonography and computed tomography angiography revealed no renal abnormalities; the bladder appeared pristine under cystoscopy. The diagnosis of sickle cell trait associated with gross hematuria was made using hemoglobin electrophoresis; renal biopsy and its complications were avoided. Urine was clear after 2 weeks of oral hydration and gamma epsilon-aminocaproic acid. Hemoglobin electrophoresis should be performed in cases of gross hematuria. Coupled with other non-invasive evaluation, this could avoid renal biopsy and its associated complications.
Alexandre Le Joncour; Laurent Mesnard; Alexandre Hertig; Thomas Robert. Red urine, updated for the nephrologist: a case report. BMC Nephrology 2018, 19, 133 .
AMA StyleAlexandre Le Joncour, Laurent Mesnard, Alexandre Hertig, Thomas Robert. Red urine, updated for the nephrologist: a case report. BMC Nephrology. 2018; 19 (1):133.
Chicago/Turabian StyleAlexandre Le Joncour; Laurent Mesnard; Alexandre Hertig; Thomas Robert. 2018. "Red urine, updated for the nephrologist: a case report." BMC Nephrology 19, no. 1: 133.
INTRODUCTION AND AIMS: Among the severe complications of preeclampsia (PE), acute kidney injury (AKI) poses a dilemma if features of thrombotic microangiopathy (TMA) are present. Although a HELLP syndrome is considerably more frequent, ruling out a flare of atypical haemolytic and uremic syndrome (HUS) is then of utmost importance.We aim to improve the differential diagnosis procedure in cases of post-partum AKI.
Matthieu Jamme; Fleuria Meybodi; Vassilis Tsataris; François Provôt; Mercédès Jourdain; Anne Sophie Ducloy Bouthors; Yahsou Delmas; Pierre Perez; Julian Darmian; Alain Wynckel; Jean Michel Rebibou; Jerome Lambert; Véronique Frémeaux Bacchi; Paul Coppo; Cedric Rafat; Luc Frimat; Alexandre Hertig. FP268POST PARTUM ACUTE KIDNEY INJURY: SORTING PLACENTAL AND NON-PLACENTAL THROMBOTIC MICROANGIOPATHIES USING THE TRAJECTORY OF BIOMARKERS. Nephrology Dialysis Transplantation 2018, 33, i120 -i121.
AMA StyleMatthieu Jamme, Fleuria Meybodi, Vassilis Tsataris, François Provôt, Mercédès Jourdain, Anne Sophie Ducloy Bouthors, Yahsou Delmas, Pierre Perez, Julian Darmian, Alain Wynckel, Jean Michel Rebibou, Jerome Lambert, Véronique Frémeaux Bacchi, Paul Coppo, Cedric Rafat, Luc Frimat, Alexandre Hertig. FP268POST PARTUM ACUTE KIDNEY INJURY: SORTING PLACENTAL AND NON-PLACENTAL THROMBOTIC MICROANGIOPATHIES USING THE TRAJECTORY OF BIOMARKERS. Nephrology Dialysis Transplantation. 2018; 33 (suppl_1):i120-i121.
Chicago/Turabian StyleMatthieu Jamme; Fleuria Meybodi; Vassilis Tsataris; François Provôt; Mercédès Jourdain; Anne Sophie Ducloy Bouthors; Yahsou Delmas; Pierre Perez; Julian Darmian; Alain Wynckel; Jean Michel Rebibou; Jerome Lambert; Véronique Frémeaux Bacchi; Paul Coppo; Cedric Rafat; Luc Frimat; Alexandre Hertig. 2018. "FP268POST PARTUM ACUTE KIDNEY INJURY: SORTING PLACENTAL AND NON-PLACENTAL THROMBOTIC MICROANGIOPATHIES USING THE TRAJECTORY OF BIOMARKERS." Nephrology Dialysis Transplantation 33, no. suppl_1: i120-i121.
