This page has only limited features, please log in for full access.

Unclaimed
Saïd Kamel
Department of Biochemistry, Amiens University Medical Center, F-80000 Amiens, France

Basic Info

Basic Info is private.

Honors and Awards

The user has no records in this section


Career Timeline

The user has no records in this section.


Short Biography

The user biography is not available.
Following
Followers
Co Authors
The list of users this user is following is empty.
Following: 0 users

Feed

Review
Published: 26 January 2021 in Toxins
Reads 0
Downloads 0

Chronic kidney disease (CKD) is a highly prevalent condition and is associated with a high comorbidity burden, polymedication, and a high mortality rate. A number of conventional and nonconventional risk factors for comorbidities and mortality in CKD have been identified. Among the nonconventional risk factors, uremic toxins are valuable therapeutic targets. The fact that some uremic toxins are gut-derived suggests that intestinal chelators might have a therapeutic effect. The phosphate binders used to prevent hyperphosphatemia in hemodialysis patients act by complexing inorganic phosphate in the gastrointestinal tract but might conceivably have a nonspecific action on gut-derived uremic toxins. Since phosphorous is a major nutrient for the survival and reproduction of bacteria, changes in its intestinal concentration may impact the gut microbiota’s activity and composition. Furthermore, AST-120 is an orally administered activated charcoal adsorbent that is widely used in Asian countries to specifically decrease uremic toxin levels. In this narrative review, we examine the latest data on the use of oral nonspecific and specific intestinal chelators to reduce levels of gut-derived uremic toxins.

ACS Style

Solène Laville; Ziad Massy; Said Kamel; Jean Chillon; Gabriel Choukroun; Sophie Liabeuf. Intestinal Chelators, Sorbants, and Gut-Derived Uremic Toxins. Toxins 2021, 13, 91 .

AMA Style

Solène Laville, Ziad Massy, Said Kamel, Jean Chillon, Gabriel Choukroun, Sophie Liabeuf. Intestinal Chelators, Sorbants, and Gut-Derived Uremic Toxins. Toxins. 2021; 13 (2):91.

Chicago/Turabian Style

Solène Laville; Ziad Massy; Said Kamel; Jean Chillon; Gabriel Choukroun; Sophie Liabeuf. 2021. "Intestinal Chelators, Sorbants, and Gut-Derived Uremic Toxins." Toxins 13, no. 2: 91.

Review
Published: 21 December 2020 in Toxins
Reads 0
Downloads 0

Vascular calcification (VC) is a cardiovascular complication associated with a high mortality rate, especially in patients with diabetes, atherosclerosis or chronic kidney disease (CKD). In CKD patients, VC is associated with the accumulation of uremic toxins, such as indoxyl sulphate or inorganic phosphate, which can have a major impact in vascular remodeling. During VC, vascular smooth muscle cells (VSMCs) undergo an osteogenic switch and secrete extracellular vesicles (EVs) that are heterogeneous in terms of their origin and composition. Under physiological conditions, EVs are involved in cell-cell communication and the maintenance of cellular homeostasis. They contain high levels of calcification inhibitors, such as fetuin-A and matrix Gla protein. Under pathological conditions (and particularly in the presence of uremic toxins), the secreted EVs acquire a pro-calcifying profile and thereby act as nucleating foci for the crystallization of hydroxyapatite and the propagation of calcification. Here, we review the most recent findings on the EVs’ pathophysiological role in VC, the impact of uremic toxins on EV biogenesis and functions, the use of EVs as diagnostic biomarkers and the EVs’ therapeutic potential in CKD.

ACS Style

Linda Yaker; Saïd Kamel; Jérôme Ausseil; Agnès Boullier. Effects of Chronic Kidney Disease and Uremic Toxins on Extracellular Vesicle Biology. Toxins 2020, 12, 811 .

AMA Style

Linda Yaker, Saïd Kamel, Jérôme Ausseil, Agnès Boullier. Effects of Chronic Kidney Disease and Uremic Toxins on Extracellular Vesicle Biology. Toxins. 2020; 12 (12):811.

Chicago/Turabian Style

Linda Yaker; Saïd Kamel; Jérôme Ausseil; Agnès Boullier. 2020. "Effects of Chronic Kidney Disease and Uremic Toxins on Extracellular Vesicle Biology." Toxins 12, no. 12: 811.

Review
Published: 18 June 2020 in Toxins
Reads 0
Downloads 0

Vascular dysfunction is an essential element found in many cardiovascular pathologies and in pathologies that have a cardiovascular impact such as chronic kidney disease (CKD). Alteration of vasomotricity is due to an imbalance between the production of relaxing and contracting factors. In addition to becoming a determining factor in pathophysiological alterations, vascular dysfunction constitutes the first step in the development of atherosclerosis plaques or vascular calcifications. In patients with CKD, alteration of vasomotricity tends to emerge as being a new, less conventional, risk factor. CKD is characterized by the accumulation of uremic toxins (UTs) such as phosphate, para-cresyl sulfate, indoxyl sulfate, and FGF23 and, consequently, the deleterious role of UTs on vascular dysfunction has been explored. This accumulation of UTs is associated with systemic alterations including inflammation, oxidative stress, and the decrease of nitric oxide production. The present review proposes to summarize our current knowledge of the mechanisms by which UTs induce vascular dysfunction.

ACS Style

Isabelle Six; Nadia Flissi; Gaëlle Lenglet; Loïc Louvet; Said Kamel; Marlène Gallet; Ziad A. Massy; Sophie Liabeuf. Uremic Toxins and Vascular Dysfunction. Toxins 2020, 12, 1 .

AMA Style

Isabelle Six, Nadia Flissi, Gaëlle Lenglet, Loïc Louvet, Said Kamel, Marlène Gallet, Ziad A. Massy, Sophie Liabeuf. Uremic Toxins and Vascular Dysfunction. Toxins. 2020; 12 (6):1.

Chicago/Turabian Style

Isabelle Six; Nadia Flissi; Gaëlle Lenglet; Loïc Louvet; Said Kamel; Marlène Gallet; Ziad A. Massy; Sophie Liabeuf. 2020. "Uremic Toxins and Vascular Dysfunction." Toxins 12, no. 6: 1.

