7 Consequently, PTH and FGF-23 maintain normal calcium and phosphate levels in early stages of CKD,8 but progressive renal damage results in hyperphosphataemia, increasing learn more FGF-23 levels (up to 1000 times the normal range) and the development of secondary hyperparathyroidism (SHPT) in many patients.9 Current management of disordered mineral homeostasis in CKD involves the control of hyperphosphataemia

by dietary modification or phosphate binders and the use of calcium, calciferol or active vitamin D compounds to maintain normal PTH levels in CKD stages 1–5. Calcimimetic agents may be added when patients are dialysis dependent and if PTH levels are high or patients have hypercalcaemia thought because of SHPT. Unfortunately, difficulties with phosphate control increase when patients reach CKD stage 5, or patients commence dialysis, and despite dietary restriction and phosphate binder therapy, patients often have poor phosphate control unless they advance to longer dialysis sessions. Patients with CKD have

an excessive burden of CVD and related mortality.10,11 Age-standardised rates of all-cause mortality and cardiovascular (CV) events are 5–20 times higher in people with CKD as compared with those with normal kidney function12 and a collaborative meta-analysis of general population BMN 673 molecular weight cohorts, consisting of more than 1.2 million people, showed that an estimated glomerular filtration rate (eGFR) of <60 mL/min per 1.73 m2 was an independent predictor of all-cause and CV mortality.13 The risk of CV morbidity and mortality progressively worsen with decline in eGFR.

Traditional CVD risk factors (hypertension, older age, hyperlipidaemia and diabetes) are highly prevalent in patients with CKD although they do not explain the heightened CV risk in stages 4–5D. For these patients, ‘non-traditional’ factors, particularly relating to abnormal selleck screening library mineral metabolism, are associated with the increased risk of CVD (Fig. 1).14,15 Recognizing the intimate associations between CVD and abnormalities of bone and mineral metabolism, the term ‘chronic kidney disease-mineral and bone disorder’ (CKD-MBD) was applied, encompassing the disturbances of mineral metabolism, renal bone disease and vascular calcification, together with patient-level outcomes of fracture, CVD and mortality in patients with CKD.16 Hyperphosphataemia, a key component of CKD-MBD, is strongly associated with adverse outcomes in CKD patients, including CVD, vascular calcification and increased arterial stiffness (Table 1).29,30 The relationship between phosphate and CVD may be explained by several putative mechanisms.31–34 The most plausible mechanism concerns the accelerated progression of vascular calcification, which is conceptually linked to the positive phosphate balance seen in CKD (as well as excessive doses of calcium-based phosphate binders).

This double-blind trial included men aged over 40 years with frequency, urgency, and at least moderate problems reported on the Patient Perception of Bladder Condition (PPBC), despite being on a stable dose of alpha-blocker for more than 1 month. Subjects were randomized to tolterodine ER 4 mg per day or placebo for 12-week treatment with their prescribed alpha-blocker. At baseline and week DAPT purchase 12, subjects completed the PPBC, IPSS, Overactive Bladder Questionnaire (OAB-q), and 5-day bladder

diaries using the five-point Urinary Sensation Scale (USS). Frequency–urgency sum was defined as the sum of USS ratings for all micturitions. PPBC improvement was reported by 63.6 and 61.6% of subjects receiving tolterodine ER plus alpha-blocker and placebo plus alpha-blocker, respectively; this treatment difference, which was the primary endpoint, was not statistically significant. At week 12, subjects receiving tolterodine ER plus alpha-blocker had significantly greater improvements in 24 h micturitions, daytime micturitions, Erastin in vitro 24-h urgency episodes, daytime urgency episodes, nocturnal urgency episodes, frequency–urgency sum, IPSS storage subscale, OAB-q symptom bother scale and coping domain. AUR occurred in less than 1% of either group. There

were no clinically meaningful changes in PVR or Qmax. The authors concluded that men with bothersome OAB symptoms despite continued alpha-blocker therapy showed significantly greater improvements when receiving additional tolterodine ER. However, the study had some limitations. It lacked a true no-treatment group. Moreover, the use of bladder diaries may have led to behavioral modification due to increased awareness Selleckchem Regorafenib of symptoms. The authors could not assess whether treatment response was influenced by prostate size because the size was not measured. In addition, the duration of this trial was limited to 12 weeks. A long-term result needs to be studied. Kaplan et al.24 conducted a 12-week, double-blind, placebo controlled trial assessing the safety and tolerability of solifenacin (5 mg once daily)