Kidneys may fail post-partum in a number of circumstances due, for example, to post-partum haemorrhage, preeclampsia, amniotic fluid embolism or septic abortion. All these conditions in pregnancy and post partum represent a threat not only to the endothelium but also to the renal tubular epithelium, and as such may lead to rapid and also irreversible impairment of the renal function. This paper is a non-systematic review of the literature and of our experience, in which we discuss the main open issues on kidney disease in pregnancy and following delivery, in particular as regards tubular damage, with the aim to help reasoning on acute kidney injury (AKI) following delivery. The review will emphasize the often under-estimated importance of the tubular epithelium in the peri-partum period and will: (1) describe the main characteristics of the renal tissues around delivery; (2) define pregnancy-related AKI according to recent Kidney Disease/Improving Global Outcome (KDIGO) guidelines; (3) discuss the most common circumstances of post-partum AKI; and (4) describe the input expected from urinalysis, renal imaging and kidney biopsy.
Patricia Villie; Marc Dommergues; Isabelle Brocheriou; Giorgina Barbara Piccoli; Jérôme Tourret; Alexandre Hertig. Why kidneys fail post-partum: a tubulocentric viewpoint. Journal of Nephrology 2018, 31, 645 -651.
AMA StylePatricia Villie, Marc Dommergues, Isabelle Brocheriou, Giorgina Barbara Piccoli, Jérôme Tourret, Alexandre Hertig. Why kidneys fail post-partum: a tubulocentric viewpoint. Journal of Nephrology. 2018; 31 (5):645-651.
Chicago/Turabian StylePatricia Villie; Marc Dommergues; Isabelle Brocheriou; Giorgina Barbara Piccoli; Jérôme Tourret; Alexandre Hertig. 2018. "Why kidneys fail post-partum: a tubulocentric viewpoint." Journal of Nephrology 31, no. 5: 645-651.
Matthieu Jamme; Alexandre Hertig; Cédric Rafat. Angiotensin II for the Treatment of Vasodilatory Shock. 2017, 377, 2603 .
AMA StyleMatthieu Jamme, Alexandre Hertig, Cédric Rafat. Angiotensin II for the Treatment of Vasodilatory Shock. . 2017; 377 (26):2603.
Chicago/Turabian StyleMatthieu Jamme; Alexandre Hertig; Cédric Rafat. 2017. "Angiotensin II for the Treatment of Vasodilatory Shock." 377, no. 26: 2603.
Even in the context of physiological pregnancy, a placenta produces large amounts of anti-angiogenic proteins and steroid hormones, which circulate in the mother’s blood and greatly alters the “environment” to which its endothelium is exposed. If the placentation is defective, preeclampsia can induce up to thrombotic micro-angiopathy, localized in the maternal liver: this is the HELLP syndrome. In cases where renal or neurological failure is associated, or if hepatic cytolysis is missing in the table, then a differential diagnosis procedure is initiated in order not to ignore two pathologies that are rarer, but which will not cure spontaneously after delivery, and which are not, in themselves, indications for delivery: hemolytic and uremic syndrome and thrombotic thrombocytopenic purpura. Pregnancy is indeed a circumstance of revelation. The objective of this review is to discuss the mechanisms of these different forms of thrombotic micro-angiopathy in the context of pregnancy and to propose to the intensivist a diagnostic and therapeutic approach. Même en contexte de grossesse physiologique, un placenta produit en grande quantité des protéines antiangiogéniques et des hormones stéroïdes, qui circulent dans le sang de la mère, et modifient considérablement le « milieu » auquel son endothélium est exposé. Si la placentation est défectueuse, la pré-éclampsie peut induire jusqu’à une micro-angiopathie thrombotique, localisée dans le foie maternel: c’est le HELLP syndrome. Dans les cas où une défaillance rénale ou neurologique est associée, ou encore si la cytolyse hépatique manque au tableau, débute alors une procédure de diagnostic différentiel pour ne pas méconnaître deux pathologies plus rares, mais qui ne guériront pas spontanément après la délivrance, et qui ne sont même pas, en soi, des indications à la délivrance: le syndrome hémolytique et urémique, et le purpura thrombotique thrombocytopénique. La grossesse en est en effet une circonstance de révélation. L’objectif de cette revue est de discuter, dans ce contexte, les mécanismes de ces différentes formes de microangiopathies thrombotiques, et de proposer au réanimateur une démarche à la fois diagnostique et thérapeutique.
