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Marie Frimat
CHU Lille, 59000 Lille, France

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Journal article
Published: 26 May 2021 in Journal of Clinical Medicine
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Despite improvements in organ preservation techniques and efforts to minimize the duration of cold ischemia, ischemia–reperfusion (IR) injury remains associated with poor graft function and long-term survival in kidney transplantation. We recently demonstrated a clinically significant day-time variation in myocardial tolerance to IR, transcriptionally orchestrated by the circadian clock. Patient and graft post-transplant survival were studied in a cohort of 10,291 patients first transplanted between 2006 and 2017 to test whether kidney graft tolerance to IR depends on the time-of-the-day of clamping/declamping, and thus impacts graft and patient survival. Post-transplant 1- and 3-year survival decreased with increasing ischemia duration. Time-of-the-day of clamping did not influence outcomes. However, night-time (vs. day-time) declamping was associated with a significantly worse post-transplant survival. After adjustment for other predictors, night-time (vs. day-time) declamping remained associated with a worse 1-year (HR = 1.26 (1.08–1.47), p = 0.0028 by Cox multivariable analysis) and 3-year (HR = 1.14 (1.02–1.27), p = 0.021) outcome. Interestingly, the deleterious impact of prolonged ischemia time (>15 h) was partially compensated by day-time (vs. night-time) declamping. Compared to night-time declamping, day-time declamping was associated with a better prognosis of kidney transplantation despite a longer duration of cold ischemia.

ACS Style

David Montaigne; Nasser Alhawajri; Mathilde Jacquelinet; Amandine Coppin; Marie Frimat; Sébastien Bouyé; Gilles Lebuffe; Bart Staels; Christian Jacquelinet; Marc Hazzan. Day-Time Declamping Is Associated with Better Outcomes in Kidney Transplantation: The Circarein Study. Journal of Clinical Medicine 2021, 10, 2322 .

AMA Style

David Montaigne, Nasser Alhawajri, Mathilde Jacquelinet, Amandine Coppin, Marie Frimat, Sébastien Bouyé, Gilles Lebuffe, Bart Staels, Christian Jacquelinet, Marc Hazzan. Day-Time Declamping Is Associated with Better Outcomes in Kidney Transplantation: The Circarein Study. Journal of Clinical Medicine. 2021; 10 (11):2322.

Chicago/Turabian Style

David Montaigne; Nasser Alhawajri; Mathilde Jacquelinet; Amandine Coppin; Marie Frimat; Sébastien Bouyé; Gilles Lebuffe; Bart Staels; Christian Jacquelinet; Marc Hazzan. 2021. "Day-Time Declamping Is Associated with Better Outcomes in Kidney Transplantation: The Circarein Study." Journal of Clinical Medicine 10, no. 11: 2322.

Review
Published: 18 February 2021 in International Journal of Molecular Sciences
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The incidence of kidney disease is rising, constituting a significant burden on the healthcare system and making identification of new therapeutic targets increasingly urgent. The heme oxygenase (HO) system performs an important function in the regulation of oxidative stress and inflammation and, via these mechanisms, is thought to play a role in the prevention of non-specific injuries following acute renal failure or resulting from chronic kidney disease. The expression of HO-1 is strongly inducible by a wide range of stimuli in the kidney, consequent to the kidney’s filtration role which means HO-1 is exposed to a wide range of endogenous and exogenous molecules, and it has been shown to be protective in a variety of nephropathological animal models. Interestingly, the positive effect of HO-1 occurs in both hemolysis- and rhabdomyolysis-dominated diseases, where the kidney is extensively exposed to heme (a major HO-1 inducer), as well as in non-heme-dependent diseases such as hypertension, diabetic nephropathy or progression to end-stage renal disease. This highlights the complexity of HO-1's functions, which is also illustrated by the fact that, despite the abundance of preclinical data, no drug targeting HO-1 has so far been translated into clinical use. The objective of this review is to assess current knowledge relating HO-1’s role in the kidney and its potential interest as a nephroprotection agent. The potential therapeutic openings will be presented, in particular through the identification of clinical trials targeting this enzyme or its products.

ACS Style

Anne Grunenwald; Lubka Roumenina; Marie Frimat. Heme Oxygenase 1: A Defensive Mediator in Kidney Diseases. International Journal of Molecular Sciences 2021, 22, 2009 .

AMA Style

Anne Grunenwald, Lubka Roumenina, Marie Frimat. Heme Oxygenase 1: A Defensive Mediator in Kidney Diseases. International Journal of Molecular Sciences. 2021; 22 (4):2009.

Chicago/Turabian Style

Anne Grunenwald; Lubka Roumenina; Marie Frimat. 2021. "Heme Oxygenase 1: A Defensive Mediator in Kidney Diseases." International Journal of Molecular Sciences 22, no. 4: 2009.

Original article
Published: 12 December 2020 in The FEBS Journal
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Heme’s interaction with toll‐like receptor 4 (TLR4) does not fully explain the pro‐inflammatory properties of this hemoglobin‐derived molecule during intravascular hemolysis. The receptor for advanced glycation end‐products (RAGE) shares many features with TLR4 such as common ligands and pro‐inflammatory, ‐thrombotic and ‐oxidative signaling pathways, prompting us to study its involvement as a heme sensor. Stable RAGE‐heme complexes with micromolar affinity were detected as heme‐mediated RAGE oligomerization. The heme binding site was located in the V domain of RAGE. This interaction was Fe3+‐dependent and competitive with carboxymethyllysine, another RAGE ligand. We confirmed a strong basal gene expression of RAGE in mouse lungs. After intraperitoneal heme injection, pulmonary TNFα, IL1β and tissue factor gene expression levels increased in WT mice but were significantly lower in their RAGE‐/‐ littermates. This may be related to the lower activation of ERK1/2 and Akt observed in the lungs of heme‐treated, RAGE‐/‐ mice. Overall, heme binds to RAGE with micromolar affinity and could promote pro‐inflammatory and pro‐thrombotic signaling in vivo, suggesting that this interaction could be implicated in heme overload conditions.

