This page has only limited features, please log in for full access.
Whereas European guidelines recommend adjusting lipid-lowering therapy (LLT) to meet prespecified targets (‘treat-to-target’) for low-density lipoprotein cholesterol (LDL-C), other guidelines do not (‘fire and forget’). In a large observational prospective cohort, we sought to evaluate which strategy could be associated with better cardiovascular outcomes in chronic kidney disease (CKD). In CKD-REIN, patients (CKD stages 3 and 4) on LLT were categorized according to achievement of LDL-C targets for high and very high cardiovascular risk (< 2.6 and < 1.8 mmol/L, respectively) at baseline. Primary outcome was fatal/non-fatal atheromatous cardiovascular disease (CVD). Secondary outcomes were non-atheromatous CVD, atheromatous or non-atheromatous CVD, and major adverse cardiovascular events. The population comprised 1521 patients (68 ± 12 years, 31% women, mean estimated glomerular filtration rate [eGFR] 35 mL/min/1.73 m2). Overall, 523 (34%) met their LDL-C targets at baseline. Median follow-up was 2.9 years (interquartile range 2.2–3.0). Incidence rates per 100 patient-years were 6.2% (95% confidence interval [CI] 5.5–7.0) for atheromatous CVD, 9.2% (8.3–10.1) for non-atheromatous CVD, 15.2% (14.0–16.4) for atheromatous/non-atheromatous CVD, and 6.3% (5.5–7.1) for major adverse cardiovascular events. Corresponding rates in patients who achieved targets were 6.6%, 9.8%, 16.1%, and 6.3%, respectively. Target achievement was not associated with risk of fatal/non-fatal atheromatous CVD (adjusted hazard ratio 1.04, 95% CI 0.76–1.44, p = 0.77) or fatal/non-fatal atheromatous or non-atheromatous CVD (0.98, 0.78–1.23, p = 0.91). These findings do not appear to support a treat-to-target approach in CKD patients on LLT, and may favor the hypothesis of an advantage of fire-and-forget. Randomized trials are needed to confirm this theory.
Ziad A. Massy; Epiphane Kolla; Jean Ferrières; Eric Bruckert; Oriane Lambert; Nicolas Mansencal; Maurice Laville; Luc Frimat; Denis Fouque; Christian Combe; Roberto Pecoits-Filho; Bénédicte Stengel; Sophie Liabeuf; Ckd-Rein Collaborators. Is a treat-to-target approach to lipid-lowering therapy appropriate in patients with chronic kidney disease? A prospective French cohort study. Journal of Nephrology 2021, 1 -11.
AMA StyleZiad A. Massy, Epiphane Kolla, Jean Ferrières, Eric Bruckert, Oriane Lambert, Nicolas Mansencal, Maurice Laville, Luc Frimat, Denis Fouque, Christian Combe, Roberto Pecoits-Filho, Bénédicte Stengel, Sophie Liabeuf, Ckd-Rein Collaborators. Is a treat-to-target approach to lipid-lowering therapy appropriate in patients with chronic kidney disease? A prospective French cohort study. Journal of Nephrology. 2021; ():1-11.
Chicago/Turabian StyleZiad A. Massy; Epiphane Kolla; Jean Ferrières; Eric Bruckert; Oriane Lambert; Nicolas Mansencal; Maurice Laville; Luc Frimat; Denis Fouque; Christian Combe; Roberto Pecoits-Filho; Bénédicte Stengel; Sophie Liabeuf; Ckd-Rein Collaborators. 2021. "Is a treat-to-target approach to lipid-lowering therapy appropriate in patients with chronic kidney disease? A prospective French cohort study." Journal of Nephrology , no. : 1-11.
In end-stage kidney disease, high urea levels promote the carbamylation of lysine side chains on a variety of proteins, including albumin. Albumin carbamylation has been identified as a risk factor for mortality and sevelamer led to a decrease in urea levels in dialysis patients. In the present secondary analysis of the NICOREN trial, we investigated the putative impacts of sevelamer and nicotinamide on albumin carbamylation, and the potential correlation between carbamylation and vascular calcifications. All possible carbamylation of circulating albumin were screened for with high-resolution liquid chromatography-tandem mass spectrometry. Levels of three carbamylated peptides were then measured as a guide to the extent of albumin carbamylation. Carbamylation was measured at baseline in 55 patients included in the NICOREN trial and 29 patients at 24 weeks of treatment. Calcifications on plain radiographs were quantified as the Kauppila score and the Adragao score. Baseline albumin carbamylation was present at three different sites in subjects with end-stage kidney disease. At baseline, we observed only a correlation between urea and the KQTA carbamylation site in these patients. Albumin carbamylation levels did not decrease after 24 weeks of treatment with either sevelamer or nicotinamide. Furthermore, the proportion of carbamylated serum albumin was not correlated with vascular calcification scores in this population. Our results confirmed the presence of carbamylated albumin in patients with end-stage kidney disease and demonstrated the presence of carbamylation beyond the LRVP residues. The results also demonstrated the lack of impact of sevelamer or nicotinamide on albumin carbamylation levels. Therapeutic strategies to lower carbamylation load should probably be focused on direct anti-carbamylation processes and/or potentially anti-inflammatory therapies.
Aurelie Lenglet; Mohamad Ali Rahali; François-Ludovic Sauvage; Sophie Liabeuf; Gabriel Choukroun; Marie Essig; Souleiman El Balkhi; Ziad A. Massy. Effect of Sevelamer and Nicotinamide on Albumin Carbamylation in Patients with End-Stage Kidney Disease. Drugs in R&D 2021, 21, 231 -238.
AMA StyleAurelie Lenglet, Mohamad Ali Rahali, François-Ludovic Sauvage, Sophie Liabeuf, Gabriel Choukroun, Marie Essig, Souleiman El Balkhi, Ziad A. Massy. Effect of Sevelamer and Nicotinamide on Albumin Carbamylation in Patients with End-Stage Kidney Disease. Drugs in R&D. 2021; 21 (2):231-238.
