Here, we report that FhTeg does not induce Th2 immune responses but can induce M2-like phenotype in vivo

that modulates cytokine CHIR-99021 nmr production from CD4+ cells in response to anti-CD3 stimulation. FhTeg induces a RELMα expressing macrophage population in vitro, while in vivo, the expression of Arg1 and Ym-1/2 but not RELMα in FhTeg-stimulated macrophages was STAT6 dependent. To support this finding, FhTeg induces RELMα expression in vivo prior to the induction of IL-13. FhTeg can induce IL-13-producing peritoneal macrophages following intraperitoneal injection This study highlights the important role of FhTeg as an immune-modulatory source during F. hepatica infection and sheds further light on helminth–macrophage interactions. “
“Inflammatory disorders of the peripheral

nervous system (PNS) and central nervous system (CNS) are common, and contribute substantially to physical and emotional disability of affected individuals. Often, the afflicted are young and in their active years. In the past, physicians and scientists often had very little to offer in terms of diagnostic precision and therapeutic effectiveness. During the past two decades, both of these relative shortcomings have clearly improved. Some of the recent developments in clinical neuroimmunology are illustrated in this special edition of Clinical and Experimental Immunology. “
“Citation Karata S, Aydin Y, Ocer F, Buyru A, Balci H. Hereditary Thrombophilia, anti-beta2 glycoprotein 1 IgM, and anti-annexin V antibodies in recurrent pregnancy loss. Am J Reprod Immunol 2012; 67: 251–255 Problem selleck chemicals llc We investigated the beta2-glycoprotein I and anti-annexin V antibodies as anti-phospholipid–cofactor antibodies; and factor V G1691A Leiden, prothrombin G20210A, and methylenetetrahydrofolate

reductase else (MTHFR) C677T mutations as hereditary thrombophilia in recurrent pregnancy losses (RPL). Method of study Study group consisted of 84 women with recurrent pregnancy loss and control group consisted of 84 women having at least one live birth. Results Methylenetetrahydrofolate reductase C677T homozygous mutation was detected in 28.5% of the study group and in 14.2% of the controls, and the difference was highly significant (P < 0.001). Heterozygous mutation of this gene was found in 64.3% of the study population and in 38.1% of the controls, and difference in heterozygous mutation frequency was also significant (P < 0.001). Both homozygous and heterozygous mutations of PT G20210A and factor V G1691A were not different between the groups. There was no significant difference in anti-annexin V levels and anti-beta2-gp 1 levels of the groups. Conclusion We concluded that both homozygous and heterozygous mutations of MTHFR C677T were related with RPL in Caucasian women. "
“Studies have shown the IL-17A involvement in human ischemic stroke patients in vivo. Whether the IL-17A expression was originated from Th17 and could be stimulated by hypoxia remained unknown.

Strips were rinsed briefly with 25% 1.5 M pH 8.0 Tris before SDS–PAGE was performed using Criterion 12.5% Tris-HCl Precast gels (Bio-Rad), run at 200 V for approximately 45 min. For each sample, two gels were run simultaneously, one for silver staining and another for

immunoblotting. Gels for silver staining were fixed individually in 0.1 L fixing solution [50% (v/v) methanol, 10% (v/v) acetic acid] for CT99021 solubility dmso a minimum of 1 h, and were subsequently stained using a sensitive ammoniacal silver method based on silver nitrate. Gel images were acquired using the UMAX Powerlook 1000 flat-bed scanner. Proteins from unstained gels were transferred electrophoretically onto polyvinylidene fluoride (PVDF) membranes using the Trans-blot cell transfer system (Bio-Rad Laboratories). ABT-737 mw To visualize total proteins, membranes were stained with a Sypro Ruby blot stain (Bio-Rad

Laboratories). To detect immunoreactive proteins, membranes were destained and subsequently probed according to the Immun-Star™ WesternC™ kit protocol (Bio-Rad Laboratories). Membranes were immunolabeled with patients’ sera at a 1 : 250 dilution, and goat anti-human IgG antibodies coupled to HRP (1 : 2000; Bio-Rad) were used as a secondary antibody. The immunoreactive protein spots matched using both the Sypro Ruby stained membrane and the silver-stained gels were identified by liquid chromatography–tandem mass spectrometry (LC–MS/MS). Briefly, spots were washed twice for 10 min in 200 μL of 100 mM NH4HCO3, reduced at 37 °C for 1 h with 50 μL of 10 mM DTT, alkylated for 1 h in 50 μL of 10 mM iodoacetamide, washed for 10 min with 200 μL of 10 mM NH4HCO3, dehydrated in acetonitrile, and trypsin-digested with 10 ng μL−1 of trypsin (Promega, Annandale, NSW, Australia). After digestion for 14 h at 37 °C, peptides were extracted by washing the gel slice for 15 min with 25 μL 1% formic acid, followed by dehydration in acetonitrile. Digests were then dried in vacuo, resuspended in 10 μL 1% formic acid and submitted for

