albicans isolates under planktonic conditions according to CLSI are given in Table 1. The biofilms of tested C. albicans isolates after 24, 48 or 72 h measured by XTT assay showed no significant difference in ODs (OD24 h: 1.048 ± 0.064; OD48 h: 0.985 ± 0.122; OD72 h: 1.12 ± 0.131, P > 0.05). The results of antifungal activities of amphotericin B, CAS and POS against C. albicans biofilms grown for 24, 48, and 72  are shown in Fig. 1 (% of XTT readings, mean ± standard error). By 24 h, CAS at 1–4 × MIC reduced the biofilm OD by ≥50% vs. the untreated control (P < 0.001). Significant reduction

in the biofilm OD was observed when the biofilms were incubated with amphotericin B at ≥4 × MIC (32.7% reduction, P = 0.002) and POS at ≥2 × MIC (16.5% reduction, P = 0.012). Amphotericin B achieved the reduction in the biofilm OD by 50% at high concentration of ≥32 × MIC (P < 0.001). By 48 h, all three antifungal agents achieved Epacadostat price a significant APO866 reduction in the biofilm OD: CAS at 1 × MIC by 25% reduction (P = 0.001), amphotericin B at 8 × MIC by 27% reduction (P = 0.03),

POS at 2 × MIC by 23% reduction (P = 0.04). However, no investigated antifungal agent reached ≥50% reduction in the biofilm OD. By 72 h, C. albicans biofilm exhibited similar susceptibility to amphotericin B and CAS as by 24 h. Caspofungin at 1 × MIC (P < 0.001) and amphotericin B at 4 × MIC (P < 0.001) reduced the biofilm OD by ≥50%. Posaconazole significantly decreased the biofilm OD at 1 × MIC by 32% (P = 0.001), but failed to reach ≥50% reduction in the biofilm OD. As shown in Fig. 2, no significant reduction in the colony counts of viable cells in biofilms after antifungal

treatment was observed (Fig. 2). The mean colony cell count determined in untreated C. albicans biofilm incubated for 24, 48 and 72 h was: 6 × 107 ±0.256 × 107; 8 × 107 ± 0.2 × 107; 9 × 107 ±0.3 × 107. Amphotericin B attained the maximum decrease in the colony count reaching one log unit at concentration of 128 × MIC against C. albicans biofilm grown for 24, 48 and 72 h. The management PLEK2 of biofilm-associated implant infection requires both antimicrobial therapy and surgical intervention, preferentially with removal of the implant. However, if removal of the infected implant is not feasible, the therapy has to rely on fungal substances alone.18 The resistance of Candida biofilm to antifungal drugs is influenced by the maturation of biofilm due to consistent changes in the composition of biofilm matrix,19,20 metabolic activity11,21 and the rate of the drug diffusion through the biofilm.22In vitro data show that biofilm resistance to azoles is induced in the early stages of biofilm.11,23 On the other hand, reduced ergosterol in the cells membrane of Candida seems to be relevant for the inefficacy of amphotericin B against mature biofilm.24 However, the mechanism of echinocandin activity against biofilms formed by different Candida species remains unknown.

Solt et al. demonstrated very similar effects with the synthetic RORγt ligand SR1001, which prevented Th17-cell differentiation and ameliorated EAE [[68]]. In a model for inflammatory bowel disease, RORγt-dependent ILCs can mediate pathology [[41]]. Together these

results suggest that the RORγt antagonist SR1001 may be utilised therapeutically to target pathogenic ILCs. Interestingly, in addition to RORγt, SR1001 also inhibits the activity of the type 2 ILC-related transcription factor RORα [[68]] This opens up the possibility of using ROR antagonists such as SR1001 in the treatment of type 2 ILC-related immune pathologies, including airway hyperreactivity in allergic asthma, selleck products as well as those mediated by RORγt-dependent ILCs. However, the application of ROR agonists and antagonists needs to be carefully assessed in view of the known beneficial roles of ILCs. Future work needs to reveal how RORα/γt antagonism affects ILC functions, and how this can be applied in the clinical settings. In addition to RORγt and RORα, AhR plays a prominent role in the survival and function of the ILC22 population. The AhR agonist FICZ increases the number of intestinal IL-22-producing ILCs, cells that are crucial for clearing C. rodentium infection [[54]]. This role in the gut makes AhR an interesting target for the treatment of inflammatory bowel disease, a disease in which ILC-derived IL-22 plays a protective