Chicago/Turabian StyleAurelie Lenglet; Mohamad Ali Rahali; François-Ludovic Sauvage; Sophie Liabeuf; Gabriel Choukroun; Marie Essig; Souleiman El Balkhi; Ziad A. Massy. 2021. "Effect of Sevelamer and Nicotinamide on Albumin Carbamylation in Patients with End-Stage Kidney Disease." Drugs in R&D 21, no. 2: 231-238.
The health crisis induced by the pandemic of coronavirus 2019 disease (COVID-19) has had a major impact on dialysis patients in France. The incidence of infection with acute respiratory syndrome coronavirus 2 (SARS-CoV-2) during the first wave of the COVID-19 epidemic was 3.3% among dialysis patients—13 times higher than in the general population. The corresponding mortality rate was high, reaching 21%. As of 19th April, 2021, the cumulative prevalence of SARS-CoV-2 infection in French dialysis patients was 14%. Convergent scientific data from France, Italy, the United Kingdom and Canada show that home dialysis reduces the risk of SARS-CoV-2 infection by a factor of at least two. Unfortunately, home dialysis in France is not sufficiently developed: the proportion of dialysis patients being treated at home is only 7%. The obstacles to the provision of home care for patients with end-stage kidney disease in France include (i) an unfavourable pricing policy for home haemodialysis and nurse visits for assisted peritoneal dialysis (PD), (ii) insufficient training in home dialysis for nephrologists, (iii) the small number of administrative authorizations for home dialysis programs, and (iv) a lack of structured, objective information on renal replacement therapies for patients with advanced chronic kidney disease (CKD). We propose a number of pragmatic initiatives that could be simultaneously enacted to improve the situation in three areas: (i) the provision of objective information on renal replacement therapies for patients with advanced CKD, (ii) wider authorization of home dialysis networks and (iii) price increases in favour of home dialysis procedures.
Guy Rostoker; Belkacem Issad; Hafedh Fessi; Ziad A. Massy. Why and how should we promote home dialysis for patients with end-stage kidney disease during and after the coronavirus 2019 disease pandemic? A French perspective. Journal of Nephrology 2021, 1 -5.
AMA StyleGuy Rostoker, Belkacem Issad, Hafedh Fessi, Ziad A. Massy. Why and how should we promote home dialysis for patients with end-stage kidney disease during and after the coronavirus 2019 disease pandemic? A French perspective. Journal of Nephrology. 2021; ():1-5.
Chicago/Turabian StyleGuy Rostoker; Belkacem Issad; Hafedh Fessi; Ziad A. Massy. 2021. "Why and how should we promote home dialysis for patients with end-stage kidney disease during and after the coronavirus 2019 disease pandemic? A French perspective." Journal of Nephrology , no. : 1-5.
Cardiovascular disease is highly prevalent in patients with chronic kidney disease. Hyperphosphatemia is associated with subclinical atheromatosis in chronic kidney disease. Phosphate-induced endothelial dysfunction and vascular calcification are thought to be key inducers of atherosclerosis in this condition. Zhou et al. now demonstrate that phosphate promotes de novo cholesterol synthesis in vascular smooth muscle and macrophages through increased 3-hydroxy-3-methylglutaryl coenzyme A reductase activation. This observation may change current concepts of atherosclerosis development and management in chronic kidney disease.
Lucie Hénaut; Ziad A. Massy. Phosphate meeting cholesterol—consequences for cardiovascular disease in chronic kidney disease? Kidney International 2021, 99, 1264 -1267.
AMA StyleLucie Hénaut, Ziad A. Massy. Phosphate meeting cholesterol—consequences for cardiovascular disease in chronic kidney disease? Kidney International. 2021; 99 (6):1264-1267.
Chicago/Turabian StyleLucie Hénaut; Ziad A. Massy. 2021. "Phosphate meeting cholesterol—consequences for cardiovascular disease in chronic kidney disease?" Kidney International 99, no. 6: 1264-1267.
Background We investigated 10-year trends in deceased donor kidney quality expressed as the kidney donor risk index (KDRI) and subsequent effects on survival outcomes in a European transplant population. Methods Time trends in the crude and standardized KDRI between 2005 and 2015 by recipient age, sex, diabetic status and country were examined in 24 177 adult kidney transplant recipients in seven European countries. We determined 5-year patient and graft survival probabilities and the risk of death and graft loss by transplant cohort (Cohort 1: 2005–06, Cohort 2: 2007–08, Cohort 3: 2009–10) and KDRI quintile. Results The median crude KDRI increased by 1.3% annually, from 1.31 [interquartile range (IQR) 1.08–1.63] in 2005 to 1.47 (IQR 1.16–1.90) in 2015. This increase, i.e. lower kidney quality, was driven predominantly by increases in donor age, hypertension and donation after circulatory death. With time, the gap between the median standardized KDRI in the youngest (18–44 years) and oldest (>65 years) recipients widened. There was no difference in the median standardized KDRI by recipient sex. The median standardized KDRI was highest in Austria, the Netherlands and the Basque Country (Spain). Within each transplant cohort, the 5-year patient and graft survival probability were higher for the lowest KDRIs. There was no difference in the patient and graft survival outcomes across transplant cohorts, however, over time the survival probabilities for the highest KDRIs improved. Conclusions The overall quality of deceased donor kidneys transplanted between 2005 and 2015 has decreased and varies between age groups and countries. Overall patient and graft outcomes remain unchanged.
Maria Pippias; Vianda S Stel; Miha Arnol; Frederike Bemelman; Stefan P Berger; Jadranka Buturovic Buturovic Ponikvar; Reinhard Kramar; Ángela Magaz; Maurizio Nordio; Hessel Peters-Sengers; Anna Varberg Reisæter; Søren S Sørensen; Ziad A Massy; Kitty J Jager. Temporal trends in the quality of deceased donor kidneys and kidney transplant outcomes in Europe: an analysis by the ERA-EDTA Registry. Nephrology Dialysis Transplantation 2021, 1 .