plus tamsulosin (0.4 mg once daily) in men with residual OAB symptoms after tamsulosin monotherapy (VICTOR study). A total of 398 men aged 45 years or older were randomized. The study population had eight or more micturitions per 24 h and one or more urgency episode per 24 h after taking tamsulosin for 4 or more weeks, a total IPSS of 13 or greater, a PPBC score of 3 or greater, a PVR of 200 mL or less and a Qmax of 5 mL per sec or greater. The primary efficacy endpoint was mean change from baseline to week 12 in micturitions per 24 h. Secondary measures included mean change in urgency episodes per 24 h, and changes in PPBC, UPS and total IPSS. The most frequent adverse events in the solifenacin plus tamsulosin and placebo plus tamsulosin groups were dry mouth (7% vs 3%) and dizziness (3% vs 2%).

Importantly, adoptive transfer of antigen-loaded DCs stimulated with GLA-SE in vivo was sufficient to induce specific Th1-cell responses in naïve mice. In contrast, DCs stimulated with emulsion alone were unable to prime T cells. Since the DCs also had to express MHCII, this indicates that their T-cell immunizing function required direct presentation of antigen in the mice primed by adoptively transferred DCs. To our surprise, BGB324 research buy antibody responses were unaltered after CD11c+

depletion. In this paper, we only analyzed total IgG responses. Maturation of DCs may still have a role in antibody affinity. The type of immune response that eliminates an infection depends on the type of pathogen. Induction of CD4+ T-cell responses by vaccination was LY294002 in vivo associated with diminished simian immunodeficiency virus (siv) replication after intrarectal challenge and decreased HIV acquisition

in the Thai HIV vaccine trial 44, 45. The results presented here demonstrate that GLA-SE is an efficient adjuvant for the generation of HIV-gag-specific Th1-cell immune response. IFN-γ was produced in large amounts by antigen-specific T cells in both spleen and lymph nodes. HIV-1 vaccines will most likely need to induce mucosal immunity. Mucosal tissues are the major site of natural HIV transmission and the reservoir for HIV replication quickly leading to a rapid loss of T cells in the intestine 46, 47. In addition, Th1 type CD4+ T cells are known to improve the mobilization of the cognate antigen-specific CD8+ T cells to a site of infectious challenge 48, 49. Thus GLA-SE has the capacity to adjuvant a protein vaccine to

induce mucosal immunity that potentially is valuable to limit viral replication and curtail systemic dissemination. Previous studies successfully showed that local immune responses were able to prevent virus spread from the gut mucosa into the systemic circulation 50–52. However, the general belief is that local but not systemic immunization is required to induce robust mucosal responses 53–55. Interestingly, we DNA ligase found that s.c. injection of the GLA-SE and anti-DEC-HIV gag p24 vaccine was able to induce strong mucosal T-cell responses. Immunization with HIV-gag targeted or untargeted protein plus GLA-SE induced a broad range of different antibody isotypes and therefore a combination of Th1 and Th2-cell responses. This contrast, i.e. with polarized Th1 T-cell responses, may be explained by the different requirement for DC priming. This result is consistent with previous studies where addition of GLA-SE gives a mixed Th1/Th2-cell response but also increases the IgG2/IgG1 ratio to an existent M. Tuberculosis and Influenza vaccine 27, 56.

Further studies also reported the existence of IgM– cells in CD27+CD43lo–int subpopulations, with one report noting that IgD– cells were more prevalent with increasing age [29, 31]. Further analysis of IgM+ cells within the CD27+CD43lo–int subpopulation showed there to be a proportion of IgMhi cells (data mTOR inhibitor not shown). As high expression of surface IgM is one of the discriminatory criteria for murine B1 cells [3], we re-ran our previous immunophenotyping analysis to distinguish between