ACS Style

Olivia May; Laure Yatime; Nicolas S. Merle; Florian Delguste; Mike Howsam; Marie V. Daugan; Charles Paul‐Constant; Muriel Billamboz; Alina Ghinet; Steve Lancel; Jordan D. Dimitrov; Eric Boulanger; Lubka T. Roumenina; Marie Frimat. The receptor for advanced glycation end products is a sensor for cell‐free heme. The FEBS Journal 2020, 288, 3448 -3464.

AMA Style

Olivia May, Laure Yatime, Nicolas S. Merle, Florian Delguste, Mike Howsam, Marie V. Daugan, Charles Paul‐Constant, Muriel Billamboz, Alina Ghinet, Steve Lancel, Jordan D. Dimitrov, Eric Boulanger, Lubka T. Roumenina, Marie Frimat. The receptor for advanced glycation end products is a sensor for cell‐free heme. The FEBS Journal. 2020; 288 (11):3448-3464.

Chicago/Turabian Style

Olivia May; Laure Yatime; Nicolas S. Merle; Florian Delguste; Mike Howsam; Marie V. Daugan; Charles Paul‐Constant; Muriel Billamboz; Alina Ghinet; Steve Lancel; Jordan D. Dimitrov; Eric Boulanger; Lubka T. Roumenina; Marie Frimat. 2020. "The receptor for advanced glycation end products is a sensor for cell‐free heme." The FEBS Journal 288, no. 11: 3448-3464.

Review
Published: 13 November 2019 in Toxins
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Vascular diseases are multifactorial, often requiring multiple challenges, or ‘hits’, for their initiation. Intra-vascular hemolysis illustrates well the multiple-hit theory where a first event lyses red blood cells, releasing hemolysis-derived products, in particular cell-free heme which is highly toxic for the endothelium. Physiologically, hemolysis derived-products are rapidly neutralized by numerous defense systems, including haptoglobin and hemopexin which scavenge hemoglobin and heme, respectively. Likewise, cellular defense mechanisms are involved, including heme-oxygenase 1 upregulation which metabolizes heme. However, in cases of intra-vascular hemolysis, those systems are overwhelmed. Heme exerts toxic effects by acting as a damage-associated molecular pattern and promoting, together with hemoglobin, nitric oxide scavenging and ROS production. In addition, it activates the complement and the coagulation systems. Together, these processes lead to endothelial cell injury which triggers pro-thrombotic and pro-inflammatory phenotypes. Moreover, among endothelial cells, glomerular ones display a particular susceptibility explained by a weaker capacity to counteract hemolysis injury. In this review, we illustrate the ‘multiple-hit’ theory through the example of intra-vascular hemolysis, with a particular focus on cell-free heme, and we advance hypotheses explaining the glomerular susceptibility observed in hemolytic diseases. Finally, we describe therapeutic options for reducing endothelial injury in hemolytic diseases.

ACS Style

Marie Frimat; Idris Boudhabhay; Lubka T. Roumenina. Hemolysis Derived Products Toxicity and Endothelium: Model of the Second Hit. Toxins 2019, 11, 660 .

AMA Style

Marie Frimat, Idris Boudhabhay, Lubka T. Roumenina. Hemolysis Derived Products Toxicity and Endothelium: Model of the Second Hit. Toxins. 2019; 11 (11):660.

Chicago/Turabian Style

Marie Frimat; Idris Boudhabhay; Lubka T. Roumenina. 2019. "Hemolysis Derived Products Toxicity and Endothelium: Model of the Second Hit." Toxins 11, no. 11: 660.

Editorial
Published: 08 September 2019 in Aging
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ACS Style

Marie Frimat; Thibault Teissier; Eric Boulanger. Is RAGE the receptor for inflammaging? Aging 2019, 11, 6620 -6621.

AMA Style

Marie Frimat, Thibault Teissier, Eric Boulanger. Is RAGE the receptor for inflammaging? Aging. 2019; 11 (17):6620-6621.

Chicago/Turabian Style

Marie Frimat; Thibault Teissier; Eric Boulanger. 2019. "Is RAGE the receptor for inflammaging?" Aging 11, no. 17: 6620-6621.

Original research article
Published: 20 December 2018 in Frontiers in Immunology
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Atypical hemolytic uremic syndrome (aHUS) is a severe disease characterized by microvascular endothelial cell (EC) lesions leading to thrombi formation, mechanical hemolysis and organ failure, predominantly renal. Complement system overactivation is a hallmark of aHUS. To investigate this selective susceptibility of the microvascular renal endothelium to complement attack and thrombotic microangiopathic lesions, we compared complement and cyto-protection markers on EC, from different vascular beds, in in vitro and in vivo models as well as in patients. No difference was observed for complement deposits or expression of complement and coagulation regulators between macrovascular and microvascular EC, either at resting state or after inflammatory challenge. After prolonged exposure to hemolysis-derived heme, higher C3 deposits were found on glomerular EC, in vitro and in vivo, compared with other EC in culture and in mice organs (liver, skin, brain, lungs and heart). This could be explained by a reduced complement regulation capacity due to weaker binding of Factor H and inefficient upregulation of thrombomodulin (TM). Microvascular EC also failed to upregulate the cytoprotective heme-degrading enzyme heme-oxygenase 1 (HO-1), normally induced by hemolysis products. Only HUVEC (Human Umbilical Vein EC) developed adaptation to heme, which was lost after inhibition of HO-1 activity. Interestingly, the expression of KLF2 and KLF4—known transcription factors of TM, also described as possible transcription modulators of HO-1- was weaker in micro than macrovascular EC under hemolytic conditions. Our results show that the microvascular EC, and especially glomerular EC, fail to adapt to the stress imposed by hemolysis and acquire a pro-coagulant and complement-activating phenotype. Together, these findings indicate that the vulnerability of glomerular EC to hemolysis is a key factor in aHUS, amplifying complement overactivation and thrombotic microangiopathic lesions.