AMA StyleMaria Pippias, Vianda S Stel, Miha Arnol, Frederike Bemelman, Stefan P Berger, Jadranka Buturovic Buturovic Ponikvar, Reinhard Kramar, Ángela Magaz, Maurizio Nordio, Hessel Peters-Sengers, Anna Varberg Reisæter, Søren S Sørensen, Ziad A Massy, Kitty J Jager. Temporal trends in the quality of deceased donor kidneys and kidney transplant outcomes in Europe: an analysis by the ERA-EDTA Registry. Nephrology Dialysis Transplantation. 2021; ():1.
Chicago/Turabian StyleMaria Pippias; Vianda S Stel; Miha Arnol; Frederike Bemelman; Stefan P Berger; Jadranka Buturovic Buturovic Ponikvar; Reinhard Kramar; Ángela Magaz; Maurizio Nordio; Hessel Peters-Sengers; Anna Varberg Reisæter; Søren S Sørensen; Ziad A Massy; Kitty J Jager. 2021. "Temporal trends in the quality of deceased donor kidneys and kidney transplant outcomes in Europe: an analysis by the ERA-EDTA Registry." Nephrology Dialysis Transplantation , no. : 1.
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.
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 StyleSolène 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 StyleSolène 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.
Background The objectives were to characterize Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) disease 2019 (COVID-19) in patients with acute kidney injury (AKI). Methods Kidney biopsy samples in two Caucasian patients and one African with COVID-19 AKI were investigated. Results All patients had a high-level non-selective glomerular proteinuria. SARS-CoV-2 samples by real-time polymerase chain reaction (RT- PCR) assay were all-negative, as well as for virus particles in the kidney by electron microscopy. The three patients and patients with other AKI did not differ significantly with regard to angiotensin-converting enzyme 2 and transmembrane protease serine 2 kidney staining. Conclusions The kidney damage particularly in Caucasians in COVID-19 seems to be an AKI, possibly by the systemic inflammatory response.
Mathilde Dargelos; Aymeric Couturier; Sophie Ferlicot; Jean-Michel Goujon; Anne-Marie Roque-Afonso; Elyanne Gault; Guy Touchard; Cecile Ory; Sihem Kaaki; Eve Vilaine; Marie Essig; Ziad A Massy. Severe acute respiratory syndrome coronavirus 2 indirectly damages kidney structures. Clinical Kidney Journal 2020, 13, 1101 -1104.
AMA StyleMathilde Dargelos, Aymeric Couturier, Sophie Ferlicot, Jean-Michel Goujon, Anne-Marie Roque-Afonso, Elyanne Gault, Guy Touchard, Cecile Ory, Sihem Kaaki, Eve Vilaine, Marie Essig, Ziad A Massy. Severe acute respiratory syndrome coronavirus 2 indirectly damages kidney structures. Clinical Kidney Journal. 2020; 13 (6):1101-1104.
Chicago/Turabian StyleMathilde Dargelos; Aymeric Couturier; Sophie Ferlicot; Jean-Michel Goujon; Anne-Marie Roque-Afonso; Elyanne Gault; Guy Touchard; Cecile Ory; Sihem Kaaki; Eve Vilaine; Marie Essig; Ziad A Massy. 2020. "Severe acute respiratory syndrome coronavirus 2 indirectly damages kidney structures." Clinical Kidney Journal 13, no. 6: 1101-1104.
Although uremic osteoporosis is a component of mineral and bone disorder in chronic kidney disease, uremic toxin (UT) concentrations in patients with end-stage kidney disease and bone mineral density (BMD) changes after kidney transplantation have not previously been described. We hypothesized that elevated UT concentrations at the time of transplantation could have a negative impact on bone during the early post-transplantation period. Hence, we sought to determine whether concentrations of UTs (trimethylamine-N-oxide, indoxylsulfate, p-cresylsulfate, p-cresylglucuronide, indole-3-acetic acid, hippuric acid, and 3-carboxy-4-methyl-5-propyl-furanpropionic acid) upon transplantation are predictive markers for (i) osteoporosis one month after transplantation, and (ii) a BMD decrease and the occurrence of fractures 12 and 24 months after kidney transplantation. Between 2012 and 2018, 310 kidney transplant recipients were included, and dual-energy X-ray absorptiometry was performed 1, 12, and 24 months after transplantation. The UT concentrations upon transplantation were determined by reverse-phase high-performance liquid chromatography. Indoxylsulfate concentrations upon transplantation were positively correlated with BMD one month after transplantation for the femoral neck but were not associated with osteoporosis status upon transplantation. Concentrations of the other UTs upon transplantation were not associated with osteoporosis or BMD one month after transplantation. None of the UT concentrations were associated with BMD changes and the occurrence of osteoporotic fractures 12 and 24 months after transplantation. Hence, UT concentrations at the time of kidney transplantation were not predictive markers of osteoporosis or fractures.
Benjamin Batteux; Sandra Bodeau; Camille André; Anne-Sophie Hurtel-Lemaire; Valérie Gras-Champel; Isabelle Desailly-Henry; Kamel Masmoudi; Youssef Bennis; Ziad A. Massy; Saïd Kamel; Gabriel Choukroun; Sophie Liabeuf. Association between Uremic Toxin Concentrations and Bone Mineral Density after Kidney Transplantation. Toxins 2020, 12, 715 .
AMA StyleBenjamin Batteux, Sandra Bodeau, Camille André, Anne-Sophie Hurtel-Lemaire, Valérie Gras-Champel, Isabelle Desailly-Henry, Kamel Masmoudi, Youssef Bennis, Ziad A. Massy, Saïd Kamel, Gabriel Choukroun, Sophie Liabeuf. Association between Uremic Toxin Concentrations and Bone Mineral Density after Kidney Transplantation. Toxins. 2020; 12 (11):715.
