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Desjardins L.,University of Picardie Jules Verne | Desjardins L.,Amiens University Hospital and the Jules Verne University of Picardy | Liabeuf S.,University of Picardie Jules Verne | Liabeuf S.,Amiens University Hospital and the Jules Verne University of Picardy | And 8 more authors.
Toxins | Year: 2013

Immunoglobulin free light chains (FLCs) form part of the middle molecule group of uremic toxins. Accumulation of FLCs has been observed in patients with chronic kidney disease (CKD). The aim of the present study was to measure FLC levels in patients at different CKD stages and to assess putative associations between FLC levels on one hand and biochemical/clinical parameters and mortality on the other. One hundred and forty patients at CKD stages 2-5D were included in the present study. Routine clinical biochemistry assays and assays for FLC kappa (κ) and lambda (λ) and other uremic toxins were performed. Vascular calcification was evaluated using radiological techniques. The enrolled patients were prospectively monitored for mortality. Free light chain κ and λ levels were found to be elevated in CKD patients (especially in those on hemodialysis). Furthermore, FLC κ and λ levels were positively correlated with inflammation, aortic calcification and the levels of various uremic toxins levels. A multivariate linear regression analysis indicated that FLC κ and λ levels were independently associated with CKD stages and β2 microglobulin levels. Elevated FLC κ and λ levels appeared to be associated with mortality. However, this association disappeared after adjustment for a propensity score including age, CKD stage and aortic calcification. In conclusion, our results indicate that FLC κ and λ levels are elevated in CKD patients and are associated with inflammation, vascular calcification and levels of other uremic toxins. The observed link between elevated FLC levels and mortality appears to depend on other well-known factors. © 2013 by the authors; licensee MDPI, Basel, Switzerland. Source


Bourron O.,Diabetes and Metabolic Diseases | Bourron O.,Institute of cardiometabolism and nutrition | Aubert C.E.,Diabetes and Metabolic Diseases | Liabeuf S.,University Pierre and Marie Curie | And 13 more authors.
Journal of Clinical Endocrinology and Metabolism | Year: 2014

Objective: The aim of the study was to investigate whether there is a link between arterial calcification in type 2 diabetes and 1) conventional cardiovascular risk factors, 2) serum RANKL andOPG levels, and 3) neuropathy.Patients and Methods: We objectively scored, in a cross-sectional study, infrapopliteal vascular calcification using computed tomography scanning in 198 patients with type 2 diabetes, a high cardiovascular risk, and a glomerular filtration rate-30 mL/min. Color duplex ultrasonography was performed to assess peripheral arterial occlusive disease, and mediacalcosis. Peripheralneuropathywasdefinedby a neuropathy disability score-6. RANKL and OPG were measured in the serum by routine chemistry.Results: Below-knee arterial calcification was associated with arterial occlusive disease. In multivariate logistic regression analysis, the variables significantly and independently associated with the calcificationscorewereage(oddsratio[OR]=1.08; 95%confidenceinterval [CI] =1.04-1.13; P<.0001), male gender(OR=3.53; 95%CI=1.54-8.08; P=.003), previous cardiovascular disease(OR=2.78; 95%CI=1.39-5.59; P=.005), and neuropathy disability score (per 1 point, OR=1.21; 95% CI=1.05-1.38; P=.006). The association with ln OPG, significantly associated with calcification score in univariate analysis (OR=3.14; 95%CI=1.05-9.40; P=.045), wasnolonger significant in multivariate analysis. RANKLand OPG/RANKL were not significantly associated with the calcification score.Conclusions: Below-knee arterial calcification severity is clearly correlated with peripheral neuropathy severity and with several usual cardiovascular risk factors, but not with serum RANKL level. Source


Rezg R.,French Institute of Health and Medical Research | Barreto F.C.,French Institute of Health and Medical Research | Barreto D.V.,French Institute of Health and Medical Research | Barreto D.V.,Amiens University Hospital and the Jules Verne University of Picardy | And 6 more authors.
Journal of Nephrology | Year: 2011

Vascular calcification is frequent in the general population. Its incidence increases with age. It contributes to cardiovascular morbidity and mortality in patients with advanced atherosclerosis, in the presence or absence of diabetes mellitus and chronic kidney disease (CKD). Both diabetes and CKD aggravate its degree of severity and accelerate its progression. Vascular calcification is the result of both passive and active processes of calcium phosphate deposition in the arterial wall. These processes are more or less successfully opposed by inhibitory proteins and nonpeptidic factors. In the present overview we discuss the roles of several among these vascular calcification inhibitors which represent potential therapeutic targets. © 2011 Società Italiana di Nefrologia. Source


Liabeuf S.,French Institute of Health and Medical Research | Liabeuf S.,Amiens University Hospital and the Jules Verne University of Picardy | Glorieux G.,Ghent University | Lenglet A.,French Institute of Health and Medical Research | And 10 more authors.
PLoS ONE | Year: 2013

Background:Uremic toxins are emerging as important, non-traditional cardiovascular risk factors in chronic kidney disease (CKD). P-cresol has been defined as a prototype protein-bound uremic toxin. Conjugation of p-cresol creates p-cresylsulfate (PCS) as the main metabolite and p-cresylglucuronide (PCG), at a markedly lower concentration. The objective of the present study was to evaluate serum PCG levels, determine the latter's association with mortality and establish whether the various protein-bound uremic toxins (i.e. PCS, PCG and indoxylsulfate (IS)) differed in their ability to predict mortality.Methodology/Principal Findings:We studied 139 patients (mean ± SD age: 67±12; males: 60%) at different CKD stages (34.5% at CKD stages 2-3, 33.5% at stage 4-5 and 32% at stage 5D). A recently developed high-performance liquid chromatography method was used to assay PCG concentrations. Total and free PCG levels increased with the severity of CKD. During the study period (mean duration: 779±185 days), 38 patients died. High free and total PCG levels were correlated with overall and cardiovascular mortality independently of well-known predictors of survival, such as age, vascular calcification, anemia, inflammation and (in predialysis patients) the estimated glomerular filtration rate. In the same cohort, free PCS levels and free IS levels were both correlated with mortality. Furthermore, the respective predictive powers of three Cox multivariate models (free PCS+other risk factors, free IS+other risk factors and free PCS+other risk factors) were quite similar - suggesting that an elevated PCG concentration has much the same impact on mortality as other uremic toxins (such as PCS or IS) do.Conclusions:Although PCG is the minor metabolite of p-cresol, our study is the first to reveal its association with mortality. Furthermore, the free fraction of PCG appears to have much the same predictive power for mortality as PCS and IS do. © 2013 liabeuf et al. Source

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