ACS Style

Olivia May; Nicolas S. Merle; Anne Grunenwald; Viviane Gnemmi; Juliette Leon; Cloé Payet; Tania Robe-Rybkine; Romain Paule; Florian Delguste; Simon C. Satchell; Peter W. Mathieson; Marc Hazzan; Eric Boulanger; Jordan Dimitrov; Veronique Fremeaux-Bacchi; Marie Frimat; Lubka T. Roumenina. Heme Drives Susceptibility of Glomerular Endothelium to Complement Overactivation Due to Inefficient Upregulation of Heme Oxygenase-1. Frontiers in Immunology 2018, 9, 1 .

AMA Style

Olivia May, Nicolas S. Merle, Anne Grunenwald, Viviane Gnemmi, Juliette Leon, Cloé Payet, Tania Robe-Rybkine, Romain Paule, Florian Delguste, Simon C. Satchell, Peter W. Mathieson, Marc Hazzan, Eric Boulanger, Jordan Dimitrov, Veronique Fremeaux-Bacchi, Marie Frimat, Lubka T. Roumenina. Heme Drives Susceptibility of Glomerular Endothelium to Complement Overactivation Due to Inefficient Upregulation of Heme Oxygenase-1. Frontiers in Immunology. 2018; 9 ():1.

Chicago/Turabian Style

Olivia May; Nicolas S. Merle; Anne Grunenwald; Viviane Gnemmi; Juliette Leon; Cloé Payet; Tania Robe-Rybkine; Romain Paule; Florian Delguste; Simon C. Satchell; Peter W. Mathieson; Marc Hazzan; Eric Boulanger; Jordan Dimitrov; Veronique Fremeaux-Bacchi; Marie Frimat; Lubka T. Roumenina. 2018. "Heme Drives Susceptibility of Glomerular Endothelium to Complement Overactivation Due to Inefficient Upregulation of Heme Oxygenase-1." Frontiers in Immunology 9, no. : 1.

Journal article
Published: 21 June 2018 in JCI Insight
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In hemolytic diseases, such as sickle cell disease (SCD), intravascular hemolysis results in the release of hemoglobin, heme, and heme-loaded membrane microvesicles in the bloodstream. Intravascular hemolysis is thus associated with inflammation and organ injury. Complement system can be activated by heme in vitro. We investigated the mechanisms by which hemolysis and red blood cell (RBC) degradation products trigger complement activation in vivo. In kidney biopsies of SCD nephropathy patients and a mouse model with SCD, we detected tissue deposits of complement C3 and C5b-9. Moreover, drug-induced intravascular hemolysis or injection of heme or hemoglobin in mice triggered C3 deposition, primarily in kidneys. Renal injury markers (Kim-1, NGAL) were attenuated in C3–/– hemolytic mice. RBC degradation products, such as heme-loaded microvesicles and heme, induced alternative and terminal complement pathway activation in sera and on endothelial surfaces, in contrast to hemoglobin. Heme triggered rapid P selectin, C3aR, and C5aR expression and downregulated CD46 on endothelial cells. Importantly, complement deposition was attenuated in vivo and in vitro by heme scavenger hemopexin. In conclusion, we demonstrate that intravascular hemolysis triggers complement activation in vivo, encouraging further studies on its role in SCD nephropathy. Conversely, heme inhibition using hemopexin may provide a novel therapeutic opportunity to limit complement activation in hemolytic diseases.

ACS Style

Nicolas S. Merle; Anne Grunenwald; Helena Rajaratnam; Viviane Gnemmi; Marie Frimat; Marie-Lucile Figueres; Samantha Knockaert; Sanah Bouzekri; Dominique Charue; Remi Noe; Tania Robe-Rybkine; Marie Le-Hoang; Nathan Brinkman; Thomas Gentinetta; Monika Edler; Sara Petrillo; Emanuela Tolosano; Sylvia Miescher; Sylvain Le Jeune; Pascal Houillier; Sophie Chauvet; Marion Rabant; Jordan Dimitrov; Veronique Fremeaux-Bacchi; Olivier P. Blanc-Brude; Lubka T. Roumenina. Intravascular hemolysis activates complement via cell-free heme and heme-loaded microvesicles. JCI Insight 2018, 3, 1 .

AMA Style

Nicolas S. Merle, Anne Grunenwald, Helena Rajaratnam, Viviane Gnemmi, Marie Frimat, Marie-Lucile Figueres, Samantha Knockaert, Sanah Bouzekri, Dominique Charue, Remi Noe, Tania Robe-Rybkine, Marie Le-Hoang, Nathan Brinkman, Thomas Gentinetta, Monika Edler, Sara Petrillo, Emanuela Tolosano, Sylvia Miescher, Sylvain Le Jeune, Pascal Houillier, Sophie Chauvet, Marion Rabant, Jordan Dimitrov, Veronique Fremeaux-Bacchi, Olivier P. Blanc-Brude, Lubka T. Roumenina. Intravascular hemolysis activates complement via cell-free heme and heme-loaded microvesicles. JCI Insight. 2018; 3 (12):1.