Chicago/Turabian StyleBenjamin Batteux; Sandra Bodeau; Camille André; Anne-Sophie Hurtel-Lemaire; Valérie Gras-Champel; Isabelle Desailly-Henry; Kamel Masmoudi; Youssef Bennis; Ziad A. Massy; Saïd Kamel; Gabriel Choukroun; Sophie Liabeuf. 2020. "Association between Uremic Toxin Concentrations and Bone Mineral Density after Kidney Transplantation." Toxins 12, no. 11: 715.
Aim To compare patient and graft survival of kidney transplant recipients who received a kidney from a living‐related donor (LRD) or living‐unrelated donor (LUD). Methods Adult patients in the ERA‐EDTA Registry who received their first kidney transplant in 1998‐2017 were included. Ten‐year patient and graft survival were compared between LRD and LUD transplants using Cox regression analysis. Results In total, 14,370 patients received a kidney from a living donor. Of those, 9,212 (64.1%) grafts were from a LRD, 5,063 (35.2%) from a LUD and for 95 (0.7%) the donor type was unknown. Unadjusted five‐year risks of death and graft failure (including death as event) were lower for LRD transplants than for LUD grafts: 4.2% (95% confidence interval [CI]: 3.7‐4.6) and 10.8% (95%CI: 10.1‐11.5) versus 6.5% (95%CI: 5.7‐7.4) and 12.2% (95%CI: 11.2‐13.3), respectively. However, after adjusting for potential confounders, associations disappeared with hazard ratios of 0.99 (95%CI: 0.87‐1.13) for patient survival and 1.03 (95%CI: 0.94‐1.14) for graft survival. Unadjusted risk of death‐censored graft failure was similar, but after adjustment it was higher for LUD transplants (1.19; 95%CI: 1.04‐1.35). Conclusion Patient and graft survival of LRD and LUD kidney transplant recipients was similar, whereas death‐censored graft failure was higher in LUD. These findings confirm the importance of both living kidney donor types.
Samar Abd ElHafeez; Marlies Noordzij; Anneke Kramer; Samira Bell; Emilie Savoye; José Maria Abad Diez; Torbjörn Lundgren; Anna Varberg Reisæter; Julia Kerschbaum; Carmen Santiuste de Pablos; Fernanda Ortiz; Frederic Collart; Runolfur Palsson; Mustafa Arici; James G. Heaf; Ziad A. Massy; Kitty J. Jager. The association of living donor source with patient and graft survival among kidney transplant recipients in the ERA‐EDTA Registry – a retrospective study. Transplant International 2020, 34, 76 -86.
AMA StyleSamar Abd ElHafeez, Marlies Noordzij, Anneke Kramer, Samira Bell, Emilie Savoye, José Maria Abad Diez, Torbjörn Lundgren, Anna Varberg Reisæter, Julia Kerschbaum, Carmen Santiuste de Pablos, Fernanda Ortiz, Frederic Collart, Runolfur Palsson, Mustafa Arici, James G. Heaf, Ziad A. Massy, Kitty J. Jager. The association of living donor source with patient and graft survival among kidney transplant recipients in the ERA‐EDTA Registry – a retrospective study. Transplant International. 2020; 34 (1):76-86.
Chicago/Turabian StyleSamar Abd ElHafeez; Marlies Noordzij; Anneke Kramer; Samira Bell; Emilie Savoye; José Maria Abad Diez; Torbjörn Lundgren; Anna Varberg Reisæter; Julia Kerschbaum; Carmen Santiuste de Pablos; Fernanda Ortiz; Frederic Collart; Runolfur Palsson; Mustafa Arici; James G. Heaf; Ziad A. Massy; Kitty J. Jager. 2020. "The association of living donor source with patient and graft survival among kidney transplant recipients in the ERA‐EDTA Registry – a retrospective study." Transplant International 34, no. 1: 76-86.
Background Chronic kidney disease is associated with a high cardiovascular risk. Compared with glomerular filtration rate–matched CKD patients (CKDps), we previously reported a 2.7-fold greater risk of global mortality among kidney transplant recipients (KTRs). We then examined aortic stiffness [evaluated by carotid–femoral pulse wave velocity (CF-PWV)] and cardiovascular risk in KTRs compared with CKDps with comparable measured glomerular filtration rate (mGFR). Methods We analysed CF-PWV in two cohorts: TransplanTest (KTRs) and NephroTest (CKDps). Propensity scores were calculated including six variables: mGFR, age, sex, mean blood pressure (MBP), body mass index (BMI) and heart rate. After propensity score matching, we included 137 KTRs and 226 CKDps. Descriptive data were completed by logistic regression for CF-PWV values higher than the median (>10.6 m/s). Results At 12 months post-transplant, KTRs had significantly lower CF-PWV than CKDps (10.1 versus 11.0 m/s, P = 0.008) despite no difference at 3 months post-transplant (10.5 versus 11.0 m/s, P = 0.242). A lower occurrence of high arterial stiffness was noted among KTRs compared with CKDps (38.0% versus 57.1%, P < 0.001). It was especially associated with lower mGFR, older age, higher BMI, higher MBP, diabetes and higher serum parathyroid hormone levels. After adjustment, the odds ratio for the risk of high arterial stiffness in KTRs was 0.40 (95% confidence interval 0.23–0.68, P < 0.001). Conclusions Aortic stiffness was significantly less marked in KTRs 1 year post-transplant than in CKDps matched for GFR and other variables. This observation is compatible with the view that the pathogenesis of post-transplant cardiovascular disease differs, at least in part, from that of CKD per se.
Lynda Cheddani; Jean Philippe Haymann; Sophie Liabeuf; Nahid Tabibzadeh; Jean-Jacques Boffa; Emmanuel Letavernier; Marie Essig; Tilman B Drüeke; Michel Delahousse; Ziad A Massy; Francois Vrtovsnik; Eric Daugas; Martin Flamant; Emmanuelle Vidal-Petiot; Christian Jacquot; Alexandre Karras; Eric Thervet; Christian D’Auzac; P Houillier; M Courbebaisse; D Eladari; G Maruani; Pierre Ronco; H Fessi; Eric Rondeau; Marine Livrozet; Camille Saint-Jacques; M Metzger; B Stengel; the NephroTest Study Group. Less arterial stiffness in kidney transplant recipients than chronic kidney disease patients matched for renal function. Clinical Kidney Journal 2020, 14, 1244 -1254.