a Quadrupole-TOF analysis on a Micromass instrument which generated collision-induced dissociation. Results were analyzed using the Mascot MS/MS ion search (Matrix Science, Boston, MA), and searches were performed on the National Centre for Biotechnology all Information non-redundant (NCBI nr) database (specifically against the available genome sequence of C. concisus BAA-1457). This study was approved by the Research Ethics Committees of the University of New South Wales and the South East Sydney Area Health Service-Eastern Section, Sydney (Ethics No.: 03/163, 03/165 and 06/164). Recently, an association between the presence of C. concisus DNA and newly diagnosed CD was reported in two case–control studies using intestinal biopsies and fecal samples (Zhang et al., 2009; Man et al., 2010c). In addition, significantly higher levels of C. concisus-specific IgG antibodies were detected in children with CD as compared with controls (Zhang et al.

4 mM of AC-

or BC-primer and 0.4 mM of AV- or BV-specific primer. After an initial denaturation step of 10 min at 94°C, the reactions were subjected to 40 cycles of PCR (94°C buy Dorsomorphin for 30 s, 58°C for 40 s, 72°C for 50 s), followed by a final extension step of 5 min at 72°C. Runoff products were purified using Sephadex gel and filter plates (Multiscreen, Millipore, Billerica, MA, USA) before they were sequenced using fluorescent chain-terminating inhibitors (BigDye Terminator v1.1 kit) and an automated capillary sequencer (ABI Prism 3700 DNA Analyzer, Applied Biosystems). CDR3α and CDR3β definitions as well as AV and BV nomenclature are according to IMGT (http://imgt.cines.fr). Cytokines were selected for cluster analysis on the basis of their recognized contribution to characterize both known and potential CD4+ T-cell subsets. Cytokine secretion levels of PMA and calcium ionophore-activated CD4+ T cells were determined ex vivo at the single-cell level using a BD LSRII apparatus. Fluorescence intensity values were directly extracted from the corresponding Flow Cytometry Standard (FCS) files

using Flow Cytometry Standard Extract Utility (Earl F. Glynn, Stowers Institute for Medical Research, KS, USA) and analyzed using Ward’s method (see below). T-cell clone clustering was based on cytokine ELISA measurements in culture supernatants. In that case, the molar concentration of each cytokine measured was expressed as the percentage of the six measured cytokines produced by a given

Romidepsin chemical structure T-cell clone and normalized in order to express results independently of their measurement scale. Agglomerative hierarchical cluster analysis according to Ward’s 46 was performed using Protirelin the JMP7 software (SAS Software, NC, USA). The optimal number of clusters was identified according to the largest distance change between successive junctions of the dendrogram plot. Validity and reproducibility of the classification obtained with hierarchical cluster analysis was assessed using non-hierarchical k-means cluster analysis, in which the optimal number of clusters identified through hierarchical cluster analysis was pre-specified. Reproducibility of the classifications obtained with both hierarchical and non-hierarchical clustering was assessed by determination of the kappa value. Differences between groups and clusters were tested using Mann-Whitney U-test (unpaired), Wilcoxon signed rank test (paired) and Kruskal-Wallis test. All tests were two-sided and a p-value <0.05 was considered statistically significant. This study was supported by Inserm, by the Centre d’Investigations Biologiques (C.I.B.) Pitié-Salpêtrière, by the Université Pierre et Marie Curie “EMERGENCE” program and by the European FP6 “ATTACK” program (Contract: LSHC-CT-2005-018914).Authorship contributions: M.L., M.H., D.D., C.P., J.P., K.D., M.S. and D.S. performed research, J.P., H.Y., and L.A. contributed vital new reagents and analytical tool, S.B., M.K. and Z.A.