IgMhigh and IgMlo CD20+CD27+CD43lo–int cells. We found a ninefold higher proportion of CD5+ cells within the IgMhigh subset compared to their IgMlow counterparts, which might indicate a closer phenotypic approximation to the ‘B1 cell’ population described previously [12] (data not shown). Sotrastaurin Nevertheless, discrepancies in the CD20+CD27+CD43+ cell immunophenotype we reported raised the need for a functional study which would match with our FACS results and reconfirm the functional B1 status of these putative B1 cells. The percentage and immunophenotype differences

found in the CD20+CD27+CD43lo–int cell subpopulation in CVID patients compared to healthy controls appeared not to be specific for this B cell subpopulation, but rather reflected a more general immune dysregulation in CVID. This could, potentially, be due to a lack of analysis using absolute counts of cells rather than percentages, which provides a much more accurate measure of difference [34]. We acknowledge this as a limitation of our study. A significantly increased percentage of CD21lo B cells within not the CD20+CD27+CD43lo–int subset in CVID patients compared to controls was observed. Although CD21lo B cells are known to have some innate-like features similar to murine B1 cells [14], our analysis showed that the proportion of CD21lo cells in the CD20+CD27+CD43lo–int was not

significantly different when compared with the proportion of CD21lo cells found in the CD20+CD27+CD43– cell subpopulation of the same patients. In addition, there was an observed lack of correlation with existing EUROclass classifications on CD21lo B cells; it is therefore likely that B1 cells and CD21lo innate-like B cells are not the same population. Further work investigating CVID and putative B1 B cells should focus on the functional aspects of B1 B cells, as any potential functional abnormalities have yet to be elucidated. In conclusion, our study showed that it is possible to use a rapid whole blood flow cytometric method to identify and analyse putative human B1 B cells. We demonstrated that CD20+CD27+CD43lo–int cells most probably represent a distinct subset within CD27+ B cells.

[26, 27] To examine whether GABAA receptor (GABAA-R) signaling is involved in granule cell ectopia, we treated rat pups with either the GABAA-R antagonist picrotoxin or the positive modulator of GABAA-R phenobarbital, finding that picrotoxin inhibited febrile seizure-induced granule cell ectopia, whereas phenobarbital selleck screening library accelerated the cell ectopia. These results suggested that GABAA-R signaling regulates granule cell migration in vivo. To determine the specificity of GABAA-R signaling in regulating granule cell migration, we took advantage of the slice culture system in which pharmacological experiments can be easily performed. Hippocampal

slices were obtained from P6 rats that received a BrdU injection at P5 to label neonatally generated granule cells. By chronically applying several agonists or antagonists for the receptors of neurotransmitters for 5 days in vitro, we found that the GABAA-R agonist muscimol retarded, and the GABAA-R antagonist bicuculline facilitated, granule cell migration,

whereas glutamatergic receptor signaling was probably not involved. Another advantage of the slice culture system is that time-lapse imaging of the neuronal maturation is available under a proper environment in which CO2 concentration and temperature are well-regulated. Direct time-lapse imaging for radially migrating granule cells was lacking, even though it was reported that granule cell progenitors are associated with radial glia PF-562271 in the dentate gyrus.[28, 29] To visualize granule cell migration and further determine the effects of neurotransmitters on the migrating granule cells, we developed a slice coculture system in which we replaced the hilar region of the Atorvastatin hippocampal slice from wild-type rats with the hilar graft slices prepared from transgenic rats expressing GFP (GFP+ transgenic rats)

(Fig. 1A). A 24-h time-lapse analysis revealed that GFP+ granule cells migrated radially to the granule cell layer (Fig. 1B). Using this slice coculture system, we could also examine the functional properties of migrating granule cells by directly recording electrophysiological properties from GFP+ migrating granule cells, finding that granule cells receive excitatory GABAergic but not glutamatergic inputs during migration. The above results indicated the possibility that enhanced GABAA-R signaling induced aberrant migration of granule cells after febrile seizures. This hypothesis led us to examine mainly two possible mechanisms that take place after experiencing febrile seizures: (i) the increased GABA amount in the environment (the hilus) where neonatally generated granule cells migrate; and (ii) the increased GABAA-R response of migrating granule cells to GABA. We examined the first possibility by immunohistochemistry, finding that febrile seizures did not significantly affect the expression of glutamate decarboxylase (GAD)-67 or GABA in the dentate gyrus.