Chicago/Turabian Style

Nicolas S. Merle; Anne Grunenwald; Helena Rajaratnam; Viviane Gnemmi; Marie Frimat; Marie-Lucile Figueres; Samantha Knockaert; Sanah Bouzekri; Dominique Charue; Remi Noe; Tania Robe-Rybkine; Marie Le-Hoang; Nathan Brinkman; Thomas Gentinetta; Monika Edler; Sara Petrillo; Emanuela Tolosano; Sylvia Miescher; Sylvain Le Jeune; Pascal Houillier; Sophie Chauvet; Marion Rabant; Jordan Dimitrov; Veronique Fremeaux-Bacchi; Olivier P. Blanc-Brude; Lubka T. Roumenina. 2018. "Intravascular hemolysis activates complement via cell-free heme and heme-loaded microvesicles." JCI Insight 3, no. 12: 1.

Journal article
Published: 01 May 2018 in Nephrology Dialysis Transplantation
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INTRODUCTION AND AIMS: The atypical hemolytic uremic syndrome (aHUS) is a rare kidney-predominant thrombotic microangiopathy associated with complement system overactivation and formation of thrombi in microvessels, triggering mechanical hemolysis. The particular susceptibility of renal endothelial cells (EC) to complement-mediated injury remains poorly understood.

ACS Style

Olivia May; Nicolas Merle; Anne Grunenwald; Viviane Gnemmi; Tania Robe-Rybkine; Marc Hazzan; Jordan Dimitrov; Véronique Frémeaux-Bacchi; Lubka Roumenina; Marie Frimat. FP076ATYPICAL HEMOLYTIC UREMIC SYNDROME - WHY THE KIDNEY? Nephrology Dialysis Transplantation 2018, 33, i74 -i74.

AMA Style

Olivia May, Nicolas Merle, Anne Grunenwald, Viviane Gnemmi, Tania Robe-Rybkine, Marc Hazzan, Jordan Dimitrov, Véronique Frémeaux-Bacchi, Lubka Roumenina, Marie Frimat. FP076ATYPICAL HEMOLYTIC UREMIC SYNDROME - WHY THE KIDNEY? Nephrology Dialysis Transplantation. 2018; 33 (suppl_1):i74-i74.

Chicago/Turabian Style

Olivia May; Nicolas Merle; Anne Grunenwald; Viviane Gnemmi; Tania Robe-Rybkine; Marc Hazzan; Jordan Dimitrov; Véronique Frémeaux-Bacchi; Lubka Roumenina; Marie Frimat. 2018. "FP076ATYPICAL HEMOLYTIC UREMIC SYNDROME - WHY THE KIDNEY?" Nephrology Dialysis Transplantation 33, no. suppl_1: i74-i74.

Original research article
Published: 01 March 2018 in Frontiers in Immunology
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Intravascular erythrocyte destruction, accompanied by the release of pro-oxidative and pro-inflammatory components hemoglobin and heme, is a common event in the pathogenesis of numerous diseases with heterogeneous etiology and clinical features. A frequent adverse effect related to massive hemolysis is the renal injury and inflammation. Nevertheless, it is still unclear whether heme––a danger-associated molecular pattern––and ligand for TLR4 or upstream hemolysis-derived products are responsible for these effects. Well-characterized animal models of hemolysis with kidney impairment are needed to investigate how hemolysis drives kidney injury and to test novel therapeutic strategies. Here, we characterized the pathological processes leading to acute kidney injury and inflammation during massive intravascular hemolysis, using a mouse model of phenylhydrazine (PHZ)-triggered erythrocyte destruction. We observed profound changes in mRNA levels for markers of tubular damage (Kim-1, NGAL) and regeneration (indirect marker of tubular injury, Ki-67), and tissue and vascular inflammation (IL-6, E-selectin, P-selectin, ICAM-1) in kidneys of PHZ-treated mice, associated with ultrastructural signs of tubular injury. Moreover, mass spectrometry revealed presence of markers of tubular damage in urine, including meprin-α, cytoskeletal keratins, α-1-antitrypsin, and α-1-microglobulin. Signs of renal injury and inflammation rapidly resolved and the renal function was preserved, despite major changes in metabolic parameters of PHZ-injected animals. Mechanistically, renal alterations were largely heme-independent, since injection of free heme could not reproduce them, and scavenging heme with hemopexin in PHZ-administered mice could not prevent them. Reduced overall health status of the mice suggested multiorgan involvement. We detected amylasemia and amylasuria, two markers of acute pancreatitis. We also provide detailed characterization of renal manifestations associated with acute intravascular hemolysis, which may be mediated by hemolysis-derived products upstream of heme release. This analysis provides a platform for further investigations of hemolytic diseases and associated renal injury and the evaluation of novel therapeutic strategies that target intravascular hemolysis.

ACS Style

Nicolas S. Merle; Anne Grunenwald; Marie-Lucile Figueres; Sophie Chauvet; Marie Daugan; Samantha Knockaert; Tania Robe-Rybkine; Rémi Noé; Olivia May; Marie Frimat; Nathan Brinkman; Thomas Gentinetta; Sylvia Miescher; Pascal Houillier; Veronique Legros; Florence Gonnet; Olivier P. Blanc-Brude; Marion Rabant; Regis Daniel; Jordan Dimitrov; Lubka T. Roumenina. Characterization of Renal Injury and Inflammation in an Experimental Model of Intravascular Hemolysis. Frontiers in Immunology 2018, 9, 179 .