AMA StyleLynda Cheddani, Jean Philippe Haymann, Sophie Liabeuf, Nahid Tabibzadeh, Jean-Jacques Boffa, Emmanuel Letavernier, Marie Essig, Tilman B Drüeke, Michel Delahousse, Ziad A Massy, Francois Vrtovsnik, Eric Daugas, Martin Flamant, Emmanuelle Vidal-Petiot, Christian Jacquot, Alexandre Karras, Eric Thervet, Christian D’Auzac, P Houillier, M Courbebaisse, D Eladari, G Maruani, Pierre Ronco, H Fessi, Eric Rondeau, Marine Livrozet, Camille Saint-Jacques, M Metzger, B Stengel, the NephroTest Study Group. Less arterial stiffness in kidney transplant recipients than chronic kidney disease patients matched for renal function. Clinical Kidney Journal. 2020; 14 (4):1244-1254.
Chicago/Turabian StyleLynda Cheddani; Jean Philippe Haymann; Sophie Liabeuf; Nahid Tabibzadeh; Jean-Jacques Boffa; Emmanuel Letavernier; Marie Essig; Tilman B Drüeke; Michel Delahousse; Ziad A Massy; Francois Vrtovsnik; Eric Daugas; Martin Flamant; Emmanuelle Vidal-Petiot; Christian Jacquot; Alexandre Karras; Eric Thervet; Christian D’Auzac; P Houillier; M Courbebaisse; D Eladari; G Maruani; Pierre Ronco; H Fessi; Eric Rondeau; Marine Livrozet; Camille Saint-Jacques; M Metzger; B Stengel; the NephroTest Study Group. 2020. "Less arterial stiffness in kidney transplant recipients than chronic kidney disease patients matched for renal function." Clinical Kidney Journal 14, no. 4: 1244-1254.
Objective: Restenosis is a frequent complication of angioplasty. It consists of a neointimal hyperplasia resulting from progression and migration of vascular smooth muscle cells (VSMC) into the vessel lumen. microRNA miR-223 has recently been shown to be involved in cardiovascular diseases including atherosclerosis, vascular calcification and arterial thrombosis. In this study, our aim was to assess the impact of miR-223 modulation on restenosis in a rat model of carotid artery after balloon injury. Methods: The over and down-expression of miR-223 was induced by adenoviral vectors, containing either a pre-miR-223 sequence allowing artificial miR-223 expression or a sponge sequence, trapping the native microRNA, respectively. Restenosis was quantified on stained rat carotid sections. Results: In vitro, three mRNA (Myocyte Enhancer Factor 2C (MEF2C), Ras homolog gene family, member B (RhoB) and Nuclear factor 1 A-type (NFIA)) reported as miR-223 direct targets and known to be implicated in VSMC differentiation and contractility were studied by RT-qPCR. Our findings showed that down-expression of miR-223 significantly reduced neointimal hyperplasia by 44% in carotids, and was associated with a 2-3-fold overexpression of MEF2C, RhoB and NFIA in a murine monocyte macrophage cell line, RAW 264.7 cells. Conclusions: Down-regulating miR-223 could be a potential therapeutic approach to prevent restenosis after angioplasty.
Eleonore M’Baya-Moutoula; Alexandre Marchand; Isabelle Six; Noura Bahrar; Tanja Celic; Nathalie Mougenot; Pierre Maitrias; Ziad A. Massy; Anne-Marie Lompreh; Laurent Metzinger; Valérie Metzinger-Le Meuth. Inhibition of miR-223 Expression Using a Sponge Strategy Decreases Restenosis in Rat Injured Carotids. Current Vascular Pharmacology 2020, 18, 507 -516.
AMA StyleEleonore M’Baya-Moutoula, Alexandre Marchand, Isabelle Six, Noura Bahrar, Tanja Celic, Nathalie Mougenot, Pierre Maitrias, Ziad A. Massy, Anne-Marie Lompreh, Laurent Metzinger, Valérie Metzinger-Le Meuth. Inhibition of miR-223 Expression Using a Sponge Strategy Decreases Restenosis in Rat Injured Carotids. Current Vascular Pharmacology. 2020; 18 (5):507-516.
Chicago/Turabian StyleEleonore M’Baya-Moutoula; Alexandre Marchand; Isabelle Six; Noura Bahrar; Tanja Celic; Nathalie Mougenot; Pierre Maitrias; Ziad A. Massy; Anne-Marie Lompreh; Laurent Metzinger; Valérie Metzinger-Le Meuth. 2020. "Inhibition of miR-223 Expression Using a Sponge Strategy Decreases Restenosis in Rat Injured Carotids." Current Vascular Pharmacology 18, no. 5: 507-516.
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.
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 StyleIsabelle 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 StyleIsabelle 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.
Among patients hospitalized for novel coronavirus disease (COVID-19), between 10 and 14% develop an acute kidney injury and around half display marked proteinuria and haematuria. Post-mortem analyses of COVID-19 kidney tissue suggest that renal tubular cells and podocytes are affected. Here we report two cases of collapsing glomerulopathy and tubulointerstitial lesions in living COVID-19 patients. Despite our use of sensitive reverse transcription polymerase chain reaction techniques in this study, we failed to detect the virus in blood, urine and kidney tissues. Our observations suggest that these kidney lesions are probably not due to direct infection of the kidney by severe acute respiratory syndrome coronavirus 2.