The individual

parameters were scored from 1 to 3, and a cumulative score between 0 and 19 was recorded for each biopsy. The observer was blinded (J.H.E). Values are expressed as the mean ± 2 SD. To compare the treatment group with controls, we used the Mann–Whitney U-test. To evaluate the differences between before treatment, during and after treatment, the normality of each type of measurement was evaluated using a KS test based on the residuals from a simple linear model using patient and time as factors. In no case was normality close to being rejected (P > 0.4 in all cases). Hence, one-way repeated-measures anova was used. However, to evaluate the differences between the two treatment groups, two-way repeated-measures anova was used. Three patients who received combined treatment were not evaluated at week 8 because they had started another psoriasis Selleckchem 3 MA treatment due to exacerbations: two of those patients at week 4 (Fig. 1A; BL3 and BL6) and one patient at week 7 (Fig. 1A; BL1). For these patients, PASI buy RG7204 evaluation was made at the time point their study participation was terminated, and they were not included

in the analysis at week 8. All measurements were taken using sigmastat 3.1 (Systat Software, San Jose, CA, USA). A P-value ≤ 0.05 was considered statistically significant. In order to evaluate whether clinical improvement of psoriasis following bathing in geothermal seawater combined with NB-UVB and NB-UVB alone is preceded by changes in systemic inflammatory markers, the clinical efficacy of each treatment regimen was evaluated first. As shown in Fig. 1C, both treatment regimens demonstrated significant clinical improvements. Furthermore, the data suggested that patients receiving combined treatment Histone demethylase demonstrated better clinical response, measured by the PASI score, than patients treated only with NB-UVB. This was seen both

after one week (% improvement: combined treatment 37.3 ± 10.3 versus NB-UVB treatment 18.3 ± 8.9, P < 0.05) and after three weeks (67.3 ± 11.9 versus 22.0 ± 12.0, P < 0.0001). However, this was not the main aim of the study, and larger cohort and another control group would be needed to fully address this interesting observation. Interestingly, bathing in the Blue Lagoon immediately following skin punch biopsy resulted in no infections and only minor skin irritation resolving in few days. In addition, the above clinical findings were confirmed by the histological Trozak’s score where patients in both treatment groups showed a significant histological improvement at week 3 (Trozak’s score: BL treatment = 10.3 ± 5.5 versus NB-UVB treatment = 8.0 ± 4.6; Fig. 2).

The relative importance of such conformational changes for selection of the CD4 T-cell repertoire is not known but a recent study by Nabel and colleagues suggests that different vaccine vectors Kinase Inhibitor Library datasheet carrying identical proteins can generate peptides with alternative conformations within

MHC class I molecules and elicit distinct T-cell responses after vaccination.66 Understanding the mechanisms of immune protection after vaccination is central to the rational design of all future vaccines. Vaccine adjuvants, a central component of protein subunit vaccines, have been traditionally optimized based on their capacity to increase the magnitude of the adaptive immune response. It is, however,

clear that adjuvants also control some more qualitative aspects of the immune response that could play an important role in determining vaccine efficacy, such as the specificity and clonotypic diversity of the responding CD4 T-cell compartment. A precise understanding of the mechanisms by which vaccine adjuvants modulate the immune repertoire of the adaptive immune response should lead, in the future, to the development of improved vaccines. The authors Atezolizumab manufacturer have nothing to disclose. This work was supported by NIH grant U19 A162627, the American Cancer Society and the Medical College of Wisconsin Cancer Center. C.B. was supported by a fellowship from FWF – the Austrian Science Fund. “
“Regulatory T cells (Tregs) are known to play an immunosuppressive role in the response of contact hypersensitivity (CHS) but

neither the dynamics of Tregs during the CHS response nor the exaggerated inflammatory response after depletion of Tregs has been characterized in details. In this study we show that the number of Tregs in the challenged tissue peak at the same time as the ear swelling reaches its maximum day 1 after challenge whereas the number of Tregs in the draining lymph nodes peaks at day 2. As expected, depletion of Tregs by injection of a monoclonal antibody to CD25 prior to sensitization, led to a prolonged 3-mercaptopyruvate sulfurtransferase and sustained inflammatory response which was dependent on CD8 T cells, and co-stimulatory blockade with CTLA4-Ig suppressed the exaggerated inflammation. In contrast, blockade of the IL-10-receptor (IL-10R) did not further increase the exaggerated inflammatory response in the Treg-depleted mice. In the absence of Tregs, the response changed from a mainly acute reaction with heavy infiltration of neutrophils to a sustained response with more chronic characteristics (fewer neutrophils and dominated by macrophages).