AMA Style

Nicolas S. Merle, Anne Grunenwald, Marie-Lucile Figueres, Sophie Chauvet, Marie Daugan, Samantha Knockaert, Tania Robe-Rybkine, Rémi Noé, Olivia May, Marie Frimat, Nathan Brinkman, Thomas Gentinetta, Sylvia Miescher, Pascal Houillier, Veronique Legros, Florence Gonnet, Olivier P. Blanc-Brude, Marion Rabant, Regis Daniel, Jordan Dimitrov, Lubka T. Roumenina. Characterization of Renal Injury and Inflammation in an Experimental Model of Intravascular Hemolysis. Frontiers in Immunology. 2018; 9 ():179.

Chicago/Turabian Style

Nicolas S. Merle; Anne Grunenwald; Marie-Lucile Figueres; Sophie Chauvet; Marie Daugan; Samantha Knockaert; Tania Robe-Rybkine; Rémi Noé; Olivia May; Marie Frimat; Nathan Brinkman; Thomas Gentinetta; Sylvia Miescher; Pascal Houillier; Veronique Legros; Florence Gonnet; Olivier P. Blanc-Brude; Marion Rabant; Regis Daniel; Jordan Dimitrov; Lubka T. Roumenina. 2018. "Characterization of Renal Injury and Inflammation in an Experimental Model of Intravascular Hemolysis." Frontiers in Immunology 9, no. : 179.

Journal article
Published: 01 September 2017 in Molecular Immunology
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ACS Style

Lubka T. Roumenina; Olivia May; Anne Grunenwald; Nicolas S. Merle; Viviane Gnemmi; Tania Robe-Rybkine; Marc Hazzan; Jordan D. Dimitrov; Veronique Fremeaux-Bacchi; Marie Frimat. Atypical hemolytic uremic syndrome – Why the kidney? Molecular Immunology 2017, 89, 172 -173.

AMA Style

Lubka T. Roumenina, Olivia May, Anne Grunenwald, Nicolas S. Merle, Viviane Gnemmi, Tania Robe-Rybkine, Marc Hazzan, Jordan D. Dimitrov, Veronique Fremeaux-Bacchi, Marie Frimat. Atypical hemolytic uremic syndrome – Why the kidney? Molecular Immunology. 2017; 89 ():172-173.

Chicago/Turabian Style

Lubka T. Roumenina; Olivia May; Anne Grunenwald; Nicolas S. Merle; Viviane Gnemmi; Tania Robe-Rybkine; Marc Hazzan; Jordan D. Dimitrov; Veronique Fremeaux-Bacchi; Marie Frimat. 2017. "Atypical hemolytic uremic syndrome – Why the kidney?" Molecular Immunology 89, no. : 172-173.

Journal article
Published: 01 September 2017 in Molecular Immunology
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ACS Style

Nicolas S. Merle; Anne Grunenwald; Helena Rajaratnam; Viviane Gnemmi; Marie Frimat; Marie-Lucile Figueres; Sanah Bouzekri; Dominique Charue; Remi Noe; Tania Robe-Rybkine; Nathan Brinkman; Sylvia Miescher; Sylvain Le Jeune; Pascal Houillier; Jordan D. Dimitrov; Veronique Fremeaux-Bacchi; Olivier P. Blanc-Brude; Lubka. T. Roumenina. Intravascular hemolysis induces complement system activation. Molecular Immunology 2017, 89, 164 .

AMA Style

Nicolas S. Merle, Anne Grunenwald, Helena Rajaratnam, Viviane Gnemmi, Marie Frimat, Marie-Lucile Figueres, Sanah Bouzekri, Dominique Charue, Remi Noe, Tania Robe-Rybkine, Nathan Brinkman, Sylvia Miescher, Sylvain Le Jeune, Pascal Houillier, Jordan D. Dimitrov, Veronique Fremeaux-Bacchi, Olivier P. Blanc-Brude, Lubka. T. Roumenina. Intravascular hemolysis induces complement system activation. Molecular Immunology. 2017; 89 ():164.

Chicago/Turabian Style

Nicolas S. Merle; Anne Grunenwald; Helena Rajaratnam; Viviane Gnemmi; Marie Frimat; Marie-Lucile Figueres; Sanah Bouzekri; Dominique Charue; Remi Noe; Tania Robe-Rybkine; Nathan Brinkman; Sylvia Miescher; Sylvain Le Jeune; Pascal Houillier; Jordan D. Dimitrov; Veronique Fremeaux-Bacchi; Olivier P. Blanc-Brude; Lubka. T. Roumenina. 2017. "Intravascular hemolysis induces complement system activation." Molecular Immunology 89, no. : 164.

Case reports
Published: 01 June 2017 in Medicine
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BRAF and MEK inhibitors have significantly improved the prognosis of metastatic melanoma, by inhibiting both the mitogen-activated protein kinase (MAP-kinase) pathway. They are associated with infrequent adverse kidney events. Most of these are related to the use of BRAF inhibitors and involve interstitial nephritis with acute tubular necrosis. We report a unique case of glomerulonephritis with renal granulomatous vasculitis in a patient diagnosed with metastatic melanoma treated with BRAF and MEK inhibitors. The patient was a 55-year old woman, who presented a melanoma of the right thigh with pulmonary metastasis. Treatment started in November 2015, with Encorafenib and Binimetinib, new BRAF and MEK inhibitors, respectively. Two months after the beginning of the treatment, there was a worsening of her renal function with significant proteinuria. Kidney biopsy showed extracapillary proliferation in the glomeruli with a granulomatous reaction. Renal function recovered completely after withdrawal of the chemotherapy. All the reported kidney adverse events secondary to BRAF and MEK inhibitors in the literature are related to the use of BRAF inhibitors. Some previous reported mechanistic investigations also provide insight between BRAF inhibitors and podocytes injuries. Therefore, encorafenib most likely is the main responsible of the disease. However, evidence has emerged that inhibition of the MAP kinase pathway could also enhance autoimmunity. Thus, binimetinib may also have played a role and the combination of BRAF and MEK inhibitors may have facilitated this autoimmune kidney disease.