Journal article
Published: 17 June 2020 in International Journal of Molecular Sciences
Reads 0
Downloads 0

This study addressed the hypothesis that soluble epoxide hydrolase (sEH), which metabolizes endothelium-derived epoxyeicosatrienoic acids, plays a role in vascular calcification. The sEH inhibitor trans-4-(4-(3-adamantan-1-yl-ureido)-cyclohexyloxy)-benzoic acid (t-AUCB) potentiated the increase in calcium deposition of rat aortic rings cultured in high-phosphate conditions. This was associated with increased tissue-nonspecific alkaline phosphatase activity and mRNA expression level of the osteochondrogenic marker Runx2. The procalcifying effect of t-AUCB was prevented by mechanical aortic deendothelialization or inhibition of the production and action of epoxyeicosatrienoic acids using the cytochrome P450 inhibitor fluconazole and the antagonist 14,15-epoxyeicosa-5(Z)-enoic acid (14,15-EEZE), respectively. Similarly, exogenous epoxyeicosatrienoic acids potentiated the calcification of rat aortic rings through a protein kinase A (PKA)-dependent mechanism and of human aortic vascular smooth muscle cells when sEH was inhibited by t-AUCB. Finally, a global gene expression profiling analysis revealed that the mRNA expression level of sEH was decreased in human carotid calcified plaques compared to adjacent lesion-free sites and was inversely correlated with Runx2 expression. These results show that sEH hydrolase plays a protective role against vascular calcification by reducing the bioavailability of epoxyeicosatrienoic acids.

ACS Style

Olivier Varennes; Romuald Mentaverri; Thomas Duflot; Gilles Kauffenstein; Thibaut Objois; Gaëlle Lenglet; Carine Avondo; Christophe Morisseau; Michel Brazier; Saïd Kamel; Isabelle Six; Jeremy Bellien. The Metabolism of Epoxyeicosatrienoic Acids by Soluble Epoxide Hydrolase Is Protective against the Development of Vascular Calcification. International Journal of Molecular Sciences 2020, 21, 1 .

AMA Style

Olivier Varennes, Romuald Mentaverri, Thomas Duflot, Gilles Kauffenstein, Thibaut Objois, Gaëlle Lenglet, Carine Avondo, Christophe Morisseau, Michel Brazier, Saïd Kamel, Isabelle Six, Jeremy Bellien. The Metabolism of Epoxyeicosatrienoic Acids by Soluble Epoxide Hydrolase Is Protective against the Development of Vascular Calcification. International Journal of Molecular Sciences. 2020; 21 (12):1.

Chicago/Turabian Style

Olivier Varennes; Romuald Mentaverri; Thomas Duflot; Gilles Kauffenstein; Thibaut Objois; Gaëlle Lenglet; Carine Avondo; Christophe Morisseau; Michel Brazier; Saïd Kamel; Isabelle Six; Jeremy Bellien. 2020. "The Metabolism of Epoxyeicosatrienoic Acids by Soluble Epoxide Hydrolase Is Protective against the Development of Vascular Calcification." International Journal of Molecular Sciences 21, no. 12: 1.

Review
Published: 12 September 2019 in Toxins
Reads 0
Downloads 0

Cardiovascular disease (CVD) is an important cause of death in patients with chronic kidney disease (CKD), and cardiovascular calcification (CVC) is one of the strongest predictors of CVD in this population. Cardiovascular calcification results from complex cellular interactions involving the endothelium, vascular/valvular cells (i.e., vascular smooth muscle cells, valvular interstitial cells and resident fibroblasts), and monocyte-derived macrophages. Indeed, the production of pro-inflammatory cytokines and oxidative stress by monocyte-derived macrophages is responsible for the osteogenic transformation and mineralization of vascular/valvular cells. However, monocytes/macrophages show the ability to modify their phenotype, and consequently their functions, when facing environmental modifications. This plasticity complicates efforts to understand the pathogenesis of CVC—particularly in a CKD setting, where both uraemic toxins and CKD treatment may affect monocyte/macrophage functions and thereby influence CVC. Here, we review (i) the mechanisms by which each monocyte/macrophage subset either promotes or prevents CVC, and (ii) how both uraemic toxins and CKD therapies might affect these monocyte/macrophage functions.

ACS Style

Lucie Hénaut; Alexandre Candellier; Cédric Boudot; Maria Grissi; Romuald Mentaverri; Gabriel Choukroun; Michel Brazier; Saïd Kamel; Ziad A. Massy. New Insights into the Roles of Monocytes/Macrophages in Cardiovascular Calcification Associated with Chronic Kidney Disease. Toxins 2019, 11, 529 .

AMA Style

Lucie Hénaut, Alexandre Candellier, Cédric Boudot, Maria Grissi, Romuald Mentaverri, Gabriel Choukroun, Michel Brazier, Saïd Kamel, Ziad A. Massy. New Insights into the Roles of Monocytes/Macrophages in Cardiovascular Calcification Associated with Chronic Kidney Disease. Toxins. 2019; 11 (9):529.

Chicago/Turabian Style

Lucie Hénaut; Alexandre Candellier; Cédric Boudot; Maria Grissi; Romuald Mentaverri; Gabriel Choukroun; Michel Brazier; Saïd Kamel; Ziad A. Massy. 2019. "New Insights into the Roles of Monocytes/Macrophages in Cardiovascular Calcification Associated with Chronic Kidney Disease." Toxins 11, no. 9: 529.

Original research
Published: 22 August 2019 in EJNMMI Research
Reads 0
Downloads 0

Preclinical imaging of endothelial activation and mineralization using both positron emission tomography (PET) and magnetic resonance (MR) remains scarce. A group of uremic ApoE−/− (Ur), non-uremic ApoE−/− (NUr), and control C57Bl/6 J mice (Ctl) were investigated. Mineralization process was assessed using sodium fluoride ([18F]NaF) PET, and MR imaging combined with intravenous injection of MPIO-αVCAM-1 was used to evaluate endothelial activation. Micro- and macrocalcifications were evaluated by flame atomic absorption spectroscopy and von Kossa staining, respectively. Ur mice showed an active and sustained mineralization process compared to Ctl mice (p = 0.002) using [18F]NaF PET imaging. Calcium plasma level was increased in Ur (2.54 ± 0.09 mM, n = 17) compared to NUr and Ctl mice (2.24 ± 0.01, n = 22, and 2.14 ± 0.02, n = 27, respectively; p < 0.0001). Likewise, vascular calcium content was increased in Ur (0.51 ± 0.06 μg Ca2+ per milligram of dry weight aorta, n = 11) compared to NUr (0.27 ± 0.05, n = 9, p = 0.013) and Ctl (0.28 ± 0.05, n = 11, p = 0.014). Ur mice also had a higher inflammatory state using MPIO-αVCAM-1 MR (p global = 0.01, post hoc analysis Ur vs. Ctl p = 0.003) associated with increased VCAM-1 expression (p global = 0.02). Aortic remodeling at the level of the brachiocephalic trunk, brachiocephalic trunk itself, and aortic arch in Ur mice was also demonstrated using MR. Preclinical molecular imaging allowed in vivo characterization of the early phase of atherosclerosis. [18F]NaF PET showed early and sustained vascular mineralization in uremic ApoE−/− mice. MPIO-αVCAM-1 MR imaging demonstrated aortic endothelial activation, predominantly in segments with vascular remodeling.