2 μg/mL phytohemagglutinin (PHA) and supplemented with 10 per cent foetal calf serum (Gibco, Eggenstein, Germany). Cell viability was 95 percent by the trypan blue exclusion test as described by Ribeiro DA et al. (17). The plate cultures of anaerobic group were incubated in sealed jars under an anaerobic environment produced by the method of Marshall (18). The RPMI 1640 medium cultured PBMC in 12 well plates of aerobic control groups were incubated in 5 per cent CO2 at 37°C. Samples of negative control group were cultured without PHA stimulation. At 6 hr and 24 hr hypoxia interference, 1 μg/mL Brefeldin A were added into culture wells and incubated

for 4 hr. The culture contents were then transferred into tubes and SAHA HDAC clinical trial centrifuged. The culture supernatants were removed and stored at −80°C until assay, while the remaining PBMC were resuspended at a concentration of 1 × 106 cells/mL for FACS. Prepared PBMC (100 μL) were stained for surface markers with 20 μL APC antihuman CD4 for 20 min at 4°C, washed twice with the staining buffer and fixed with 100 μL fixation buffer for 30 min at 4°C. After being permeabilized

with 1 mL permeabilization buffer for 30 min at 4°C, cells were then stained with 20 μL FITC antihuman IL-17A or FITC Omipalisib datasheet antihuman IFN-γ for 30 min at 4°C. Cells were washed twice in permeabilizing solution, suspended with 0.5 mL staining buffer, and finally measured on a FACS Aria Cell Sorter (BD Biosciences Pharmingen Inc., San Diego, CA, USA). Isotype-matched monoclonal antibody were

used as controls. Purified APC-CD4 and FITC-IL-17A (or IFN-γ) double-positive lymphocytes were used as positive controls. The levels of IL-1β, IFN-γ, IL-23 and IL-17A protein in collected supernatants were double evaluated with commercially available ELISA kits following the procedures suggested by the manufacturer. The concentration of chemokines was determined spectrophotometrically. The absorbance was read at 450 nm. The assay sensitivity Bumetanide was less than 1 pg/mL. For each data group, results are expressed as means ± standard error of the mean and n refers to the number of independent experiments. Statistical analysis was performed using Student’s t-test (SPSS ver. 13.01). For statistical analysis, each treatment was compared with its respective control, and differences were considered significant at *P < 0.05, **P < 0.01 and ***P < 0.001. All Th1/Th17 ratios were obtained by FACS method and typical results are shown in Figure 1. Both Th1 and Th17 ratios presented upregulation after ischemia stimulation in SCI group but not in other groups. Th17 ratios peaked at 6 hr (mean 10.9%, n= 10) and diminished at 24 hr (mean 7.

With regard to treatment, surgical resection or percutaneous techniques such as ethanol injection

and radiofrequency ablation are considered to be choices for the curable treatment of localized HCC, whereas transarterial chemo-embolization is a well-established technique for more advanced HCC [3]. www.selleckchem.com/screening/pi3k-signaling-inhibitor-library.html Recently the Sorafenib Hepatocellular carcinoma Assessment Randomized Protocol (SHARP) trial has demonstrated that sorafenib, a multi-targeting kinase molecule that inhibits receptor tyrosine kinases [vascular endothelial growth factor receptor (VEFGR)-2, VEGFR-3, Flt ligand (Flt)-3, platelet-derived growth factor receptor beta (PDGFR) and fibroblast growth factor receptors (FGFR)-1] as well as Raf serine–threonine kinase in the signal transduction, is effective for prolonging median survival and time-to-progression in patients with advanced HCC [4]. The liver contains a large compartment of innate immune cells [natural killer (NK) cells and NK T cells] and acquired immune cells (T cells) [5,6]. However, what remain unclear are the details of the activation of these immune cells in the process of HCC development. If the mechanism of tumour surveillance drug discovery by immune cells in HCC development can be elucidated, this could lead to the establishment

of new strategies for HCC treatment. α-Fetoprotein (AFP), a glycoprotein of molecular mass 68–72 kDa, is a tumour-associated antigen in HCC and a target for immunotherapy [7]. Measurement of serum levels of AFP is important for the diagnosis of HCC and monitoring of treatment [8]. Recently, several biological properties of AFP have been identified in its regulatory effects on immune responses [9–13]. AFP induces the suppression of cytotoxic T lymphocytes (CTLs) activity and antibody responses of B lymphocytes [9–11]. Alisa et al. demonstrated that AFP may contain specific epitopes which activate the expansion of inducible transforming