Aymeric Couturier; Sophie Ferlicot; Kévin Chevalier; Matthieu Guillet; Marie Essig; Stéphane Jauréguiberry; Rocco Collarino; Mathilde Dargelos; Alice Michaut; Guillaume Geri; Anne-Marie Roque-Afonso; Mohamad Zaidan; Ziad A Massy. Indirect effects of severe acute respiratory syndrome coronavirus 2 on the kidney in coronavirus disease patients. Clinical Kidney Journal 2020, 13, 347 -353.
AMA StyleAymeric Couturier, Sophie Ferlicot, Kévin Chevalier, Matthieu Guillet, Marie Essig, Stéphane Jauréguiberry, Rocco Collarino, Mathilde Dargelos, Alice Michaut, Guillaume Geri, Anne-Marie Roque-Afonso, Mohamad Zaidan, Ziad A Massy. Indirect effects of severe acute respiratory syndrome coronavirus 2 on the kidney in coronavirus disease patients. Clinical Kidney Journal. 2020; 13 (3):347-353.
Chicago/Turabian StyleAymeric Couturier; Sophie Ferlicot; Kévin Chevalier; Matthieu Guillet; Marie Essig; Stéphane Jauréguiberry; Rocco Collarino; Mathilde Dargelos; Alice Michaut; Guillaume Geri; Anne-Marie Roque-Afonso; Mohamad Zaidan; Ziad A Massy. 2020. "Indirect effects of severe acute respiratory syndrome coronavirus 2 on the kidney in coronavirus disease patients." Clinical Kidney Journal 13, no. 3: 347-353.
Background: Uremic toxins have emerged as potential mediators of morbidity and mortality in patients with chronic kidney disease (CKD). Indole-3-acetic acid (IAA, a tryptophan-derived uremic toxin) might be a useful biomarker in patients with CKD. The objectives of the present study were to (i) describe IAA concentrations in a cohort of non-transplanted patients with CKD and a cohort of transplanted patients with CKD, and (ii) investigate the possible relationship between IAA levels and adverse outcomes in the two cohorts. Methods: Levels of free and total IAA were assayed in the two prospective CKD cohorts (140 non-transplanted patients and 311 transplanted patients). Cox multivariate analyses were used to evaluate the association between IAA levels and outcomes (mortality, cardiovascular events, and graft loss). Results: In the non-transplanted CKD cohort, free and total IAA increased progressively with the CKD stage. In the transplanted CKD cohort, free and total IAA levels were elevated at the time of transplantation but had fallen substantially at one-month post-transplantation. Indole acetic acid concentrations were lower in transplanted patients than non-dialysis non-transplanted patients matched for estimated glomerular filtration rate (eGFR), age, and sex. After adjustment for multiple confounders, the free IAA level predicted overall mortality and cardiovascular events in the non-transplanted CKD cohort (hazard ratio [95% confidence interval]: 2.5 [1.2–5.1] and 2.5 [1.3–4.8], respectively). In the transplanted CKD cohort, however, no associations were found between free or total IAA on one hand, and mortality, CV event, or graft survival on the other. Conclusion: We demonstrated that levels of IAA increase with the CKD stage, and fall substantially, even normalizing, after kidney transplantation. Free IAA appears to be a valuable outcome-associated biomarker in non-transplanted patients, but—at least in our study setting—not in transplanted patients.
Sophie Liabeuf; Solène M. Laville; Griet Glorieux; Lynda Cheddani; François Brazier; Dimitri Titeca Beauport; Raymond Vanholder; Gabriel Choukroun; Ziad A. Massy. Difference in Profiles of the Gut-Derived Tryptophan Metabolite Indole Acetic Acid between Transplanted and Non-Transplanted Patients with Chronic Kidney Disease. International Journal of Molecular Sciences 2020, 21, 2031 .
AMA StyleSophie Liabeuf, Solène M. Laville, Griet Glorieux, Lynda Cheddani, François Brazier, Dimitri Titeca Beauport, Raymond Vanholder, Gabriel Choukroun, Ziad A. Massy. Difference in Profiles of the Gut-Derived Tryptophan Metabolite Indole Acetic Acid between Transplanted and Non-Transplanted Patients with Chronic Kidney Disease. International Journal of Molecular Sciences. 2020; 21 (6):2031.
Chicago/Turabian StyleSophie Liabeuf; Solène M. Laville; Griet Glorieux; Lynda Cheddani; François Brazier; Dimitri Titeca Beauport; Raymond Vanholder; Gabriel Choukroun; Ziad A. Massy. 2020. "Difference in Profiles of the Gut-Derived Tryptophan Metabolite Indole Acetic Acid between Transplanted and Non-Transplanted Patients with Chronic Kidney Disease." International Journal of Molecular Sciences 21, no. 6: 2031.
Vitamin K is a key cofactor for the activation of proteins involved in blood coagulation, apoptosis, bone mineralization regulation, and vessel health. Scientific evidence shows an important role of activated osteocalcin and matrix-Gla protein in bone and vessels, markedly affected along the course of chronic kidney disease (CKD). In fact, CKD corresponds to an unique condition of vitamin K deficiency caused by dietary restriction, intestinal dysfunction, and impaired vitamin K recycling. Clinical data suggest that vitamin K status can be modulated and this prompts us to speculate whether patients with CKD might benefit from vitamin K supplementation. However, as important as whether the improvement in vitamin K status would be able to result in better bone quality, less vascular calcification, and lower mortality rates, several issues need to be clarified. These include better standardized methods for measuring vitamin K levels, and definition of the optimal concentration range for supplementation in different subgroups. Here, we review the literature data concerning the impact of vitamin K deficiency and supplementation on CKD-associated mineral and bone disorders (CKD-MBD). We present and discuss the available evidence from basic science and clinical studies, and highlight perspectives for further research.
Rodrigo Bueno de Oliveira; Andréa Emilia Marques Stinghen; Ziad A. Massy. Vitamin K role in mineral and bone disorder of chronic kidney disease. Clinica Chimica Acta 2019, 502, 66 -72.
AMA StyleRodrigo Bueno de Oliveira, Andréa Emilia Marques Stinghen, Ziad A. Massy. Vitamin K role in mineral and bone disorder of chronic kidney disease. Clinica Chimica Acta. 2019; 502 ():66-72.