ACS Style

Guillaume Rucher; on behalf of the STOP-AS investigators; Lucie Cameliere; Jihene Fendri; Antoine Anfray; Ahmed Abbas; Saïd Kamel; Quentin Dupas; Nicolas Delcroix; Ludovic Berger; Alain Manrique. Molecular imaging of endothelial activation and mineralization in a mouse model of accelerated atherosclerosis. EJNMMI Research 2019, 9, 1 -9.

AMA Style

Guillaume Rucher, on behalf of the STOP-AS investigators, Lucie Cameliere, Jihene Fendri, Antoine Anfray, Ahmed Abbas, Saïd Kamel, Quentin Dupas, Nicolas Delcroix, Ludovic Berger, Alain Manrique. Molecular imaging of endothelial activation and mineralization in a mouse model of accelerated atherosclerosis. EJNMMI Research. 2019; 9 (1):1-9.

Chicago/Turabian Style

Guillaume Rucher; on behalf of the STOP-AS investigators; Lucie Cameliere; Jihene Fendri; Antoine Anfray; Ahmed Abbas; Saïd Kamel; Quentin Dupas; Nicolas Delcroix; Ludovic Berger; Alain Manrique. 2019. "Molecular imaging of endothelial activation and mineralization in a mouse model of accelerated atherosclerosis." EJNMMI Research 9, no. 1: 1-9.

Journal article
Published: 01 April 2019 in Journal of Molecular and Cellular Cardiology
Reads 0
Downloads 0

Calcific aortic valve disease (CAVD) is the most common heart valve disease in western countries. It has been reported that activation of the calcium-sensing receptor(CaSR) expressed by vascular smooth muscle cells prevents vascular calcification. However, to date, the CaSR's expression and function in cardiac valves have not been studied. The present study sought to evaluate the presence of the CaSR within human valvular interstitial cells (hVICs), assess the CaSR's functionality, and ascertain its involvement in hVIC calcification. Data from Western blot, flow cytometry and immunocytochemistry experiments demonstrated that primary hVICs express the CaSR. The receptor was functional, since the incubation of hVICs with the calcimimetic R-568 significantly increased Ca2+-induced ERK1/2 phosphorylation, and exposure to the calcilytic NPS2143 reduced ERK1/2 activation. A reduction in endogenous CaSR expression by hVICs (using siRNA) was associated with significantly lower levels of Ca2+-induced mineralization (quantified using Alizarin Red staining). Similar data were obtained after the pharmacological inhibition of CaSR activity by the calcilytic NPS2143. In contrast, overexpression of a functional CaSR amplified Ca2+-induced calcification. Pharmacological activation of the CaSR with the calcimimetic R-568 showed similar effects. CaSR's procalcific properties are associated with increased osteogenic transition (as characterized by elevated mRNA expression of bone morphogenetic protein 2 and osterix), and reduced the expression of the calcification inhibitor osteopontin. Histological analysis of 12 human aortic tricuspid valves showed that CaSR expression was greater in calcified areas than in non-calcified areas. These data were confirmed by Western blots. To the best of our knowledge, this study is the first to have demonstrated that hVICs express a functional CaSR. Taken as a whole, our data suggest that activation of the CaSR expressed by hVICs might be a key promoter of CAVD progression.

ACS Style

Hawraa Issa; Lucie Hénaut; Jeanne Bou Abdallah; Cédric Boudot; Gaëlle Lenglet; Carine Avondo; Aida Ibrik; Thierry Caus; Michel Brazier; Romuald Mentaverri; Kazem Zibara; Saïd Kamel. Activation of the calcium-sensing receptor in human valvular interstitial cells promotes calcification. Journal of Molecular and Cellular Cardiology 2019, 129, 2 -12.

AMA Style

Hawraa Issa, Lucie Hénaut, Jeanne Bou Abdallah, Cédric Boudot, Gaëlle Lenglet, Carine Avondo, Aida Ibrik, Thierry Caus, Michel Brazier, Romuald Mentaverri, Kazem Zibara, Saïd Kamel. Activation of the calcium-sensing receptor in human valvular interstitial cells promotes calcification. Journal of Molecular and Cellular Cardiology. 2019; 129 ():2-12.

Chicago/Turabian Style

Hawraa Issa; Lucie Hénaut; Jeanne Bou Abdallah; Cédric Boudot; Gaëlle Lenglet; Carine Avondo; Aida Ibrik; Thierry Caus; Michel Brazier; Romuald Mentaverri; Kazem Zibara; Saïd Kamel. 2019. "Activation of the calcium-sensing receptor in human valvular interstitial cells promotes calcification." Journal of Molecular and Cellular Cardiology 129, no. : 2-12.

Review
Published: 22 July 2018 in Toxins
Reads 0
Downloads 0

Individuals at all stages of chronic kidney disease (CKD) have a higher risk of developing cognitive disorders and dementia. Stroke is also highly prevalent in this population and is associated with a higher risk of neurological deterioration, in-hospital mortality, and poor functional outcomes. Evidence from in vitro studies and in vivo animal experiments suggests that accumulation of uremic toxins may contribute to the pathogenesis of stroke and amplify vascular damage, leading to cognitive disorders and dementia. This review summarizes current evidence on the mechanisms by which uremic toxins may favour the occurrence of cerebrovascular diseases and neurological complications in CKD.

ACS Style

Maryam Assem; Mathilde Lando; Maria Grissi; Saïd Kamel; Ziad A. Massy; Jean-Marc Chillon; Lucie Hénaut. The Impact of Uremic Toxins on Cerebrovascular and Cognitive Disorders. Toxins 2018, 10, 303 .

AMA Style

Maryam Assem, Mathilde Lando, Maria Grissi, Saïd Kamel, Ziad A. Massy, Jean-Marc Chillon, Lucie Hénaut. The Impact of Uremic Toxins on Cerebrovascular and Cognitive Disorders. Toxins. 2018; 10 (7):303.