Smad inhibitor role [[28, 30]]. In summary, as discussed in this review, the transcriptional programs that govern the development of the various branches of the ILC family, including RORγt and RORα dependent ILCs, are

beginning to be unraveled. Future studies should aim to address the precise requirements of specific transcription factors at different stages of ILC development and to unravel how these transcription factors are regulated, what the effects of antagonism are, and how the potential interactions between Dehydratase the various transcription factors affect ILC development and function. With such knowledge, attention can be turned to specific therapeutics based on regulating these family members. “
“The function of IL-10 producing regulatory B cells (Breg) during gestation is unknown. Here, we aimed to understand their participation in early pregnancy. CD19+CD24hiCD27+B cell frequency, measured by flow cytometry, increased with pregnancy onset but not in the case of spontaneous abortions. B cells from non-pregnant women cultured with serum from normal pregnant women produced higher IL-10 levels than those cultured with serum from spontaneous abortion patients or autologous serum. CD19+-activated B cells from pregnant women strongly suppressed TNF-a production by CD4+T cells when cocultured. We identified hCG as an important factor regulating the number and function of Breg during pregnancy. Breg emerge as important players in pregnancy; they suppress undesired immune responses from maternal T cells and are therefore important for tolerance acquisition.

We measured increased promoter activity of the human TAP1 gene and detected enhanced expression of TAP1 protein in HTNV-infected A549 cells. Similarly, paramyxoviruses have been shown to enhance TAP1 expression [30]. Thus, hantaviruses may augment transport of peptides ABT-888 ic50 into the ER similar to flaviviruses [31, 32]. Type I IFN was not absolutely required for HTNV-induced HLA-I expression. First, HTNV only moderately increased the number of IFN-β transcripts in A549

cells in line with recent studies [26, 33]. Second, Vero E6 cells, which lack type I IFN genes [25], also upregulate MHC-I upon HTNV infection. Third, although HTNV-infected A549 cells produced type III IFN (IFN-λ1 and IFN-λ2) transcripts confirming

a previous report [26], exogenously added type IFN-λ1 did not significantly increase MHC-I expression in Vero E6 cells. In addition, transfection of RNA derived from HTNV-infected cells triggered MHC-I upregulation, although Peptide 17 mw type III IFN could not be detected in the supernatant. Finally, IFN-λ1 was not detectable in HTNV stocks prepared from Vero E6 cells [34]. This points to an IFN-independent mechanism contributing to HTNV-associated MHC-I upregulation. On the other hand, we have previously observed that upregulation of HLA-I on human endothelial cells infected with hantavirus can be blocked in part by antibodies directed against type I IFN [35]. Taken together, our results suggest that both direct and indirect (IFN-driven) hantaviral mechanisms are required for efficient HLA-I upregulation. Activation of NF-κB could increase MHC-I transcription independently of IFN during hantavirus infection as reported for flaviviruses [36, 37]. In accordance, HTNV RNA has recently been described Fossariinae to trigger NF-κB promoter activity through RIG-I stimulation [21]. On the other hand, the HTNV N protein has been demonstrated to interfere with NF-κB activation [38]. Thus, hantavirus-triggered PRRs may facilitate the assembly of a MHC-I-specific enhanceosome that binds to promoter sequences different from the NF-κB binding site as shown for NLRC5 [39, 40]. Compared to DCs stimulated with TNF-α, HTNV-infected

DCs show increased macropinocytosis and receptor-mediated endocytosis [23], a prerequisite of cross-presentation. Indeed, we observed in this study that HTNV confers upon DCs the capacity to efficiently cross-present pp65, a HCMV-encoded model antigen. It is likely that HTNV-infected DCs also cross-present HTNV-derived antigens. In contrast, cross-presenting uninfected DCs that are activated indirectly by proinflammatory cytokines may induce tolerance rather than immunity [41]. It has been shown that HTNV-infected DCs do not undergo cell death [23]. Thus, lung DCs infected with HTNV after inhalation of virion containing aerosols could migrate to the draining lymph nodes and cross-prime powerful antiviral cytotoxic T cells.