To evade destruction by the host immune system, the spirochete has developed evasion strategies such as antigenic variation of surface proteins. Zhang and co-workers first

described antigenic variation of a 35-kDa surface lipoprotein in PDE inhibitor B. burgdorferi which they termed VlsE (variable major protein-like sequence; Zhang et al., 1997). VlsE is similar to the well characterized variable major protein (Vmp) of the relapsing fever Borrelia (Barbour, 1993). The vlsE locus is encoded on the lp28-1 plasmid and consists of the vlsE expression site and 15 silent cassettes (Zhang et al., 1997). Within each silent cassette, there are six variable regions (VR-I through VR-VI) and six highly conserved regions. Importantly, the VlsE regions of variability are located on the membrane distal portion of the protein, which is more likely to

come in contact with antibody during mammalian infection (Eicken et al., 2001). During mammalian infection, regions of the expressed vlsE cassette are replaced with regions of the silent cassettes through a gene conversion mechanism that can result in numerous vlsE sequence products (Zhang et al., 1997; Zhang & Norris, 1998a, b). Sequence variation occurs in all six of the variable regions of the expression site, but the sequence of the silent cassettes is conserved (Zhang et al., 1997; Zhang & Norris, 1998a, b). In mice, variability of vlsE is observed as early as 4 days postinfection (Zhang & Norris, 1998b). These changes selleck products continue during the duration of the infection and occur at greater frequencies at later time points postinfection (Zhang & Norris, 1998b). Interestingly, clonal populations of B. burgdorferi grown in vitro or maintained within ticks retain the parental vlsE sequence, and sequence variation in immunocompetent mice occurred at a greater rate as compared to variation of vlsE in SCID mice (Zhang & Norris, 1998b). These data suggest that conversion is dependent on mammalian factors and that selection of vlsE variants occurs in the presence of an intact

immune response (Zhang et al., 1997; Zhang & Norris, 1998b; Indest et al., 2001). Presence of lp28-1, the vlsE encoding plasmid, is correlated with an intermediate infectivity phenotype of B. burgdorferi in which the spirochetes are unable to persist BCKDHA in tissues (Purser & Norris, 2000; Labandeira-Rey & Skare, 2001). However, strains lacking lp28-1 are able to infect and persist in SCID mice, suggesting that lp28-1 is required for B. burgdorferi to survive in the presence of an intact immune system (Labandeira-Rey et al., 2003; Purser et al., 2003). A B. burgdorferi strain lacking vlsE expression was developed by deleting the region encoding this locus (Bankhead & Chaconas, 2007). Importantly, the VlsE-mutant strain demonstrated a phenotype similar to an lp28-1-deficient B. burgdorferi strain. The combined data suggest VlsE as an important virulence determinant of B. burgdorferi.

The transcription

of pro-IL-1β was also substantially induced by LPS and strongly enhanced by RWE treatment (Fig. 4f) and a substantially stronger production of processed IL-1β protein was detected in the lysate of LPS and RWE plus NADPH-treated cells compared with the LPS-treated ones (Fig. 4g). To see how NLRP3 and pro-IL-1β expression depends on RWE NADPH oxidase-generated ROS, we studied the RWE-induced transcription of the corresponding genes in the absence or presence of NADPH (Fig. 5). Our results show that all of the studied gene inductions by RWE appeared to be NADPH dependent. Furthermore, we found that ROS-inhibitor DPI substantially inhibited pro-IL-1β and NLRP3 gene expression in the LPS-treated or RWE-treated cells, as well as in those STI571 treated with their combination. Interestingly, while the LPS-induced caspase-1 production was not affected by DPI, significant down-regulation was observed in the case of the RWE-treated THP-1 macrophages, regardless of the LPS treatment. To see whether the LPS-activated

signal transduction pathways are affected by RWE we studied the phosphorylation of JNK, p38 MAPK and IκBα in response to treatment by various combinations of compounds used in this study. Unlike the phosphorylation of IκBα (data not shown), the RWE-induced p38 MAPK and JNK phosphorylation appeared to be NADPH dependent (Fig. 6a). Furthermore, RWE in the presence of NADPH substantially enhanced the LPS-induced p38 MAPK and JNK phosphorylation (Fig. 6b). p38 and JNK are members of the MAPK family that has been described to activate RG7204 supplier AP-1 transcription factors.[21] To demonstrate the activation of these downstream signalling

events we studied the expression and phosphorylation of c-Jun and c-Fos transcription factors. Our results show that the expression of c-Fos and c-Jun was not affected by the NADPH[21] (Fig. 6c) or the RWE plus NADPH treatment (Fig. 6d). However, we found that co-treatment with RWE and NADPH significantly increased the phosphorylation Ribociclib supplier of c-Fos and c-Jun compared with that of the RWE-treated cells (Fig. 6c). Similarly, these transcription factors were more phosphorylated in the LPS-activated and RWE plus NADPH-treated cells compared with the only LPS-treated ones (Fig. 6d). These results suggest that the ROS-dependent enhancement of LPS-induced IL-1β production by RWE involves the p38 MAPK and JNK pathways. Allergic rhinitis is one of the most common inflammatory disorders accompanied by high levels of IL-1β production. It is hypothesized that combined exposure to endotoxin and an allergen would enhance the influx and activity of macrophages in the lung and increase the symptoms of allergic airway reactions.[7, 22] Supporting this assumption, here we demonstrate that RWE significantly enhances LPS-induced IL-1β secretion in THP-1 macrophages, as well as in human primary macrophages and dendritic cells. Both pollen grain and pollen extract have been reported to be able to modify inflammatory responses.