Chicago/Turabian Style

Maryam Assem; Mathilde Lando; Maria Grissi; Saïd Kamel; Ziad A. Massy; Jean-Marc Chillon; Lucie Hénaut. 2018. "The Impact of Uremic Toxins on Cerebrovascular and Cognitive Disorders." Toxins 10, no. 7: 303.

Review
Published: 29 May 2018 in Toxins
Reads 0
Downloads 0

Chronic kidney disease (CKD) is associated with profound vascular remodeling, which accelerates the progression of cardiovascular disease. This remodeling is characterized by intimal hyperplasia, accelerated atherosclerosis, excessive vascular calcification, and vascular stiffness. Vascular smooth muscle cell (VSMC) dysfunction has a key role in the remodeling process. Under uremic conditions, VSMCs can switch from a contractile phenotype to a synthetic phenotype, and undergo abnormal proliferation, migration, senescence, apoptosis, and calcification. A growing body of data from experiments in vitro and animal models suggests that uremic toxins (such as inorganic phosphate, indoxyl sulfate and advanced-glycation end products) may directly impact the VSMCs’ physiological functions. Chronic, low-grade inflammation and oxidative stress—hallmarks of CKD—are also strong inducers of VSMC dysfunction. Here, we review current knowledge about the impact of uremic toxins on VSMC function in CKD, and the consequences for pathological vascular remodeling.

ACS Style

Lucie Hénaut; Aurélien Mary; Jean-Marc Chillon; Saïd Kamel; Ziad A. Massy. The Impact of Uremic Toxins on Vascular Smooth Muscle Cell Function. Toxins 2018, 10, 218 .

AMA Style

Lucie Hénaut, Aurélien Mary, Jean-Marc Chillon, Saïd Kamel, Ziad A. Massy. The Impact of Uremic Toxins on Vascular Smooth Muscle Cell Function. Toxins. 2018; 10 (6):218.

Chicago/Turabian Style

Lucie Hénaut; Aurélien Mary; Jean-Marc Chillon; Saïd Kamel; Ziad A. Massy. 2018. "The Impact of Uremic Toxins on Vascular Smooth Muscle Cell Function." Toxins 10, no. 6: 218.

Journal article
Published: 01 May 2018 in Revue Francophone des Laboratoires
Reads 0
Downloads 0

Les tissus cardiovasculaires et osseux sont particulièrement affectés au cours des diabètes. Ainsi le risque cardiovasculaire est multiplié par un facteur 2 à 5 chez le patient diabétique. Les calcifications vasculaires (CV), très fréquentes dans le diabète, représentent un déterminant majeur de ce risque. Les produits terminaux de la glycation des protéines (AGE), résultant de l'hyperglycémie chronique, joue un rôle prépondérant dans leur pathogenèse. L'évaluation des CV est nécessaire pour stratifier le risque cardiovasculaire du patient diabétique. L'exploration fait appel à des méthodes d'imagerie mais également à la mesure au niveau sanguin de plusieurs marqueurs biologiques dont la protéine matricielle GLA (MGP), la fétuine A ou encore le dosage des AGE. Les patients diabétiques présentent également une augmentation du risque de fractures, non expliqué par les variations de la masse osseuse. Des défauts dans la qualité de la trame osseuse ont été évoqués pour expliquer cette augmentation du risque de fractures et les AGE jouent un rôle clé dans ces défauts. L'exploration du remodelage osseux, grâce à la mesure des marqueurs de formation et de résorption osseuse au niveau sanguin, permet de rendre compte, au moins en partie, de la qualité osseuse. L'utilisation de ces marqueurs a permis de montrer que le diabète est un état de bas remodelage osseux. Bone and vascular complications in diabetes Cardiovascular and bone alterations are major complications in diabetes. It is now clearly established that cardiovascular risk is 2- to 5 fold increased in diabetic patients. Vascular calcifications (VC) occurs frequently in diabetes and constitutes an independent risk factor for cardiovascular diseases. Chronic hyperglycemia lead to formation of Advanced Glycation End Products (AGEs) involved in the pathophysiological mechanisms of VC. VC assesment is important to stratify the cardiovascular risk in diabetes. This can be achieved using imaging but also by the measurement of biochemical markers in blood including Matrix Gla Proptein (MGP), Fetuin A and AGEs. Diabetic patients have also an increased risk of fractures that cannot be fully explained by bone mass. A poor bone quality has been evoked to explain this increased risk and AGEs are largely involved in these bone defects. Bone turnover markers, including bone resorption and bone formation markers, represent useful non invasive tools to explore bone quality. Their measurements in several cohorts have demonstrated that diabetes is a state of low bone turnover with lower values in both bone resorption and bone formation markers.

ACS Style

Aurélien Mary; L Said Kamel. Complications vasculaires et osseuses des diabètes. Revue Francophone des Laboratoires 2018, 2018, 56 -64.

AMA Style

Aurélien Mary, L Said Kamel. Complications vasculaires et osseuses des diabètes. Revue Francophone des Laboratoires. 2018; 2018 (502):56-64.

Chicago/Turabian Style

Aurélien Mary; L Said Kamel. 2018. "Complications vasculaires et osseuses des diabètes." Revue Francophone des Laboratoires 2018, no. 502: 56-64.

Review
Published: 01 May 2018 in Seminars in Nephrology
Reads 0
Downloads 0

In chronic kidney disease (CKD), the progressive decrease in renal function leads to disturbances of mineral metabolism that generally cause secondary hyperparathyroidism. The increase in serum parathyroid hormone is associated with reduced serum calcium and calcitriol levels and/or increased serum fibroblast growth factor-23 and phosphate levels. The resulting CKD-associated disorder of mineral and bone metabolism is associated with various other metabolic dysregulations such as acidosis, malnutrition, inflammation, and accumulation of uremic toxins. It favors the occurrence of vascular calcification, which results from an imbalance between numerous inhibitors and promoters of soft-tissue mineralization. This review provides an overview of the most recent state of knowledge concerning the mechanisms that lead to the development of vascular calcification in the CKD setting. It further proposes directions for potential new therapeutic targets.

ACS Style

Lucie Hénaut; Jean-Marc Chillon; Saïd Kamel; Ziad A. Massy. Updates on the Mechanisms and the Care of Cardiovascular Calcification in Chronic Kidney Disease. Seminars in Nephrology 2018, 38, 233 -250.

AMA Style

Lucie Hénaut, Jean-Marc Chillon, Saïd Kamel, Ziad A. Massy. Updates on the Mechanisms and the Care of Cardiovascular Calcification in Chronic Kidney Disease. Seminars in Nephrology. 2018; 38 (3):233-250.