Similarly, bleomycin-induced fibrosis of the skin was enhanced in Lsp−/− mice [26]. Fibrocytes from patients with thermal burns and those from normal donors have substantially less capacity for collagen production than do dermal fibroblasts [27]. When conditioned medium from fibrocytes derived from burned individuals was incubated

with dermal fibroblasts, they exhibited accelerated proliferation when compared to those incubated in medium from control fibrocytes. These effects could be blocked with TGF-β neutralizing antibodies [27]. These same investigators have shown that IFN-α2b can reduce scar formation following Fostamatinib thermal injury by attenuating fibrocyte activity and reducing their numbers [28]. With regard to the kidney, the participation of bone marrow-derived stem cells remains controversial selleck chemical [29]. Results generated in a number of models of renal injury suggest that these stem cells can localize to specific areas of the kidney and might facilitate tissue regeneration. Thus, their therapeutic potential in several forms of human kidney dysfunction is under evaluation. The outcome of such studies will probably influence the research being conducted in allied

disease processes involving other organs and tissues. Graves’ disease represents an autoimmune process where the thyroid becomes enlarged and overactive [30]. The basis for the over-production of thyroid hormones and gland enlargement in this disease involves the production and activity of autoantibodies targeting the thyrotrophin (aka thyroid-stimulating

hormone) receptor (TSHR). In addition, the IGF-1 receptor (IGF-1R) is over-expressed by orbital fibroblasts Rebamipide [31], B [32] and T cells [33,34] in patients with the disease. IGF-1R represents a second potentially pathogenic autoantigen that may account for abnormal thyroid enlargement and underlie the trafficking of lymphocytes to affected tissues, including the pretibial skin and orbit. Pritchard et al. [31] have suggested that T cell trafficking to the orbit in Graves’ disease might be mediated through fibroblast responses to IGF-1 and Graves’ disease-immunoglobulin G (GD-IgG). When exposed to either agent, these fibroblasts express high levels of the T cell chemoattractants, IL-16 and regulated on activation normal T cell expressed and secreted (RANTES). The fibroblast response is mediated through IGF-1R activation and post-receptor signalling through the FRAP/mTor/Akt/p70s6k pathway. It is absent in fibroblasts derived from healthy donors [35]. In addition to the generation of chemoattractants, thyroid-associated ophthalmopathy (TAO) orbital fibroblasts synthesize high levels of hyaluronan, in response to either GD-IgGs or IGF-1. Hyaluronan is a non-sulphated glycosaminoglycan, the accumulation of which is thought to result in tissue oedema [36]. Orbital connective tissue derives in large part from neural ectoderm [37]. This tissue has a special propensity for inflammation.

These intrinsic reparative processes tend to become less marked with age, but nevertheless are there throughout life so can, and have been, exploited therapeutically. In this special issue of Neuropathology and Applied Neurobiology we have sought to explore several of these aspects of regenerative neurobiology around a range of disorders which also serves to highlight some of the problems that such approaches generate as well as their ability to provide new insights into disease processes themselves The ability of the mature mammalian CNS to generate new neurones has become increasingly recognised over the last 10–20 years, although evidence

suggesting that this was the case existed from the 1960s [1]. However the extent to which this occurs https://www.selleckchem.com/products/CAL-101.html in the adult human CNS has been debated in terms of

its rate, where it occurs and its normal physiological role but there now seems overwhelming evidence that it does occur at least in two sites – the subventricular zone with the cells so generated heading primarily to the olfactory bulb and the hippocampal subgranular zone where the cells integrate Protein Tyrosine Kinase inhibitor into the dentate gyrus [2,3]. In either site the cells so generated probably have a role in certain forms of cognition (e.g. pattern separation in the dentate gyrus [4]), but may also be involved in disease processes [5]. Thus manipulating these populations Amobarbital of cells may be a therapeutic route by which to treat a number of disorders, and this has been explored in many conditions – in terms of trying to upregulate the intrinsic neurogenic process as well as redirect it to areas of damage now in need of repair. This whole area of adult neurogenesis forms the topic for the review by S.M.G. Braun and S. Jessberger (pp. 3–12) and covers not just neurological disorders but also aspects of neuropsychiatry given the posited role of abnormalities in hippocampal neurogenesis in depression. The fact that neurogenesis occurs and can be dynamically altered by disease and drugs

is not restricted to these areas as it can also be influenced by environmental enrichment – the condition in which animals are placed in environments with a large number of cognitive and physical stimulants. Under such circumstances animals interact more and appear to be able to upregulate neurogenesis along with the central production of growth factors such as brain neurotrophic factor (BDNF) and with this synaptic formation and function. This has generated a great deal of interest as it would suggest that patients placed in programmes of high intensity rehabilitation may do very well and as such many trials exploring this are being pursued globally (e.g. [6]). However one of the problems in this field is that much of what is seen experimentally looks at animals placed in enriched environments vs.