Chicago/Turabian StyleRodrigo Bueno de Oliveira; Andréa Emilia Marques Stinghen; Ziad A. Massy. 2019. "Vitamin K role in mineral and bone disorder of chronic kidney disease." Clinica Chimica Acta 502, no. : 66-72.
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.
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 StyleLucie 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 StyleLucie 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.
Chronic kidney disease (CKD) is commonly associated with mineral and bone metabolism disorders, but these are less frequently studied in non-dialysis CKD patients than in dialysis patients. We examined and described international variation in mineral and bone disease (MBD) markers and their treatment and target levels in Stage 3–5 CKD patients. Prospective cohort study of 7658 adult patients with eGFR <60 ml/min/1.73 m2, excluding dialysis or transplant patients, participating in the Chronic Kidney Disease Outcomes and Practice Patterns Study (CKDopps) in Brazil, France, Germany, and the US. CKD-MBD laboratory markers included serum levels of phosphorus (P), calcium (Ca), intact parathyroid hormone (iPTH), and 25-hydroxyvitamin D (25-D). MBD treatment data included phosphate binders and vitamin D (nutritional and active). Nephrologist survey data were collected on target MBD marker levels. Over two-thirds of the patients had MBD markers measured at time intervals in line with practice guidelines. P and iPTH increased and Ca decreased gradually from eGFR 60–20 ml/min/1.73m2 and more sharply for eGFR 5.5 mg/dL, phosphate binder use was 14% to 43% across the four countries. Among patients with PTH >300 pg/mL, use of active (calcitriol and related analogs) vitamin D was 12%–51%, and use of any (active or nutritional) vitamin D was 60%–87%. Although monitoring of CKD-MBD laboratory markers by nephrologists in CKDopps countries is consistent with guidelines, target levels vary notably and prescription of medications to treat abnormalities in these laboratory markers is generally low in these cross-sectional analyses. While there are opportunities to increase treatment of hyperphosphatemia, hyperparathyroidism, and vitamin D deficiency in advanced CKD, the effect on longer-term complications of these conditions requires study.
Sophie Liabeuf; Keith McCullough; Eric W. Young; Ronald Pisoni; Jarcy Zee; Helmut Reichel; Roberto Pecoits-Filho; Friedrich K. Port; Bénédicte Stengel; Philipp A. Csomor; Marie Metzger; Bruce Robinson; Ziad A. Massy. International variation in the management of mineral bone disorder in patients with chronic kidney disease: Results from CKDopps. Bone 2019, 129, 115058 .
AMA StyleSophie Liabeuf, Keith McCullough, Eric W. Young, Ronald Pisoni, Jarcy Zee, Helmut Reichel, Roberto Pecoits-Filho, Friedrich K. Port, Bénédicte Stengel, Philipp A. Csomor, Marie Metzger, Bruce Robinson, Ziad A. Massy. International variation in the management of mineral bone disorder in patients with chronic kidney disease: Results from CKDopps. Bone. 2019; 129 ():115058.
Chicago/Turabian StyleSophie Liabeuf; Keith McCullough; Eric W. Young; Ronald Pisoni; Jarcy Zee; Helmut Reichel; Roberto Pecoits-Filho; Friedrich K. Port; Bénédicte Stengel; Philipp A. Csomor; Marie Metzger; Bruce Robinson; Ziad A. Massy. 2019. "International variation in the management of mineral bone disorder in patients with chronic kidney disease: Results from CKDopps." Bone 129, no. : 115058.
The strengths and the limitations of research activities currently present in Europe are explored in order to outline how to proceed in the near future. Epidemiological and clinical research and public policy in Europe are generally considered to be comprehensive and successful, and the European Renal Association – European Dialysis and Transplant Association (ERA-EDTA) is playing a key role in the field of nephrology research. The Nephrology and Public Policy Committee (NPPC) aims to improve the current situation and translation into public policy by planning eight research topics to be supported in the coming 5 years by ERA-EDTA.
Ziad A Massy; Fergus J Caskey; Patrik Finne; Jerome Harambat; Kitty J Jager; Evi Nagler; Benedicte Stengel; Mehmet Sukru Sever; Raymond Vanholder; Peter J Blankestijn; Annette Bruchfeld; Giovambattista Capasso; Danilo Fliser; Denis Fouque; Dimitrios Goumenos; Maria Jose Soler; Ivan Rychlík; Goce Spasovski; Kathryn Stevens; Christoph Wanner; Carmine Zoccali. Nephrology and Public Policy Committee propositions to stimulate research collaboration in adults and children in Europe. Nephrology Dialysis Transplantation 2019, 34, 1469 -1480.
AMA StyleZiad A Massy, Fergus J Caskey, Patrik Finne, Jerome Harambat, Kitty J Jager, Evi Nagler, Benedicte Stengel, Mehmet Sukru Sever, Raymond Vanholder, Peter J Blankestijn, Annette Bruchfeld, Giovambattista Capasso, Danilo Fliser, Denis Fouque, Dimitrios Goumenos, Maria Jose Soler, Ivan Rychlík, Goce Spasovski, Kathryn Stevens, Christoph Wanner, Carmine Zoccali. Nephrology and Public Policy Committee propositions to stimulate research collaboration in adults and children in Europe. Nephrology Dialysis Transplantation. 2019; 34 (9):1469-1480.
Chicago/Turabian StyleZiad A Massy; Fergus J Caskey; Patrik Finne; Jerome Harambat; Kitty J Jager; Evi Nagler; Benedicte Stengel; Mehmet Sukru Sever; Raymond Vanholder; Peter J Blankestijn; Annette Bruchfeld; Giovambattista Capasso; Danilo Fliser; Denis Fouque; Dimitrios Goumenos; Maria Jose Soler; Ivan Rychlík; Goce Spasovski; Kathryn Stevens; Christoph Wanner; Carmine Zoccali. 2019. "Nephrology and Public Policy Committee propositions to stimulate research collaboration in adults and children in Europe." Nephrology Dialysis Transplantation 34, no. 9: 1469-1480.