Chicago/Turabian Style

Lucie Hénaut; Jean-Marc Chillon; Saïd Kamel; Ziad A. Massy. 2018. "Updates on the Mechanisms and the Care of Cardiovascular Calcification in Chronic Kidney Disease." Seminars in Nephrology 38, no. 3: 233-250.

Journal article
Published: 18 April 2018 in Annals of Intensive Care
Reads 0
Downloads 0

Bowel ischemia is a life-threatening emergency defined as an inadequate vascular perfusion leading to bowel inflammation resulting from impaired colonic/small bowel blood supply. Main issue for physicians regarding bowel ischemia diagnosis lies in the absence of informative and specific clinical or biological signs leading to delayed management, resulting in a poorer prognosis, especially after cardiac surgery. The aim of the present series was to propose a simple scoring system based on biological data for the diagnosis of bowel ischemia. In a retrospective monocentric study, patients admitted in cardiac ICU, after cardiovascular surgery, were screened for inclusion. According to a 1:2 ratio (case–control), matching between two groups was based on sex, type of cardiovascular surgery, and the operative period (per month). Patients were divided into two groups: “ischemic group” which corresponds to patients with confirmed bowel ischemia and “non-ischemic group” which corresponds to patients without bowel ischemia. Primary objective was the conception of a scoring system for the diagnosis of bowel ischemia. Secondary objectives were to detail the postoperative morbidity and the diagnostic features for the distinction between acute mesenteric ischemia and ischemic colitis. Forty-eight patients (1.3%) had confirmed bowel ischemia (“ischemic group”). According to the 2:1 matching, 96 patients were included in the “non-ischemic group.” Aspartate aminotransferase > 449 UI/L, lactate > 4 mmol/L, procalcitonin > 4.7 μg/L, and myoglobin > 1882 μg/L were found to be independently associated with bowel ischemia. Based on their respective odds ratios, points were assigned to each item ranging from 4 to 8. AUROCC [95% confidence interval] of the scoring system to diagnose bowel ischemia was 0.93 [0.91–0.95], p < 0.001. The optimal threshold after bootstrapping was ≥ 14 points; this yielded a sensitivity of 85.4%, a specificity of 94.8%, a positive likelihood ratio of 16.42, a negative likelihood ratio of 0.15, a Youden’s index of 0.802, and a diagnostic odds ratio of 106.62. A biological scoring system based on PCT, ASAT, lactate, and myoglobin measurement allows the diagnosis of bowel ischemia after cardiac surgery with high accuracy. This score could help clinician to propose an early diagnosis and an early treatment in this high mortality disease.

ACS Style

Elie Zogheib; Cyril Cosse; Charles Sabbagh; Simon Marx; Thierry Caus; Marc Henry; Joseph Nader; Mathurin Fumery; Michael Bernasinski; Patricia Besserve; Faouzi Trojette; Cedric Renard; Pierre Duhaut; Said Kamel; Jean-Marc Regimbeau; Hervé Dupont. Biological scoring system for early prediction of acute bowel ischemia after cardiac surgery: the PALM score. Annals of Intensive Care 2018, 8, 46 .

AMA Style

Elie Zogheib, Cyril Cosse, Charles Sabbagh, Simon Marx, Thierry Caus, Marc Henry, Joseph Nader, Mathurin Fumery, Michael Bernasinski, Patricia Besserve, Faouzi Trojette, Cedric Renard, Pierre Duhaut, Said Kamel, Jean-Marc Regimbeau, Hervé Dupont. Biological scoring system for early prediction of acute bowel ischemia after cardiac surgery: the PALM score. Annals of Intensive Care. 2018; 8 (1):46.

Chicago/Turabian Style

Elie Zogheib; Cyril Cosse; Charles Sabbagh; Simon Marx; Thierry Caus; Marc Henry; Joseph Nader; Mathurin Fumery; Michael Bernasinski; Patricia Besserve; Faouzi Trojette; Cedric Renard; Pierre Duhaut; Said Kamel; Jean-Marc Regimbeau; Hervé Dupont. 2018. "Biological scoring system for early prediction of acute bowel ischemia after cardiac surgery: the PALM score." Annals of Intensive Care 8, no. 1: 46.

Journal article
Published: 11 July 2017 in Nephrology Dialysis Transplantation
Reads 0
Downloads 0

Nephrol Dial Transplant 2017; 32 (5): 870-879. doi: 10.1093/ndt/gfw042

ACS Style

Aurélie Lenglet; Sophie Liabeuf; Najeh El Esper; Sandrine Brisset; Janette Mansour; Anne-Sophie Lemaire-Hurtel; Aurelien Mary; Michel Brazier; Said Kamel; Romuald Mentaverri; Gabriel Choukroun; Albert Fournier; Ziad A. Massy. Efficacy and safety of nicotinamide in haemodialysis patients: the NICOREN study. Nephrology Dialysis Transplantation 2017, 32, 1597 -1597.

AMA Style

Aurélie Lenglet, Sophie Liabeuf, Najeh El Esper, Sandrine Brisset, Janette Mansour, Anne-Sophie Lemaire-Hurtel, Aurelien Mary, Michel Brazier, Said Kamel, Romuald Mentaverri, Gabriel Choukroun, Albert Fournier, Ziad A. Massy. Efficacy and safety of nicotinamide in haemodialysis patients: the NICOREN study. Nephrology Dialysis Transplantation. 2017; 32 (9):1597-1597.

Chicago/Turabian Style

Aurélie Lenglet; Sophie Liabeuf; Najeh El Esper; Sandrine Brisset; Janette Mansour; Anne-Sophie Lemaire-Hurtel; Aurelien Mary; Michel Brazier; Said Kamel; Romuald Mentaverri; Gabriel Choukroun; Albert Fournier; Ziad A. Massy. 2017. "Efficacy and safety of nicotinamide in haemodialysis patients: the NICOREN study." Nephrology Dialysis Transplantation 32, no. 9: 1597-1597.