C. Vigneron; A. Hertig. Micro-angiopathies thrombotiques du péripartum : physiopathologie, diagnostic et traitement. Médecine Intensive Réanimation 2017, 26, 296 -310.
AMA StyleC. Vigneron, A. Hertig. Micro-angiopathies thrombotiques du péripartum : physiopathologie, diagnostic et traitement. Médecine Intensive Réanimation. 2017; 26 (4):296-310.
Chicago/Turabian StyleC. Vigneron; A. Hertig. 2017. "Micro-angiopathies thrombotiques du péripartum : physiopathologie, diagnostic et traitement." Médecine Intensive Réanimation 26, no. 4: 296-310.
Our work shows the diversity of host-microbial interactions which precede extra-intestinal virulence.
Parvine Tashk; Marie Lecronier; Olivier Clermont; Aurélie Renvoisé; Alexandra Aubry; Benoît Barrou; Alexandre Hertig; Mathilde Lescat; Olivier Tenaillon; Erick Denamur; Jérôme Tourret. Épidémiologie moléculaire et cinétique des infections urinaires précoces à Escherichia coli chez les sujets transplantés d’un rein. Néphrologie & Thérapeutique 2017, 13, 236 -244.
AMA StyleParvine Tashk, Marie Lecronier, Olivier Clermont, Aurélie Renvoisé, Alexandra Aubry, Benoît Barrou, Alexandre Hertig, Mathilde Lescat, Olivier Tenaillon, Erick Denamur, Jérôme Tourret. Épidémiologie moléculaire et cinétique des infections urinaires précoces à Escherichia coli chez les sujets transplantés d’un rein. Néphrologie & Thérapeutique. 2017; 13 (4):236-244.
Chicago/Turabian StyleParvine Tashk; Marie Lecronier; Olivier Clermont; Aurélie Renvoisé; Alexandra Aubry; Benoît Barrou; Alexandre Hertig; Mathilde Lescat; Olivier Tenaillon; Erick Denamur; Jérôme Tourret. 2017. "Épidémiologie moléculaire et cinétique des infections urinaires précoces à Escherichia coli chez les sujets transplantés d’un rein." Néphrologie & Thérapeutique 13, no. 4: 236-244.
Preeclampsia (PE) results in placental dysfunction and is one of the primary causes of maternal and fetal mortality and morbidity. During pregnancy, estrogen is produced primarily in the placenta by conversion of androgen precursors originating from maternal and fetal adrenal glands. These processes lead to increased plasma estrogen concentrations compared with levels in nonpregnant women. Aberrant production of estrogens could play a key role in PE symptoms because they are exclusively produced by the placenta and they promote angiogenesis and vasodilation. Previous assessments of estrogen synthesis during PE yielded conflicting results, possibly because of the lack of specificity of the assays. However, with the introduction of reliable analytical protocols using liquid chromatography/mass spectrometry or gas chromatography/mass spectrometry, more recent studies suggest a marked decrease in estradiol levels in PE. The aim of this review is to summarize current knowledge of estrogen synthesis, regulation in the placenta, and biological effects during pregnancy and PE. Moreover, this review highlights the links among the occurrence of PE, estrogen biosynthesis, angiogenic factors, and cardiovascular risk factors. A close link between estrogen dysregulation and PE occurrence might validate estrogen levels as a biomarker but could also reveal a potential approach for prevention or cure of PE.
Nadia Berkane; Philippe Liere; Jean-Paul Oudinet; Alexandre Hertig; Guillaume Lefèvre; Nicola Pluchino; Michael Schumacher; Nathalie Chabbert-Buffet. From Pregnancy to Preeclampsia: A Key Role for Estrogens. Endocrine Reviews 2017, 38, 123 -144.
AMA StyleNadia Berkane, Philippe Liere, Jean-Paul Oudinet, Alexandre Hertig, Guillaume Lefèvre, Nicola Pluchino, Michael Schumacher, Nathalie Chabbert-Buffet. From Pregnancy to Preeclampsia: A Key Role for Estrogens. Endocrine Reviews. 2017; 38 (2):123-144.