5c). This observation indicates that even though the programmed DCs check details continue to internalize and process antigens, chemokine pre-treatment may delay

up-regulating peptide–MHC II complexes on the cell surface, thereby failing to effectively present antigens to T cells. Hence, in Part II of this study, we are quantifying the antigen presentation capacity of these programmed DCs and the subsequent T-cell response. In addition to higher levels of IL-1β and IL-10 secretions from iDCs programmed by CCL3 + 19 (7 : 3) versus untreated iDCs before subsequent LPS treatment, programmed DCs secreted IL-23, after subsequent LPS treatment, at higher levels (44%) than iDCs treated with only LPS. These differential outcomes of various cytokines secreted from DCs also suggest that chemokine programming has a multifunctional

impact on modulating the adaptive immunity by signals other than antigens or co-stimulatory molecules. For example, IL-1β and IL-23 secreted from the programmed DCs can accumulate until after subsequent TLR stimulation, and then induce Th17 polarization,[63] which plays a critical role in autoimmune diseases or anti-microbial immunity. Hence, hypothetically chemokine programming of DCs could provide immunomodulating strategies for both innate and adaptive immunity against various pathologies. As the chemokine combination of CCL3 + 19 (7 : 3) induced DC learn more endocytic capacity retained at high levels even after subsequent LPS treatment, we have examined how the chemokine receptor expressions on the DC surface are modulated upon treatment of DCs with chemokines and subsequent LPS. In this examination, DCs were pre-treated with single CCL3 (70 ng/ml), CCL19 (30 ng/ml), or their combination (7 : 3), and then chemokine receptor expressions on the DC surface were measured

using flow cytometry and fluorescently labelled antibodies against mouse CCR5 or CCR7 on Day 1 and Day 2 schedules, as shown in Fig. 1. Unexpectedly, it was not possible to observe any statistically meaningful data of CCR expressions between DC treatments. Also, CCR5 expressions on JAWSII DC line surface were at very low levels (data not shown). Possibly Thalidomide because of the DC line’s unknown immunobiological functions, which are not exactly the same as the primary DCs,[64] we could not determine how CCR5 or CCR7 expressions are modulated upon pre-treatments of this DC line with individual chemokines or their combination. However, we found that CCR5 expressions on untreated iDCs decreased or CCR7 expressions on untreated iDCs increased upon DC maturation (data not shown). Therefore, we can conclude, at least, that even though this JAWSII DC line up-regulates CCR5 or CCR7 at low levels, this cell line still expresses these two chemokine receptors that respond to DC maturation in the same way as other DCs in the literature. Further study using other measurements (e.g.

[12], namely the HLA-DQB1*02:02 subtype, an eventual allele for ABPA–CF susceptibility and HLA-DQB1*02:01, a possible allele of ABPA–CF protection. The difference between DQB1*02:01 and DQB1*02:02 is in exon 3 (amino acid 135). The DQB1*02:01 allele is genetically linked to DQA1*05:01 and has classically been associated with celiac disease, Type 1 diabetes and other autoimmune diseases. However, DQB1*02:02 is linked to several DQA1 alleles, namely DQA1*02:01 and DQA1*03:03. Thus, in future studies we will investigate other HLA genes to clarify other possible associations. In addition, because ABPA is an uncommon complication of CF, it will also be important to further investigate and corroborate

these interesting findings with a larger number selleck products of patients in the future. We found no differences between the groups used as comparison controls, which consolidates our findings. Our findings allow us to both corroborate and rule out partnerships with primary genetic pathology in patients with CF. With regard to patients with asthma, they allow us to discard possible associations with other allergic pulmonary pathology and, by making comparisons with healthy subjects, to determine general population frequencies. learn more In this context, several reports have shown that a strong Th2 response to A. fumigatus antigens, as indicated by prominent eosinophil infiltration, could be responsible for development of ABPA [21, 22].