Research article
Published: 01 July 2017 in Arteriosclerosis, Thrombosis, and Vascular Biology
Reads 0
Downloads 0

Objective— Cardiovascular diseases constitute the leading cause of mortality worldwide. Calcification of the vessel wall is associated with cardiovascular morbidity and mortality in patients having many diseases, including diabetes mellitus, atherosclerosis, and chronic kidney disease. Vascular calcification is actively regulated by inductive and inhibitory mechanisms (including vascular smooth muscle cell adaptation) and results from an active osteogenic process. During the calcification process, extracellular vesicles (also known as matrix vesicles) released by vascular smooth muscle cells interact with type I collagen and then act as nucleating foci for calcium crystallization. Our primary objective was to identify new, natural molecules that inhibit the vascular calcification process. Approach and Results— We have found that oligogalacturonic acids (obtained by the acid hydrolysis of polygalacturonic acid) reduce in vitro inorganic phosphate–induced calcification of vascular smooth muscle cells by 80% and inorganic phosphate–induced calcification of isolated rat aortic rings by 50%. A specific oligogalacturonic acid with a degree of polymerization of 8 (DP8) was found to inhibit the expression of osteogenic markers and, thus, prevent the conversion of vascular smooth muscle cells into osteoblast-like cells. We also evidenced in biochemical and immunofluorescence assays a direct interaction between matrix vesicles and type I collagen via the GFOGER sequence (where single letter amino acid nomenclature is used, O=hydroxyproline) thought to be involved in interactions with several pairs of integrins. Conclusions— DP8 inhibits vascular calcification development mainly by inhibition of osteogenic marker expression but also partly by masking the GFOGER sequence—thereby, preventing matrix vesicles from binding to type I collagen.

ACS Style

Ahmed Hodroge; Eric Trécherel; Marjorie Cornu; Walaa Darwiche; Ali Mansour; Katia Ait-Mohand; Thomas Verissimo; Cathy Gomila; Carole Schembri; Sophie Da Nascimento; Redouan Elboutachfaiti; Agnès Boullier; Emmanuel Lorne; Josiane Courtois; Emmanuel Petit; Sylvestre Toumieux; José Kovensky; Pascal Sonnet; Ziad A. Massy; Saïd Kamel; Claire Rossi; Jérôme Ausseil. Oligogalacturonic Acid Inhibits Vascular Calcification by Two Mechanisms. Arteriosclerosis, Thrombosis, and Vascular Biology 2017, 37, 1391 -1401.

AMA Style

Ahmed Hodroge, Eric Trécherel, Marjorie Cornu, Walaa Darwiche, Ali Mansour, Katia Ait-Mohand, Thomas Verissimo, Cathy Gomila, Carole Schembri, Sophie Da Nascimento, Redouan Elboutachfaiti, Agnès Boullier, Emmanuel Lorne, Josiane Courtois, Emmanuel Petit, Sylvestre Toumieux, José Kovensky, Pascal Sonnet, Ziad A. Massy, Saïd Kamel, Claire Rossi, Jérôme Ausseil. Oligogalacturonic Acid Inhibits Vascular Calcification by Two Mechanisms. Arteriosclerosis, Thrombosis, and Vascular Biology. 2017; 37 (7):1391-1401.

Chicago/Turabian Style

Ahmed Hodroge; Eric Trécherel; Marjorie Cornu; Walaa Darwiche; Ali Mansour; Katia Ait-Mohand; Thomas Verissimo; Cathy Gomila; Carole Schembri; Sophie Da Nascimento; Redouan Elboutachfaiti; Agnès Boullier; Emmanuel Lorne; Josiane Courtois; Emmanuel Petit; Sylvestre Toumieux; José Kovensky; Pascal Sonnet; Ziad A. Massy; Saïd Kamel; Claire Rossi; Jérôme Ausseil. 2017. "Oligogalacturonic Acid Inhibits Vascular Calcification by Two Mechanisms." Arteriosclerosis, Thrombosis, and Vascular Biology 37, no. 7: 1391-1401.

Journal article
Published: 01 May 2017 in Nephrology Dialysis Transplantation
Reads 0
Downloads 0
ACS Style

Lucie Hénaut; François Brazier; Maria Grissi; Maryam Assem; Ziad Massy; Saïd Kamel; Jean-Marc Chillon. MP065CHRONIC RENAL FAILURE WORSENS ISCHEMIC STROKE SIZE AND ALTERS NEUROLOGICAL FUNCTIONS IN MICE. Nephrology Dialysis Transplantation 2017, 32, 1 .

AMA Style

Lucie Hénaut, François Brazier, Maria Grissi, Maryam Assem, Ziad Massy, Saïd Kamel, Jean-Marc Chillon. MP065CHRONIC RENAL FAILURE WORSENS ISCHEMIC STROKE SIZE AND ALTERS NEUROLOGICAL FUNCTIONS IN MICE. Nephrology Dialysis Transplantation. 2017; 32 (suppl_3):1.

Chicago/Turabian Style

Lucie Hénaut; François Brazier; Maria Grissi; Maryam Assem; Ziad Massy; Saïd Kamel; Jean-Marc Chillon. 2017. "MP065CHRONIC RENAL FAILURE WORSENS ISCHEMIC STROKE SIZE AND ALTERS NEUROLOGICAL FUNCTIONS IN MICE." Nephrology Dialysis Transplantation 32, no. suppl_3: 1.

Journal article
Published: 10 April 2017 in Oncotarget
Reads 0
Downloads 0

Osteolytic bone metastases are observed in advanced cases of breast cancer. In vitro data suggest that the activity of the calcium-sensing receptor (CaSR) expressed by metastatic cells could potentiate their osteolytic potential. This study aimed to demonstrate in vivo the involvement of the CaSR in breast cancer cells osteolytic potential and to identify potential targets linked to CaSR activity. MDA-MB-231 stably transfected with plasmids containing either a full-length wild-type CaSR (CaSR-WT), or a functionally inactive dominant negative mutant (CaSR-DN) or an empty vector (EV) were intratibially injected into Balb/c-Nude mice. X-ray analysis performed 19 days after injection showed a dramatic increase of osteolytic lesions in mice injected with CaSR-WT-transfected cells as compared to mice injected with EV- or CaSR-DN-transfected cells. This was associated with decreased BV/TV ratio and increased tumor burden. Epiregulin, an EGF-like ligand, was identified by a DNA microarray as a possible candidate involved in CaSR-mediated osteolysis. Indeed, in vitro, CaSR overexpression increased both epiregulin expression and secretion as compared to EV- or CaSR-DN-transfected cells. Increased epiregulin expression was also detected in osteolytic bone lesions from mice injected with CaSR-WT-transfected MDA-MB-231. In vitro, exposure of osteoblastic cells (HOB and SaOS2) to exogenous epiregulin significantly decreased OPG mRNA expression. Exposure of osteoblastic cells to conditioned media prepared from CaSR-WT-transfected cells also decreased OPG expression. This effect was partially blocked after addition of an anti-epiregulin antibody. Overexpression of a functional CaSR in metastatic breast cancer cells dramatically amplifies their osteolytic potential through epiregulin-mediated OPG downregulation.