ACS Style

Mehdi Maanaoui; Camille Saint-Jacques; Viviane Gnemmi; Marie Frimat; Arnaud Lionet; Marc Hazzan; Christian Noël; François Provot. Glomerulonephritis and granulomatous vasculitis in kidney as a complication of the use of BRAF and MEK inhibitors in the treatment of metastatic melanoma. Medicine 2017, 96, e7196 -e7196.

AMA Style

Mehdi Maanaoui, Camille Saint-Jacques, Viviane Gnemmi, Marie Frimat, Arnaud Lionet, Marc Hazzan, Christian Noël, François Provot. Glomerulonephritis and granulomatous vasculitis in kidney as a complication of the use of BRAF and MEK inhibitors in the treatment of metastatic melanoma. Medicine. 2017; 96 (25):e7196-e7196.

Chicago/Turabian Style

Mehdi Maanaoui; Camille Saint-Jacques; Viviane Gnemmi; Marie Frimat; Arnaud Lionet; Marc Hazzan; Christian Noël; François Provot. 2017. "Glomerulonephritis and granulomatous vasculitis in kidney as a complication of the use of BRAF and MEK inhibitors in the treatment of metastatic melanoma." Medicine 96, no. 25: e7196-e7196.

Review
Published: 17 May 2017 in Clinical Science
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Advanced glycation end-product (AGE) is the generic term for a heterogeneous group of derivatives arising from a non-enzymatic reaction between reducing sugars and proteins. In recent years, evidence has accumulated that incriminates AGEs in pathogenic processes associated with both chronic hyperglycaemia and age-related diseases. Regardless of their exogenous or endogenous origin, the accumulation of AGEs and their derivatives could promote accelerated ageing by leading to protein modifications and activating several inflammatory signalling pathways via AGE-specific receptors. However, it remains to be demonstrated whether preventing the accumulation of AGEs and their effects is an important therapeutic option for successful ageing. The present review gives an overview of the current knowledge on the pathogenic role of AGEs by focusing on three AGE target organs: kidney, heart and brain. For each of these organs we concentrate on an age-related disease, each of which is a major public health issue: chronic kidney disease, heart dysfunction and neurodegenerative diseases. Even though strong connections have been highlighted between glycation and age-related pathogenesis, causal links still need to be validated. In each case, we report evidence and uncertainties suggested by animal or epidemiological studies on the possible link between pathogenesis and glycation in a chronic hyperglycaemic state, in the absence of diabetes, and with exogenous AGEs alone. Finally, we present some promising anti-AGE strategies that are currently being studied.

ACS Style

Marie Frimat; Maité Daroux; Rachel Litke; Remi Neviere; Frederic Tessier; Eric Boulanger. Kidney, heart and brain: three organs targeted by ageing and glycation. Clinical Science 2017, 131, 1069 -1092.

AMA Style

Marie Frimat, Maité Daroux, Rachel Litke, Remi Neviere, Frederic Tessier, Eric Boulanger. Kidney, heart and brain: three organs targeted by ageing and glycation. Clinical Science. 2017; 131 (11):1069-1092.

Chicago/Turabian Style

Marie Frimat; Maité Daroux; Rachel Litke; Remi Neviere; Frederic Tessier; Eric Boulanger. 2017. "Kidney, heart and brain: three organs targeted by ageing and glycation." Clinical Science 131, no. 11: 1069-1092.

Journal article
Published: 01 May 2017 in Nephrology Dialysis Transplantation
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INTRODUCTION AND AIMS: Effects of endogeneous advanced glycation end-products (AGEs) are well-known, especially for their impact on inflammation and fibrosis. They are thought to play a key role in processes such as the pathogenesis of diabetic nephropathy or ageing. Nonetheless, these effects have yet to be described for dietary AGEs (dAGEs). We here studied whether a prolonged exposure to the dAGE carboxymethyl lysine (CML) can influence the process of ageing in kidneys and whether RAGE (receptor for AGEs) is a modulator of this process.

ACS Style

Thibault Tessier; Valentine Quersin; Viviane Gnemmi; Florian Delguste; Maité Daroux; Frederic Tessier; Eric Boulanger; Marie Frimat. MP081RENAL AGEING AND GLYCATION: IMPLICATION OF RECEPTOR FOR ADVANCED GLYCATION END-PRODUCTS. Nephrology Dialysis Transplantation 2017, 32, iii456 -iii456.

AMA Style

Thibault Tessier, Valentine Quersin, Viviane Gnemmi, Florian Delguste, Maité Daroux, Frederic Tessier, Eric Boulanger, Marie Frimat. MP081RENAL AGEING AND GLYCATION: IMPLICATION OF RECEPTOR FOR ADVANCED GLYCATION END-PRODUCTS. Nephrology Dialysis Transplantation. 2017; 32 (suppl_3):iii456-iii456.

Chicago/Turabian Style

Thibault Tessier; Valentine Quersin; Viviane Gnemmi; Florian Delguste; Maité Daroux; Frederic Tessier; Eric Boulanger; Marie Frimat. 2017. "MP081RENAL AGEING AND GLYCATION: IMPLICATION OF RECEPTOR FOR ADVANCED GLYCATION END-PRODUCTS." Nephrology Dialysis Transplantation 32, no. suppl_3: iii456-iii456.