Chicago/Turabian StyleNadia Berkane; Philippe Liere; Jean-Paul Oudinet; Alexandre Hertig; Guillaume Lefèvre; Nicola Pluchino; Michael Schumacher; Nathalie Chabbert-Buffet. 2017. "From Pregnancy to Preeclampsia: A Key Role for Estrogens." Endocrine Reviews 38, no. 2: 123-144.
Parmi les facteurs anti-angiogéniques produits par le placenta, sFlt-1 joue un rôle majeur dans la physiopathologie du syndrome maternel de pré-éclampsie. Son élévation est détectable dans le sang maternel plusieurs semaines avant les signes cliniques. L’étude MOMA (MOrbiMortality Amelioration in preeclamptic primiparas) a été conçue pour déterminer si la prédiction de la pré-éclampsie grâce au dosage de sFlt1 au sixième mois de grossesse permettrait de diminuer la morbi-mortalité maternelle et fœtale. MOMA est une étude interventionnelle prospective et randomisée ayant inclus dans le Centre d’obstétrique de Tenon des patientes adultes primipares, ayant accepté le dosage de sFlt-1 entre 24 et 29 semaines d’aménorrhée (SA), et un Doppler aux artères utérines à 22 SA ± 10 jours. Le risque de pré-éclampsie était d’abord stratifié sur la base du Doppler, puis calculé sur la base de la concentration de sFlt-1 (> 957 ng/mL), et communiqué à l’obstétricien dans un cas sur 2. En cas de risque jugé élevé de pré-éclampsie (sFlt-1 élevé), les patientes étaient soumises à une surveillance accrue. Dans le groupe témoin, le risque était mesuré mais non communiqué. Le critère de jugement principal était composite, associant différents facteurs de morbidité maternelle et fœtale. Au total, 939 femmes ont été incluses, parmi lesquelles 466 ont constitué le groupe « sFlt-1 connu », et 473 le groupe « sFlt-1 masqué ». L’incidence de la pré-éclampsie a été de 7,3 % dans le groupe connu, 4,9 % dans le groupe masqué. Le score de morbidité a été identique dans les deux groupes, suggérant que le suivi rapproché des patientes à risque ne change pas le pronostic du syndrome. Le seuil choisi de la concentration de sFlt-1 a été, a posteriori, bas. Mais sFlt-1 a une valeur pronostique : le score était le plus élevé dans le quartile le plus élevé des concentrations. Si la concentration de sFlt-1 dans le sang maternel, entre 24 et 29 SA, est associée à la morbidité du syndrome de pré-éclampsie, le suivi rapproché des patientes à risque (même si le risque a ici été surestimé) ne semble pas diminuer la morbidité, ce qui est logique en l’absence de traitement spécifique disponible. La mesure de la concentration de sFlt-1 dans le sang maternel entre 24 et 29 SA ne permet pas de diminuer la morbidité de la pré-éclampsie.
N. Berkane; G. Lefevre; M. Boulvain; A. Rousseau; A. Oppenheimer; T. Simon; J. Seror; A. Hertig. Mesure de la concentration sérique de sFlt-1 pour diminuer la morbi-mortalité de la pré-éclampsie : résultats de l’étude MOMA. Néphrologie & Thérapeutique 2016, 12, 272 .
AMA StyleN. Berkane, G. Lefevre, M. Boulvain, A. Rousseau, A. Oppenheimer, T. Simon, J. Seror, A. Hertig. Mesure de la concentration sérique de sFlt-1 pour diminuer la morbi-mortalité de la pré-éclampsie : résultats de l’étude MOMA. Néphrologie & Thérapeutique. 2016; 12 (5):272.
Chicago/Turabian StyleN. Berkane; G. Lefevre; M. Boulvain; A. Rousseau; A. Oppenheimer; T. Simon; J. Seror; A. Hertig. 2016. "Mesure de la concentration sérique de sFlt-1 pour diminuer la morbi-mortalité de la pré-éclampsie : résultats de l’étude MOMA." Néphrologie & Thérapeutique 12, no. 5: 272.