ACS Style

Cédric Boudot; Lucie Hénaut; Ursula Thiem; Sandra Geraci; Mariangela Galante; Paulo Saldanha; Zuzana Saidak; Isabelle Six; Philippe Clézardin; Said Kamel; Romuald Mentaverri. Overexpression of a functional calcium-sensing receptor dramatically increases osteolytic potential of MDA-MB-231 cells in a mouse model of bone metastasis through epiregulin-mediated osteoprotegerin downregulation. Oncotarget 2017, 8, 56460 -56472.

AMA Style

Cédric Boudot, Lucie Hénaut, Ursula Thiem, Sandra Geraci, Mariangela Galante, Paulo Saldanha, Zuzana Saidak, Isabelle Six, Philippe Clézardin, Said Kamel, Romuald Mentaverri. Overexpression of a functional calcium-sensing receptor dramatically increases osteolytic potential of MDA-MB-231 cells in a mouse model of bone metastasis through epiregulin-mediated osteoprotegerin downregulation. Oncotarget. 2017; 8 (34):56460-56472.

Chicago/Turabian Style

Cédric Boudot; Lucie Hénaut; Ursula Thiem; Sandra Geraci; Mariangela Galante; Paulo Saldanha; Zuzana Saidak; Isabelle Six; Philippe Clézardin; Said Kamel; Romuald Mentaverri. 2017. "Overexpression of a functional calcium-sensing receptor dramatically increases osteolytic potential of MDA-MB-231 cells in a mouse model of bone metastasis through epiregulin-mediated osteoprotegerin downregulation." Oncotarget 8, no. 34: 56460-56472.

Journal article
Published: 01 March 2017 in Joint Bone Spine
Reads 0
Downloads 0

Our results indicate that CaSR expression in synovial derived monocytes is higher in osteoarthritis than in inflammatory rheumatisms and that CaSR expression is modulated by the nature of the synovial fluid. Given the role played by monocytes in the pathogenesis of chronic rheumatisms, monocytes could be interesting therapeutic targets via the CaSR.

ACS Style

Alice Séjourné; Cédric Boudot; Thibaut Objois; Patrice Fardellone; Michel Brazier; Isabelle Six; Saïd Kamel; Romuald Mentaverri; Vincent Goeb. Expression of the calcium-sensing receptor in monocytes from synovial fluid is increased in osteoarthritis. Joint Bone Spine 2017, 84, 175 -181.

AMA Style

Alice Séjourné, Cédric Boudot, Thibaut Objois, Patrice Fardellone, Michel Brazier, Isabelle Six, Saïd Kamel, Romuald Mentaverri, Vincent Goeb. Expression of the calcium-sensing receptor in monocytes from synovial fluid is increased in osteoarthritis. Joint Bone Spine. 2017; 84 (2):175-181.

Chicago/Turabian Style

Alice Séjourné; Cédric Boudot; Thibaut Objois; Patrice Fardellone; Michel Brazier; Isabelle Six; Saïd Kamel; Romuald Mentaverri; Vincent Goeb. 2017. "Expression of the calcium-sensing receptor in monocytes from synovial fluid is increased in osteoarthritis." Joint Bone Spine 84, no. 2: 175-181.

Journal article
Published: 15 February 2017 in Cardiovascular Diabetology
Reads 0
Downloads 0

Vascular calcification (VC) is common in type 2 diabetes, and is associated with cardiovascular complications. Recent preclinical data suggest that metformin inhibits VC both in vitro and in animal models. However, metformin's effects in patients with diabetic VC have not previously been characterized. The present study investigated the association between metformin use and lower-limb arterial calcification in patients with type 2 diabetes and high cardiovascular risk. The DIACART cross-sectional cohort study included 198 patients with type 2 diabetes but without severe chronic kidney disease. Below-the-knee calcification scores were assessed by computed tomography and supplemented by colour duplex ultrasonography. Data on anti-diabetic drugs were carefully collected from the patients' medical records and during patient interviews. Biochemical and clinical data were studied as potential confounding factors. Metformin-treated patients had a significantly lower calcification score than metformin-free patients (mean ± standard deviation: 2033 ± 4514 and 4684 ± 9291, respectively; p = 0.01). A univariate analysis showed that metformin was associated with a significantly lower prevalence of severe below-the-knee arterial calcification (p = 0.02). VC was not significantly associated with the use of other antidiabetic drugs, including sulfonylureas, insulin, gliptin, and glucagon like peptide-1 analogues. A multivariate logistic regression analysis indicated that the association between metformin use and calcification score (odds ratio [95% confidence interval] = 0.33 [0.11-0.98]; p = 0.045) was independent of age, gender, tobacco use, renal function, previous cardiovascular disease, diabetes duration, neuropathy, retinopathy, HbA1c levels, and inflammation. In patients with type 2 diabetes, metformin use was independently associated with a lower below-the-knee arterial calcification score. This association may contribute to metformin's well-known vascular protective effect. Further prospective investigations of metformin's potential ability to inhibit VC in patients with and without type 2 diabetes are now needed to confirm these results.

ACS Style

Aurélien Mary; Agnes Hartemann; Sophie Liabeuf; Carole Elodie Aubert; Salim Kemel; Joe Elie Salem; Philippe Cluzel; Aurélie Lenglet; Ziad A. Massy; Jean-Daniel Lalau; Romuald Mentaverri; Olivier Bourron; Saïd Kamel. Association between metformin use and below-the-knee arterial calcification score in type 2 diabetic patients. Cardiovascular Diabetology 2017, 16, 24 .

AMA Style

Aurélien Mary, Agnes Hartemann, Sophie Liabeuf, Carole Elodie Aubert, Salim Kemel, Joe Elie Salem, Philippe Cluzel, Aurélie Lenglet, Ziad A. Massy, Jean-Daniel Lalau, Romuald Mentaverri, Olivier Bourron, Saïd Kamel. Association between metformin use and below-the-knee arterial calcification score in type 2 diabetic patients. Cardiovascular Diabetology. 2017; 16 (1):24.