Journal article
Published: 01 May 2017 in Nephrology Dialysis Transplantation
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ACS Style

Marc Ulrich; Viviane Gnemmi; Marie Frimat; Evelyne Mac Namara; Laurence Vrigneaud; Céline LeBas; Francois Provôt; Gerard Cardon; Pierre Bataille; Francois Glowacki. MO037PROLIFERATIVE GLOMERULONEPHRITIS WITH MONOCLONAL IMMUNOGLOBULIN DEPOSITS: A CASE SERIES. Nephrology Dialysis Transplantation 2017, 32, 1 .

AMA Style

Marc Ulrich, Viviane Gnemmi, Marie Frimat, Evelyne Mac Namara, Laurence Vrigneaud, Céline LeBas, Francois Provôt, Gerard Cardon, Pierre Bataille, Francois Glowacki. MO037PROLIFERATIVE GLOMERULONEPHRITIS WITH MONOCLONAL IMMUNOGLOBULIN DEPOSITS: A CASE SERIES. Nephrology Dialysis Transplantation. 2017; 32 (suppl_3):1.

Chicago/Turabian Style

Marc Ulrich; Viviane Gnemmi; Marie Frimat; Evelyne Mac Namara; Laurence Vrigneaud; Céline LeBas; Francois Provôt; Gerard Cardon; Pierre Bataille; Francois Glowacki. 2017. "MO037PROLIFERATIVE GLOMERULONEPHRITIS WITH MONOCLONAL IMMUNOGLOBULIN DEPOSITS: A CASE SERIES." Nephrology Dialysis Transplantation 32, no. suppl_3: 1.

Journal article
Published: 01 April 2017 in Néphrologie & Thérapeutique
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In renal transplant medicine, several scores have been recently developed in order to help decision-making in clinical practice. The aim of this update is to focus on these new scores that allow to better estimate the quality of the renal transplant, to refine the allocation policy, to help registration of old recipients on the waiting list, or to evaluate the risk to develop end-stage renal failure after living donation.

ACS Style

Marc Hazzan; Marie Frimat; François Glowacki; Arnaud Lionet; François Provot; Christian Noël. Nouveaux scores en transplantation rénale : comment peut-on les utiliser ? Néphrologie & Thérapeutique 2017, 13, S131 -S136.

AMA Style

Marc Hazzan, Marie Frimat, François Glowacki, Arnaud Lionet, François Provot, Christian Noël. Nouveaux scores en transplantation rénale : comment peut-on les utiliser ? Néphrologie & Thérapeutique. 2017; 13 ():S131-S136.

Chicago/Turabian Style

Marc Hazzan; Marie Frimat; François Glowacki; Arnaud Lionet; François Provot; Christian Noël. 2017. "Nouveaux scores en transplantation rénale : comment peut-on les utiliser ?" Néphrologie & Thérapeutique 13, no. : S131-S136.

Journal article
Published: 17 January 2017 in Journal of the American Society of Nephrology
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In C3 glomerulopathy (C3G), the alternative pathway of complement is frequently overactivated by autoantibodies that stabilize the C3 convertase C3bBb. Anti-C3b and anti-factor B (anti-FB) IgG have been reported in three patients with C3G. We screened a cohort of 141 patients with C3G and Ig-associated membranoproliferative GN (Ig-MPGN) for anti-FB and anti-C3b autoantibodies using ELISA. We identified seven patients with anti-FB IgG, three patients with anti-C3b IgG, and five patients with anti-FB and anti-C3b IgG. Of these 15 patients, ten were diagnosed with Ig-MPGN. Among those patients with available data, 92% had a nephrotic syndrome, 64% had AKI, and 67% had a documented infection. Patients negative for anti-C3b and anti-FB IgG had much lower rates of infection (17 [25%] patients with C3G and one [10%] patient with Ig-MPGN). After 48 months, four of 15 (26%) positive patients had developed ESRD or died. All 15 patients had high plasma Bb levels, six (40%) patients had low levels of C3, and nine (60%) patients had high levels of soluble C5b9. In vitro, IgG purified from patients with anti-FB Abs selectively enhanced C3 convertase activity; IgG from patients with anti-C3b/anti-FB Abs enhanced C3 and C5 cleavage. IgG from patients with anti-C3b Abs stabilized C3bBb and perturbed C3b binding to complement receptor 1 but did not perturb binding to factor H. In conclusion, the prevalence of anti-C3b/anti-FB Abs and alternative pathway activation is similar in Ig-MPGN and C3G, suggesting similar pathogenic mechanisms. Identification of the underlying defect in Ig-MPGN could lead to improved treatment.

ACS Style

Maria Chiara Marinozzi; Lubka T. Roumenina; Sophie Chauvet; Alexandre Hertig; Dominique Bertrand; Jérome Olagne; Marie Frimat; Tim Ulinski; Georges Deschênes; Stephane Burtey; Michel Delahousse; Bruno Moulin; Christophe Legendre; Véronique Frémeaux-Bacchi; Moglie Le Quintrec. Anti-Factor B and Anti-C3b Autoantibodies in C3 Glomerulopathy and Ig-Associated Membranoproliferative GN. Journal of the American Society of Nephrology 2017, 28, 1603 -1613.

AMA Style

Maria Chiara Marinozzi, Lubka T. Roumenina, Sophie Chauvet, Alexandre Hertig, Dominique Bertrand, Jérome Olagne, Marie Frimat, Tim Ulinski, Georges Deschênes, Stephane Burtey, Michel Delahousse, Bruno Moulin, Christophe Legendre, Véronique Frémeaux-Bacchi, Moglie Le Quintrec. Anti-Factor B and Anti-C3b Autoantibodies in C3 Glomerulopathy and Ig-Associated Membranoproliferative GN. Journal of the American Society of Nephrology. 2017; 28 (5):1603-1613.