The CHOICE study performed by Jaar et al.11 studied 1041 patients on HD and PD from 81 dialysis clinics in the United States. They were prospectively studied for up to 7 years after commencement. Data were gathered on coexisting diseases and disease severity along with age, sex, ethnicity, serum albumin, Hb, C-reactive protein, residual urine output and BMI. After adjustment, the risk of death did not differ between HD and PD patients undergoing treatment for the first 12 months. However, after the second year, the mortality risk was significantly higher in the PD group. This study did not find an increased risk of death with

PD for diabetic or elderly patients; however, there was a somewhat greater risk of death for some groups on Torin 1 order PD if the patient had a history of CVD (not statistically significant in all subgroups). Limitations: Measured dialysis adequacy was not available for all patients to make a comparison between modalities and possibly associate with survival. A selection bias could influence results due to the observational nature of this study. This study allowed for modality switching without analysis of the reasons and the survival outcome. Registry data analysis from

the USA, the Netherlands, Canada, Italy and Denmark is included here. Canadian Organ Replacement Register data analysis by Fenton et al.5 studied 11 970 patients with stage 5 kidney disease commencing Neratinib research buy treatment in Canada from 1990 until 1994 with up to 5 years of follow up. Deaths were allocated to the treatment the patient was

receiving at the time of their death. Data were adjusted for age, primary renal disease, centre size and predialysis comorbidities. Lumacaftor purchase Results indicated that the mortality risk for patients commencing treatment with PD was 73% that of those commencing with HD when adjusting for various prognostic factors; however, this became less pronounced when various subgroups were teased out (especially for those with diabetes and over the age of 65 years). The mortality rate for those on PD tended to increase over time while the HD survival was represented by a U shape. Limitations: This study did not adjust registry data for the impact of dialysis adequacy, nutritional status, patient compliance, comorbidity severity and the effect of late referral on patient mortality. United States Renal Data System (USRDS) registry data analysis. This registry data study by Vonesh and Moran3 extracted mortality data on nearly 204 000 patients from the USRDS for incident and prevalent patients over a 7-year period from 1987 to 1993. The results showed significant variations in mortality rates according to specific cohorts studied such as age, diabetes and gender. Importantly, there were no statistically significant differences in the adjusted death rates among non-diabetic PD and HD patients across age, gender or race.

Moreover, in the subgroup of learn more patients without previous immunosuppressant treatment, there was no disability progression during the treatment period. Hence, mycophenolate mofetil might serve as an alternative therapy for RRMS [41]. Moreover, recent studies examined the safety and efficacy of combinations of ‘classic’ immunosuppressive

drugs with recombinant IFN-β and showed equivocal results [42]. Moreover, some novel oral immunomodulatory drugs have recently been tested alone or in combination with IFN-β or GA in Phase III trials in patients with CIS or RRMS (see below). A parallel approach, however, is lacking in CIDP. Mitoxantrone is an anthracenedione derivative related to the anthracyclines doxorubicin and daunorubicin. It interacts with topoisomerase-2, stabilizes its cleavable complex with DNA, and thus prevents the ligation of DNA strands and consecutively delays cell-cycle progression. Preparations and administration: mitoxantrone is approved in Europe for the disease-modifying monotherapy of patients with highly active RRMS and SPMS

Dorsomorphin mouse (‘escalation therapy’) [43]. Its use, however, is limited by cardiotoxicity (the standard cumulative lifetime dose of mitoxantrone is 96 mg/m2, which can be extended up to a maximum lifetime dose of 140 mg/m2 under careful risk–benefit weighting and monitoring) and the risk of therapy-associated leukaemia (especially acute myelogenous leukaemia, AML). Given these limitations and the broadening spectrum of drugs available for patients with highly active RRMS, the use of mitoxantrone is limited in clinical practice to patients with SPMS. Mitoxantrone is administered intravenously at a dosage of 12 mg/m2 every 3 months for a total of 2 years, according to the mitoxantrone