Chicago/Turabian Style

Aurélien Mary; Agnes Hartemann; Sophie Liabeuf; Carole Elodie Aubert; Salim Kemel; Joe Elie Salem; Philippe Cluzel; Aurélie Lenglet; Ziad A. Massy; Jean-Daniel Lalau; Romuald Mentaverri; Olivier Bourron; Saïd Kamel. 2017. "Association between metformin use and below-the-knee arterial calcification score in type 2 diabetic patients." Cardiovascular Diabetology 16, no. 1: 24.

Review
Published: 15 November 2016 in Toxins
Reads 0
Downloads 0

N-methyl-2-pyridone-5-carboxamide (2PY, a major metabolite of nicotinamide, NAM) was recently identified as a uremic toxin. Recent interventional trials using NAM to treat high levels of phosphorus in end-stage renal disease have highlighted new potential uremic toxicities of 2PY. In the context of uremia, the accumulation of 2PY could be harmful—perhaps by inhibiting poly (ADP-ribose) polymerase-1 activity. Here, we review recently published data on 2PY’s metabolism and toxicological profile.

ACS Style

Aurélie Lenglet; Sophie Liabeuf; Sandra Bodeau; Loïc Louvet; Aurélien Mary; Agnès Boullier; Anne Sophie Lemaire-Hurtel; Alexia Jonet; Pascal Sonnet; Said Kamel; Ziad A. Massy. N-methyl-2-pyridone-5-carboxamide (2PY)—Major Metabolite of Nicotinamide: An Update on an Old Uremic Toxin. Toxins 2016, 8, 339 .

AMA Style

Aurélie Lenglet, Sophie Liabeuf, Sandra Bodeau, Loïc Louvet, Aurélien Mary, Agnès Boullier, Anne Sophie Lemaire-Hurtel, Alexia Jonet, Pascal Sonnet, Said Kamel, Ziad A. Massy. N-methyl-2-pyridone-5-carboxamide (2PY)—Major Metabolite of Nicotinamide: An Update on an Old Uremic Toxin. Toxins. 2016; 8 (11):339.

Chicago/Turabian Style

Aurélie Lenglet; Sophie Liabeuf; Sandra Bodeau; Loïc Louvet; Aurélien Mary; Agnès Boullier; Anne Sophie Lemaire-Hurtel; Alexia Jonet; Pascal Sonnet; Said Kamel; Ziad A. Massy. 2016. "N-methyl-2-pyridone-5-carboxamide (2PY)—Major Metabolite of Nicotinamide: An Update on an Old Uremic Toxin." Toxins 8, no. 11: 339.

Journal article
Published: 01 November 2015 in Revue Francophone des Laboratoires
Reads 0
Downloads 0

Par ses implications dans de nombreuses réactions biologiques et son rôle capital dans la structure du squelette, le phosphate apporté par notre alimentation, est indispensable à la vie. La phosphatémie, marqueur de la charge phosphatée de l’organisme, est maintenue dans des limites physiologiques grâce à des systèmes hormonaux agissant de concert sur l’intestin et le rein. L’hyperphosphatémie est considérée aujourd’hui comme un important facteur de risque non-traditionnel, prédictif de la morbi-mortalité cardiovasculaire. Plusieurs études épidémiologiques et expérimentales récentes ont en effet démontré un lien positif entre les concentrations sériques élevées de phosphate et la survenue de différentes maladies cardiovasculaires. Le phosphate, par des effets à la fois directs et indirects, est capable d’accélérer le processus de calcification vasculaire, d’induire une dysfonction endothéliale et une hypertrophie ventriculaire gauche, contribuant ainsi au risque cardiovasculaire. Le lien entre phosphatémie et événements cardiovasculaires a été mis en évidence non seulement dans la maladie rénale chronique, condition pathologique qui s’accompagne fréquemment d’une hyperphosphatémie, mais également, et de façon plus surprenante, dans la population générale, pour laquelle des valeurs de phosphate sérique situées autour de la limite supérieure de la normale, sont également prédictives d’accidents cardiovasculaires. Cette relation n’est pas encore clairement comprise, mais pourrait s’expliquer par l’augmentation constatée au cours de ces dernières années, de l’apport de phosphate inorganique alimentaire, présent dans les aliments transformés contenant des additifs phosphatés. Des stratégies préventives et curatives de l’hyperphosphatémie basées sur des régimes alimentaires ou sur l’utilisation de substances thérapeutiques visant à diminuer l’absorption intestinale des phosphates sont mises en place aujourd’hui, en particulier dans la maladie rénale chronique. De futures études seront encore nécessaires pour préciser le rôle de l’excès de phosphates alimentaires sur le système cardiovasculaire et l’intérêt d’utiliser des stratégies préventives et thérapeutiques dans la population générale. Phosphate is an essential mineral that plays a key role in human body. Phosphatemia, which can reflect the pool of phosphate, is maintained within a normal range thanks to a tight hormonal regulation. Several recent epidemiological and experimental studies have demonstrated that hyperphosphatemia is associated with increased risk of cardiovascular disease and mortality. Indeed, phosphate can exert deleterious effect directly or indirectly on cardiovascular system by accelerating cardiovascular calcification, promoting endothelial dysfunction and left ventricular hypertrophy. The association between phosphate and cardiovascular risk has been found in patients with chronic kidney disease, a pathological condition where hyperphosphatemia is frequent, due to an unbalance in mineral metabolism. More surprisingly, this association has been also established among people without chronic kidney disease. In the general population, studies have reported an increased risk of cardiovascular disease even at modestly elevated phosphatemia. The reason of this association is not yet clear, but could be due to, at least in part, to the increasing dietary intake of phosphate linked to a greater consumption of processed foods with phosphate additives. A better understanding of mechanisms of impaired phosphate metabolism in CKD as well as in the general population would help to clarify the possible role of excess dietary phosphate as a health risk factor.

ACS Style

Haifa Rahabi-Layachi; Isabelle Six; Said Kamel. L’excès de phosphate peut-il s’avérer aussi dangereux pour le système cardiovasculaire que l’excès de cholestérol ? Revue Francophone des Laboratoires 2015, 2015, 27 -34.

AMA Style

Haifa Rahabi-Layachi, Isabelle Six, Said Kamel. L’excès de phosphate peut-il s’avérer aussi dangereux pour le système cardiovasculaire que l’excès de cholestérol ? Revue Francophone des Laboratoires. 2015; 2015 (476):27-34.

Chicago/Turabian Style

Haifa Rahabi-Layachi; Isabelle Six; Said Kamel. 2015. "L’excès de phosphate peut-il s’avérer aussi dangereux pour le système cardiovasculaire que l’excès de cholestérol ?" Revue Francophone des Laboratoires 2015, no. 476: 27-34.