Chicago/Turabian Style

Maria Chiara Marinozzi; Lubka T. Roumenina; Sophie Chauvet; Alexandre Hertig; Dominique Bertrand; Jérome Olagne; Marie Frimat; Tim Ulinski; Georges Deschênes; Stephane Burtey; Michel Delahousse; Bruno Moulin; Christophe Legendre; Véronique Frémeaux-Bacchi; Moglie Le Quintrec. 2017. "Anti-Factor B and Anti-C3b Autoantibodies in C3 Glomerulopathy and Ig-Associated Membranoproliferative GN." Journal of the American Society of Nephrology 28, no. 5: 1603-1613.

Journal article
Published: 01 January 2017 in American Journal of Kidney Diseases
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ACS Style

Marie Frimat; François Provôt; Alexandre Hertig. In Reply to ‘Risk of Tranexamic Acid for Treatment of Postpartum Hemorrhage’. American Journal of Kidney Diseases 2017, 69, 160 -161.

AMA Style

Marie Frimat, François Provôt, Alexandre Hertig. In Reply to ‘Risk of Tranexamic Acid for Treatment of Postpartum Hemorrhage’. American Journal of Kidney Diseases. 2017; 69 (1):160-161.

Chicago/Turabian Style

Marie Frimat; François Provôt; Alexandre Hertig. 2017. "In Reply to ‘Risk of Tranexamic Acid for Treatment of Postpartum Hemorrhage’." American Journal of Kidney Diseases 69, no. 1: 160-161.

Journal article
Published: 01 December 2016 in Kidney International
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Thrombotic microangiopathy (TMA) is a poorly recognized cause of collapsing glomerulopathy. The frequency and significance of collapsing glomerulopathy associated with renal TMA have not been specifically studied in native kidney biopsy specimens. Here we retrospectively documented clinicopathologic features of 53 patients with histologically proven TMA in the native kidney, with special emphasis on changes due to focal segmental glomerulosclerosis (FSGS). Histological TMA was related to hypertensive nephropathy in 21 patients, genetic complement abnormalities in 9, drugs in 7, and to other causes in 16 patients. Almost half (26 patients) presented with arteriolar, 6 with glomerular, and 21 with mixed TMA. Using the Columbia classification system for the 53 patients with histological TMA, 33 had concurrent FSGS lesions with collapsing glomerulopathy the dominant variant in 19 patients (58% of the FSGS cases), not otherwise specified in 9 patients, cellular in 3, and perihilar or tip lesions in 1 patient each. The presence of FSGS was associated with a poor renal prognosis, with no prognostic difference between collapsing glomerulopathy and other FSGS variants. Thus, collapsing glomerulopathy is frequently found in native kidney biopsies with TMA, suggesting that endothelial injury may play an important role in the pathophysiology of FSGS.

ACS Style

David Buob; Mélanie Decambron; Viviane Gnemmi; Marie Frimat; Maxime Hoffmann; Raymond Azar; Jean-Dominique Gheerbrant; Thomas Guincestre; Christian Noël; Marie-Christine Copin; Francois Glowacki. Collapsing glomerulopathy is common in the setting of thrombotic microangiopathy of the native kidney. Kidney International 2016, 90, 1321 -1331.

AMA Style

David Buob, Mélanie Decambron, Viviane Gnemmi, Marie Frimat, Maxime Hoffmann, Raymond Azar, Jean-Dominique Gheerbrant, Thomas Guincestre, Christian Noël, Marie-Christine Copin, Francois Glowacki. Collapsing glomerulopathy is common in the setting of thrombotic microangiopathy of the native kidney. Kidney International. 2016; 90 (6):1321-1331.

Chicago/Turabian Style

David Buob; Mélanie Decambron; Viviane Gnemmi; Marie Frimat; Maxime Hoffmann; Raymond Azar; Jean-Dominique Gheerbrant; Thomas Guincestre; Christian Noël; Marie-Christine Copin; Francois Glowacki. 2016. "Collapsing glomerulopathy is common in the setting of thrombotic microangiopathy of the native kidney." Kidney International 90, no. 6: 1321-1331.

Review
Published: 26 October 2016 in Immunological Reviews
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Endothelium is strategically located at the interface between blood and interstitial tissues, placing thus endothelial cell as a key player in vascular homeostasis. Endothelial cells are in a dynamic equilibrium with their environment and constitute concomitantly a source, a barrier, and a target of defensive mediators. This review will discuss the recent advances in our understanding of the complex crosstalk between the endothelium, the complement system and the hemostasis in health and in disease. The first part will provide a general introduction on endothelial cells heterogeneity and on the physiologic role of the complement and hemostatic systems. The second part will analyze the interplay between complement, hemostasis and endothelial cells in physiological conditions and their alterations in diseases. Particular focus will be made on the prototypes of thrombotic microangiopathic disorders, resulting from complement or hemostasis dysregulation-mediated endothelial damage: atypical hemolytic uremic syndrome and thrombotic thrombocytopenic purpura. Novel aspects of the pathophysiology of the thrombotic microangiopathies will be discussed.

ACS Style

Lubka T. Roumenina; Julie Rayes; Marie Frimat; Veronique Fremeaux-Bacchi. Endothelial cells: source, barrier, and target of defensive mediators. Immunological Reviews 2016, 274, 307 -329.

AMA Style

Lubka T. Roumenina, Julie Rayes, Marie Frimat, Veronique Fremeaux-Bacchi. Endothelial cells: source, barrier, and target of defensive mediators. Immunological Reviews. 2016; 274 (1):307-329.

Chicago/Turabian Style

Lubka T. Roumenina; Julie Rayes; Marie Frimat; Veronique Fremeaux-Bacchi. 2016. "Endothelial cells: source, barrier, and target of defensive mediators." Immunological Reviews 274, no. 1: 307-329.