Endothelial microparticles (EMPs) are vesicles derived from cell membranes, which contain outsourced phosphatidylserine and express adhesion molecules, such as cadherin, intercellular cell adhesion molecule-1 (ICAM-1), E-selectin, and integrins. EMPs are expressed under physiological conditions and continue circulating in the plasma. However, in pathologic conditions their levels increase, and they assume a pro-inflammatory and pro-coagulant role via interactions with monocytes; these effects are related to the development of atherosclerosis. Chronic kidney dysfunction (CKD) characterizes this dysfunctional scenario through the accumulation of uremic solutes in the circulating plasma, whose toxicity is related to the development of cardiovascular diseases. Therefore, this review aims to discuss the formation of EMPs and their biological effects in the uremic environment. Data from previous research demonstrate that uremic toxins are closely associated with the activation of inflammatory biomarkers, cardiovascular dysfunction processes, and the release of EMPs. The impact of a decrease in circulating EMPs in clinical studies has not yet been evaluated. Thus, whether MPs are biochemical markers and/or therapeutic targets has yet to be established.
Giane Favretto; Regiane Stafim Da Cunha; Maria Aparecida Dalboni; Rodrigo Bueno De Oliveira; Fellype De Carvalho Barreto; Ziad A. Massy; Andréa Emilia Marques Stinghen. Endothelial Microparticles in Uremia: Biomarkers and Potential Therapeutic Targets. Toxins 2019, 11, 267 .
AMA StyleGiane Favretto, Regiane Stafim Da Cunha, Maria Aparecida Dalboni, Rodrigo Bueno De Oliveira, Fellype De Carvalho Barreto, Ziad A. Massy, Andréa Emilia Marques Stinghen. Endothelial Microparticles in Uremia: Biomarkers and Potential Therapeutic Targets. Toxins. 2019; 11 (5):267.
Chicago/Turabian StyleGiane Favretto; Regiane Stafim Da Cunha; Maria Aparecida Dalboni; Rodrigo Bueno De Oliveira; Fellype De Carvalho Barreto; Ziad A. Massy; Andréa Emilia Marques Stinghen. 2019. "Endothelial Microparticles in Uremia: Biomarkers and Potential Therapeutic Targets." Toxins 11, no. 5: 267.
Hyperphosphatemia control is a major issue in hemodialysis patients. Both sevelamer and nicotinamide are prescribed for this purpose. In addition, they exert pleiotropic effects such as an improvement of inflammatory status and potentially enhanced clearance of uremic toxins. In the present secondary analysis of the NICOREN trial, we investigated the impact of sevelamer and nicotinamide on uremic toxins, toxin precursors, and endotoxemia in chronic hemodialysis patients. Circulating uremic toxins (including phenylacetylglutamine, trimethylamine-N-oxide, p-cresyl sulfate, indoxyl sulfate, kynurenine, hippuric acid, indole-3-acetic acid, 3-carboxy-4-methyl-5-propyl-2-furanpropionic acid, kynurenic acid, and p-cresyl glucuronide) and precursors were measured by ultra-performance liquid chromatography-tandem mass spectrometry, and urea, uric acid, phosphate, C-reactive protein, and intact parathyroid hormone by routine biochemistry methods. Serum endotoxin (evaluated by lipopolysaccharide levels) and C-terminal fibroblast growth factor-23 levels were measured using enzyme-linked immunosorbent assay kits. One hundred hemodialysis patients were randomized to receive either nicotinamide or sevelamer treatment. Among them, 63% were male, mean (± standard deviation) age was 65 ± 14 years, 47% had diabetes mellitus, and 51% had a history of cardiovascular disease. In the sevelamer group, but not the nicotinamide group, serum levels of urea, uric acid, and fibroblast growth factor-23 were significantly reduced after 6 months of treatment. The other circulating uremic toxins and toxin precursors remained unchanged in response to either phosphate-lowering agent. Sevelamer treatment led to a marked decrease in serum lipopolysaccharide (p < 0.001) whereas nicotinamide treatment induced an only modest decrease of borderline significance (p = 0.057). There was no change in C-reactive protein levels. In contrast to sevelamer, nicotinamide did not reduce circulating levels of low-molecular-weight uremic toxins other than phosphate, and neither agent reduced circulating uremic toxins of high-molecular-weight or protein-bound toxins. Sevelamer, but not nicotinamide, reduced serum endotoxin levels. Despite no change in serum C-reactive protein, the endotoxin-lowering effect of sevelamer may help to attenuate the inflammatory status of patients with chronic kidney disease.
Aurelie Lenglet; Nicolas Fabresse; Méline Taupin; Cathy Gomila; Sophie Liabeuf; Said Kamel; Jean Claude Alvarez; Tilman B. Drueke; Ziad A. Massy. Does the Administration of Sevelamer or Nicotinamide Modify Uremic Toxins or Endotoxemia in Chronic Hemodialysis Patients? Drugs 2019, 79, 855 -862.
AMA StyleAurelie Lenglet, Nicolas Fabresse, Méline Taupin, Cathy Gomila, Sophie Liabeuf, Said Kamel, Jean Claude Alvarez, Tilman B. Drueke, Ziad A. Massy. Does the Administration of Sevelamer or Nicotinamide Modify Uremic Toxins or Endotoxemia in Chronic Hemodialysis Patients? Drugs. 2019; 79 (8):855-862.
Chicago/Turabian StyleAurelie Lenglet; Nicolas Fabresse; Méline Taupin; Cathy Gomila; Sophie Liabeuf; Said Kamel; Jean Claude Alvarez; Tilman B. Drueke; Ziad A. Massy. 2019. "Does the Administration of Sevelamer or Nicotinamide Modify Uremic Toxins or Endotoxemia in Chronic Hemodialysis Patients?" Drugs 79, no. 8: 855-862.