growth factor (TGF)-β producing regulatory T cells, leading to evasion of tumour control [12]. Antigen-presenting cells (APCs) of HCC patients with high levels of AFP are dysfunctional, and AFP impairs dendritic cell (DC) function and induces their apoptosis [13]. However, the biological role of AFP on innate N-acetylglucosamine-1-phosphate transferase immune responses still remains unclear. In this study, we investigated the immunoregulation of NK activity and DC function by AFP. We demonstrate that AFP impairs NK activity via inhibition of interleukin (IL)-12 production from DCs. The present study sheds light on previously unrecognized immunological effects of AFP on NK cells, and thus suggests a role of AFP in HCC development. Cell culture was maintained in a medium (RPMI-1640 medium supplemented with 10% heat-inactivated fetal bovine serum, 100 U/ml penicillin, 100 ug/ml streptomycin and 10 mM l-glutamine: all reagents from Gibco /Life Technologies, Grand Island, NY, USA) in a humidified incubator at 5% CO2 and 37°C.

XLA patients had significantly reduced putative follicular T cells, which may depend on B cells for survival, while no significant alterations were observed in the T cells of those with IgG subclass deficiency or selective IgA deficiency. Common variable immunodeficiency disorders (CVID) are heterogeneous conditions that make up the most common group of clinically significant primary antibody deficiency (PAD). Patients with CVID are characterized by increased susceptibility to recurrent bacterial infection, coupled with low serum immunoglobulin levels and reduced specific antibody

Selleckchem Buparlisib production in response to vaccination [1]. Patients may also have numerous clinical complications, including enteropathy, lymphoid malignancy, granuloma and autoimmunity, which Selleck FDA approved Drug Library have been used recently to classify patients into clinical phenotypes with varying prognoses [2,3]. CVID probably represent a polygenic group of primary antibody deficiency disorders of unknown aetiology [4]. Other PADs include X-linked agammaglobulinaemia (XLA), immunoglobulin (Ig)G subclass deficiency and selective IgA deficiency. Patients with XLA are profoundly antibody and B cell-deficient, and therefore experience recurrent bacterial infections [5]. However, they do not encounter the other clinical complications, common to many CVID patients, which are thought to

relate to the underlying immune dysregulation. There have been suggestions that partial antibody deficiencies, in particular selective IgA deficiency, may share a genetic basis with some types of CVID [6]. This is supported by reports of progression of selective IgA deficiency to CVID in rare patients [6]. Patients with CVID have

a common feature in failure of B cell function, although a number of T cell abnormalities have been described, including reduced naive CD4 T cells [7], reduced proliferative responses to mitogens [8,9], reduced cytokine responses to mitogens and recall antigen [10,11] and reduced T regulatory cells (Tregs) [12–14] in selected patients. A subset of CVID patients are reported to have an increased susceptibility to recurrent viral infections or opportunistic infections that are more associated with T cell defects [7,15], particularly in those patients from consanguineous families [16], suggesting an unknown, autosomal recessive, combined immune very deficiency. Upon antigen encounter, naive T cells undergo a developmental pathway, resulting in the generation of central memory and effector memory T cells [17]. They can be measured in blood by use of the accepted markers, CCR7 and CD45RA [18]. In the early stages of differentiation, T cells express high levels of co-stimulatory molecules CD28 and CD27, which are lost sequentially upon differentiation [19,20]. CD31 and CD45RA co-expression is used to define recent thymic emigrants and correlates well with T cell receptor excision circle (TREC) levels [21].

falciparum-infected groups. Plasma concentrations of CXCL16 in NEG patients were 2930 pg/ml (mean) and the levels were enhanced in those with P. falciparum, to 5160 pg/ml in MM and 8840 pg/ml in SM cases. CXCL9 and CXCL16 levels were clearly higher (P < 0·0001) in SM than in NEG, and CXCL9 levels in SM were higher than those of MM patients (P < 0·0001). At 48–60 h post-anti-malarial treatment (Fig. 3), significantly diminished cytokine concentrations were detected for IL-10, IL-13 and the