Thus, it is possible that particular HLA class II alleles play critical roles in the outcome of T-cell responses (Th1 vs Th2) to A. fumigatus antigens. Thus, patients with CF but without ABPA who PRKD3 lack permissive alleles possibly have Th1 type responses against the fungus A. fumigates, which would prevent colonization of the lung and development of ABPA. The opposite situation would occur in patients with ABPA–CF and susceptibility alleles; they mount a Th2 type response [11, 15]. In this context, other authors have also demonstrated that altered T cell receptor-mediated signals can lead to altered T lymphocyte phenotypes [23]. This

does not mean that a susceptibility allele alone can cause ABPA; however, these alleles could influence the outcome of exposure to A. fumigatus. In conclusion, these data corroborate previous studies showing correlations between HLA-DRB1*15:01, –DRB1*11:01, –DRB1*11:04, –DRB1*07:01, –DRB1*04 alleles, and ABPA–CF susceptibility. Indeed, our data show that HLA-DQB1*02:01 is a possible ABPA–CF resistance allele. This work was possible in part thank to technical support from projects from Fondo de Investigación Sanitaria (FIS) (PI11/02686) (CIBERehd) funded by the Instituto de Salud Carlos III, Spain and Seneca Foundation No. 04487/GERM/O6 y CajaMurcia. None of the authors has a conflict of interest to disclose. We confirm that we have read the journal’s position on issues involved in ethical publication and we affirm that this report is consistent with those guidelines.

WANG KU-CHUNG, KUO LI-CHUEH, CHEN JIN-BOR Division of Nephrology, Kaohsiung Chang Gung Memorial Hospital and Chang Gung University College of Medicine, Kaohsiung Introduction: The aim of study was to investigate the influences of clinical variables this website on the quality of life (QoL) in incident peritoneal dialysis (PD) patients. Methods: The study was a prospective, case-control, observational design. Fifty-three incident patients who received chronic PD in one PD unit were enrolled. The mean age was 48.3 ± 12.6 year-old, men to women 21:32. The observational period was two years. SF-36 health survey questionnaires

were used to measure the QoL. Comparable variables included epidemiology, social status, concomitant medical status and biochemical data. Results: The scores of SF-36 components before PD therapy were general health 58.48 ± 20.05, pain 38.64 ± 21.84, social functioning 64.62 ± 27.54, emotional well-being 48.48 ± 18.29, energy/fatigue 56.82 ± 21.59, role limitations due to emotional problems 68.69 ± 15.74, role limitations due to physical health 54.88 ± 15.19, physical functioning 65.09 ± 20.24. After six months PD therapy, unmarried subjects demonstrated higher scores in role limitations due to emotional problems (76.19 vs 47.75, p < 0.05), role

limitations due to physical health (66.07 vs 37.16, p < 0.05) than married subjects. At the end of twenty-four months PD therapy, subjects who exchanged PD fluid by MLN0128 solubility dmso themselves showed higher scores in social functioning and physical functioning compared to those

exchanged PD fluid by assistants. Furthermore, subjects with antihypertensive demonstrated higher scores in emotional well-being than those without antihypertensive. Conclusion: PD therapy had sequential influences on the components of QoL in term of PD duration. At 6-month PD therapy, marriage status had a positive influence on QoL. In contrast, self-care and antihypertensive use had a greater contribution on QoL improvement at 24-month PD therapy. Therefore, patient-oriented PD care should be implanted into contemporary situation of PD patients. RYU HAN JAK1, HAN IN MEE1, LEE MI JUNG1, OH HYUNG JUNG1, PARK JUNG TAK1, MOON SUNG JIN3, KANG SHIN-WOOK1,2, YOO TAE-HYUN1,2 1Department of Internal Medicine, College of Medicine, Yonsei University, Seoul; 2Brain Korea 21 PLUS Project for Medical Science, Yonsei University, Seoul, Korea; Farnesyltransferase 3College of Medicine, Kwandong University, Gyeonggi-do, Korea Introduction: Endothelial dysfunction is implicated in increased cardiovascular risk in non-dialyzed population. However, the prognostic impact of endothelial dysfunction on cardiovascular outcome has not been investigated in peritoneal dialysis (PD) patients. Methods: We prospectively determined endothelial function by brachial artery endothelium-dependent vasodilation (flow-mediated dilation; FMD) in 143 non-diabetic PD patients and 32 controls. Primary outcome was a composite of fatal or nonfatal cardiovascular events.