in MS study (MIMS) [44]. To extend the total administration period, the dosage can be reduced to 5 mg/m2 upon clinical stabilization. G protein-coupled receptor kinase Clinical trials: there are no recent clinical trials with mitoxantrone in MS. Moreover, due to a lack of evidence from randomized, controlled clinical trials the use of mitoxantrone in CIDP is not established. Adverse effects, frequent: secondary amenorrhoea/azoospermia, nausea and vomiting, myelosuppression; infrequent: alopecia, cardiotoxicity, secondary leukaemia (especially AML) [45, 46]. Contraindications: severe active infections, chronic or relapsing infections, cardiomyopathy, treatment with other cardiotoxic drugs, severe liver or kidney dysfunction, pregnancy and lactation. Due to a lack of evidence from randomized, controlled clinical trials, the use of cyclophosphamide in MS and CIDP is not properly established [25, 47]. Teriflunomide is the biologically active metabolite of leflunomide, which is approved for the treatment of rheumatoid arthritis.

These data suggest that Bcl-3 may not play a significant role in the regulation of inflammation in the colon. Despite a robust inflammatory response following DSS treatment, the colonic tissue architecture in Bcl-3−/− mice, in particular the epithelial features, remain intact. Following DSS treatment intestinal epithelial cell proliferation in Bcl-3−/− mice was enhanced significantly, whereas in wild-type mice it was

absent. The increased proliferation in Bcl-3−/− mice correlates with the maintenance of tissue architecture and structure and suggests that the resistance to DSS-induced colitis of Bcl-3−/− mice results from increased regeneration of the epithelium. It is also noteworthy that Bcl-3 acts a negative regulator of myeloid progenitor proliferation and differentiation, and is essential for limiting granulopoiesis under inflammatory conditions [27]. This study identifies a novel role for Bcl-3 in regulating BMS-777607 intestinal epithelial cell proliferation under inflammatory but not homeostatic conditions. Our identification of Bcl-3 as a negative regulator of intestinal epithelial cell proliferation during colitis suggests additional physiological functions Selleck AZD1208 for Bcl-3 beyond its role as a negative regulator of proinflammatory gene expression. The dual role of NF-κB as a key mediator of inflammation

and a critical driver of epithelial cell survival and proliferation has rendered it a complex and difficult therapeutic target in IBD. Transgenic mice in which NF-κB activity has been inhibited selectively in the intestinal epithelium develop spontaneous colitis due to failure of the epithelial barrier function, while an increase in intestinal NF-κB activity also leads to severe Liothyronine Sodium inflammation [4]. The data obtained in this study, however, suggest that certain regulatory components of the NF-κB pathway such as Bcl-3 may play a more important role in the epithelium rather than the immune system

in the colon. We have demonstrated previously that Bcl-3 expression is induced by inflammation [16]. Given that the proliferation of intestinal epithelial cells is normal in Bcl-3−/− mice, it is probable that inflammation-induced expression of Bcl-3 in the epithelium during colitis contributes to the development of disease. Thus, by targeting Bcl-3 it may be possible to enhance epithelial cell proliferation and regeneration without exacerbating inflammation in the intestine. The potential therapeutic benefits to IBD are highlighted by the reduced clinical score and lack of weight loss in DSS-treated Bcl-3−/− mice. In summary, we describe a novel function for Bcl-3 in regulating epithelial cell proliferation during DSS-induced colitis. The increased epithelial cell proliferation and regeneration in Bcl-3−/− mice supports further a role for NF-κB in maintaining the integrity of the intestinal epithelium.

Our study was undertaken to establish the kinetics of sCD14 concentrations in BALF in patients with allergic asthma following segmental allergen challenge at different time points (10 min, 18, 42 and 162 h). Moreover, the study attempted to establish stimuli involved in sC14 production and/or shedding, respectively, such as LPS,

which has been shown to increase sCD14 levels in vitro [21] and in vivo [22] and leukotriene D4 (LTD4), which has been implicated in allergic inflammation and the pathogenesis of airway hyperresponsiveness [34]. Furthermore, LTD4 has been shown to induce TNF-α release from macrophages [35] that was inhibited by the leukotriene-receptor antagonist (LTRA) Verlukast [35]. IL-17 has been associated with an OTX015 in vitro increase in IL-8 and GM-CSF production from bronchial epithelial cells [36], the regulation of ICAM-1 expression [37] and the selective recruitment of neutrophils [38]. Moreover, it plays a role in the LPS-induced chemotaxis of neutrophils into the airways after LPS inhalation [39] and increases after organic dust inhalation in healthy subjects [40]. We therefore investigated whether IL-17 might influence sCD14 production in cell cultures. Eighteen patients with allergic asthma (nine men and nine women), mean age 26.3 ± 5.4 years with a duration of asthma for more than 2 years (mean duration 11.7 ± 5.2 years), were studied. Bronchial asthma had previously Apoptosis Compound Library been diagnosed