chemokines MIG/CXCL9, CXCL16 and MIP-3α/CCL20 (not shown). The mean levels of IL-17F, BMN-673 IL-27, IL-31 and IL-33 did not change at 48–60 h post-anti-malaria treatment and with reduced parasitaemia. In P. falciparum-infected infants, the levels of MIP3-α/CCL20 (r2 = 0·28; P = 0·0002) and MIG/CXCL9 (r2 = 0·33, P = 0·0005) were correlated positively with parasite density, while IL-27 displayed a weak negative correlation (r2 = −0·17; P = 0·01). Naturally acquired protective immunity against malaria requires subclass-specific antibody responses [16–18], and the secretion of cytokines, chemokines and further immune mediators is essential for the regulation both of cellular effector mechanisms against P. falciparum blood-stage parasites and of organ-specific inflammation and pathogenesis [19,20]. In MM and SM infants substantial cytokine Trametinib and chemokine levels were detected, which disclosed

both innate and memory immune responsiveness. The first parasite encounter and sensitization to P. falciparum antigens may already occur prenatally and continue in infants shortly after birth [21]. P. falciparum infection during pregnancy is a major health problem in our study area [22,23], and prenatal and early life contact with plasmodial antigens has to be considered as a regularity. In infants, antibody responses and pronounced parasite-specific IL-10 production were found to be associated with faster P. falciparum parasite clearance [24], and the higher longevity of regulatory T cell

(Treg)-type IL-10 compared to Th1-type IFN-γ responses [25] suggested that prenatal and early postnatal sensitization with P. falciparum antigens has occurred [26,27]. It is noteworthy that parasite-specific AMP deaminase IL-10 responses were observed frequently and of high magnitude in umbilical cord blood cells from newborns of infected mothers [21–23,28]. In the present work, plasma IL-10 levels were not correlated with parasite densities or the infants’ age, and this further supported early life P. falciparum-specific immune sensitization and IL-10 induction. The role of IL-10 in malaria pathogenesis is controversial. High IL-10 levels were associated with cerebral malaria [13], with high parasite density and severe disease in children [29,30], while lower plasma concentrations of IL-10 occurred in those with severe malarial anaemia [13,30].

4 vs 15.5 days) at dialysis initiation were higher in the usual care group. Estimated medical costs during 3 months before dialysis till dialysis initiation, the MDC group yielded a reduction of NT$ 59 251 for each patient (P < 0.001). Patient mortality was not significantly different. Multidisciplinary care intervention for pre-ESRD patients could not only significantly improve the quality of disease care and clinical outcome, but also reduce medical costs. "
“Date written: December 2008 Final submission: March 2009 No recommendations possible selleck inhibitor based on Level I or II evidence (Suggestions

are based on Level III and IV evidence) Registry data and data from observational cohort studies suggest that coexisting vascular disease, whether it be coronary artery disease (CAD), peripheral vascular disease (PVD) or cerebrovascular disease is associated with Staurosporine increased mortality risk for patients on dialysis. Limited studies have addressed the effect of different levels of disease severity. Dialysis itself is associated with a significantly increased risk of worsening vascular disease and nephrologists should consider these factors when a decision is being made to commence dialysis and the patient

should be adequately informed regarding the outcomes in people with these comorbidities. No recommendation. Databases searched: MeSH terms and text words for cardiovascular disease, coronary disease and myocardial ischaemia were combined with MeSH

terms and text words for renal replacement therapy and dialysis. The search was carried out in Medline (1950–March, Week 3, 2008). The Cochrane Renal Group Trials Register was also searched for trials not indexed in Medline. Date of search/es: 2 April 2008. Patients with end-stage kidney disease (ESKD) are at high risk of developing cardiovascular disease (CVD), which is considered the leading cause of mortality and morbidity in dialysis patients, accounting for 40–50% of deaths.1 Although there have only been a few studies of CVD in a population with mild renal insufficiency, several authors have reported before an elevated prevalence of CVD in patients starting dialysis compared with the general population.2–5 On admission to dialysis, patients have a high prevalence of cardiovascular risk factors. According to the Lombardy registry,6 it was estimated that 17.4% of the incident patients admitted to dialysis have CAD (9.8%) or myocardial infarction (7.6%). Congestive cardiac failure (CCF) was reported in the same study to be 8.3%. In the United States Renal Data System Registry (USRDS),7 the prevalence of CVD in incident ESKD patients should be proportionally higher, as there is a higher proportion of diabetics, however, the proportion of patients affected by ischaemic heart disease is 3 times higher (40.0%) and the proportion of patients affected by CCF is 5 times higher at 36.0%.