by an independent physician. Each patient had a positive skin prick test to either birch pollen (n = 8), rye pollen (n = 3), or house dust mite allergen (n = 7) extracts (Allergopharma, Reinbek, Germany), and all had either elevated total IgE levels (293.6 ± 233.1 kU/l) and / or elevated specific IgE levels (32.2 ± 49.1 kU/l) (Kabi Pharmacia CAP System, Uppsala, Sweden) to their respective allergen as well as a history of reversible bronchoconstriction after inhalation of these particular allergens. Obeticholic Acid nmr There was no history or clinical evidence in any of the patients, suggesting a respiratory tract infection prior to or at the time of segmental

allergen challenge. All patients were non-smokers. Baseline FEV1 (forced expiratory volume in 1 s) was 3.8 ± 0.96 l (94.9 ± 13.1% of predicted, normal values [41]). All patients received inhaled ß2-agonist therapy on an as needed basis except for three patients who did not require any medication. In addition, five patients had inhaled corticosteroids and three had inhaled cromoglycate. Both were withheld at least 10 days prior to entry into the study. All patients gave their written informed consent. The study protocol was approved by the local Ethics Committee. Prior to the segmental allergen provocation, patients underwent an inhaled allergen challenge as previously described [29, 42] to establish dual bronchial reactions to the inhaled allergen and to determine the individual PD20FEV1 for the respective allergen.

On the other hand, the authors of the DRASTIC study developed a clinical prediction rule with a reported diagnostic accuracy similar to renal scintigraphy with a sensitivity of 72% and specificity of 90%. The authors concluded that in the diagnostic work up of patients suspected of having RAS, the clinical prediction rule can help

select patients for renal angiography in an efficient manner by reducing the number of angiographic procedures without the risk of missing many true RAS. The search for ideal non-invasive or minimally invasive tests for the screening and diagnosis of RAS is incomplete. Most of the evidence cited in the meta-analyses of published trials suggests superiority of CE-MRA and CTA for screening atherosclerotic RAS. The imaging modalities used in any particular situation are going to be a combination of what best suits the patient as well as available infrastructure Talazoparib molecular weight and expertise. Kidney Disease Outcomes Quality Initiative: Guideline 4.1 For GSI-IX cost patients in whom there is suspicion of renal artery disease (RAD), the clinician should: 1 Estimate the probability of RAD using a predictive index derived from clinical characteristics. UK Renal Association: No recommendation. Canadian Society of Nephrology:

No recommendation. European Best Practice Guidelines: No recommendation. International Guidelines: No recommendation. Future research in this area is fraught with uncertainties as a result of lack of definitive

proof of benefit of endovascular intervention, and rapidly evolving technological innovations designed to improve visualization of renal arteries. Murty Mantha has no relevant financial affiliations that would cause a conflict of interest according to the conflict of interest statement Mannose-binding protein-associated serine protease set down by CARI. “
“Aim:  To compare the effects of i.v. iron sucrose and Fe chloride on the iron indices of haemodialysis patients with anaemia. Methods:  One hundred and eight haemodialysis patients receiving recombinant human erythropoiesis-stimulating agent (ESA) (mean age 59.37 years) were enrolled and randomly assigned to an iron sucrose or an Fe chloride group. Iron supplements were administered at 100 mg/week during the first 4 weeks (loading dose). Ferritin and transferrin saturation (TSAT) were then measured and dose adjusted. Ninety-eight subjects completed treatment; 51 in the iron sucrose group and 47 in the Fe chloride group. Ferritin, TSAT, haematocrit (Hct), reticulocyte count, serum albumin, fractional clearance of urea (Kt/V) and intact parathyroid hormone (iPTH) were measured. Results:  There was no significant difference in baseline characteristics between the groups. Significant differences between the groups were observed in both iron indices and ESA dosage. Hct at week 24 (31.1% vs 29.7%, P = 0.006) and ferritin at week 20 (731.3 vs 631.7 ng/mL, P = 0.006) in the iron sucrose group were significantly higher than in the Fe chloride group.