albicans (Fig. 5). The structural and bioimmunological analysis of Candida mannans has mostly been conducted using yeast cells form grown at 28 °C. Nevertheless, Candida cells become pathogenic and invade tissue in the hyphal form at 37 °C [30, 31]. Recently, it has been shown that presence of the α-1,6-linked branching

mannose residues in mannan structure is reduced in Candida hyphal form mannan [8]. IgM and IgG antibodies levels induced by both conjugates immunization were slightly higher for hyphal morphological form of C. albicans (Fig. 5). Difference in α-1,6-linked branching presence in mannan of C. albicans yeast and hyphal form and detected antibody levels indicate that recognized antigenic determinants are α-1,6-linked branching independent. Palbociclib mw We can suppose that observed difference in induction of humoral immune response by M5-BSA and M6-BSA conjugates is less related to difference in oligomannoside length and is more related to structure diversity,

concretely branching difference at non-reducing end of oligomers. Generally, oligosaccharides of intermediate length are required for the carbohydrate components of conjugate vaccines to obtain conformation similar to CB-839 price its native state on the cell surface. In the case of β-1,2-linked mannooligomers, the size of the epitopes that are able to induce protective antibodies is 2 or 3 residues [1]. We can suppose that dominant antigenic determinants of α-1,6-branched oligomannosides are not related

to branching site. In addition, whole cell ELISA assay reveal marked non-specific interaction of serum antibodies with Candida whole cells of both morphological forms. Determination of the source of non-specific interactions requires further investigation. IgGl and IgG2a subclass antibodies play a significant role in the opsonization either in the presence or absence of complement [32]. A comparison of the levels of IgGl and IgG2a indicates poor correlation between the putative Th responses oxyclozanide initiated and mice strain susceptibility to infection [33]. Experimental infection of BALB/c mice with low susceptibility to Candida infection produced increased levels of IgGl instead of IgG2a [33]. By immunization with semi-synthetic oligomannoside-BSA conjugates M5-BSA and M6-BSA, we observed in agreement with mentioned report increase in IgG1 levels instead of IgG2a. The ability of immune sera to enhance the candidacidal activity of PMN was studied according to previously published candidacidal assay [14]. The published observations of efficient yeast cells opsonophagocytosis revealed ability of mannan-specific antibodies alone to serve as sufficient opsonins [34]. These results are supported by an earlier report of C. albicans yeast cells opsonophagocytic killing by human neutrophils induced by natural anti-mannan antibodies [35].

Chlamydia pneumoniae lung infection in Barasertib cost IL-10 knockouts showed a faster clearance, but at the same time a more severe inflammation (Penttiläet

al., 2008). This is especially relevant to determine the importance of innate immune response mediators in Chlamydiales infections given the lack of genetic manipulation techniques for the bacterial genome. Furthermore, chlamydial infections not only affect cytokine expression but also cytokine receptors’ expression. Thus, C. psittaci-infected HeLa cells (229) showed an increase in TNF, interferon and IL-1 receptors. Induction was mediated by a heat-stable component of the bacteria and did not require protein synthesis (Shirey & Carlin, 2006). The component was recognized by Toll-like receptors (TLRs) that among others induce cytokine selleck screening library receptor expression. This promoted a rapid response to secreted cytokines and hence an improved clearance of C. psittaci or at least an inhibition of its growth. Conversely, the functionality of the receptors has to be assessed, because Chlamydiales might have developed mechanisms to counteract the upregulation of cytokine receptors. Because cytokines play such an important role in tissue damage, chronicity and clearance of chlamydial infection, the bacterial and cellular effectors responsible for their activation have been broadly investigated. TLRs are on the front line of inducing innate immune response. TLRs belong to the family of PRRs that can be located

intracellularly or on the plasma membrane of immune cells and also on epithelial cells, such as the type II pneumocytes (Droemann et al., 2003). There are 10 members in the TLR family in humans with a homologous cytoplasmic domain. The expression level of each TLR depends on the cell type and tissue, i.e. TLR2 is present to a greater extent than TLR4 in the reproductive Carbachol tract (Pioli et al., 2004). These TLRs present on the cell surface or inside the cell recognize PAMPs and induce an innate immune response. The PAMPs can be found on the bacterial surface, become accessible once inside the cell or be produced during replication. Interestingly, UV-inactivated C. muridarum is not able to induce TLR2-dependent TNF-α and IL-6 expression, showing the requirement for intact particles for recognition (Darville et al., 2003). In contrast, P. acanthamoebae expresses a trypsin-sensitive PAMP that is accessible only upon heat inactivation and is mainly recognized by TLR4 (Roger et al., 2010). The two major components of the TLR-induced signaling cascade are Myd88 (TLR2/TLR4) and TRIF (TLR3/TLR4) (Kawai & Akira, 2010). Both lead to the activation of NF-κB and the downstream production of pro-inflammatory cytokines (Fig. 2), such as IL-6, IL-12p40 and TNF-α. There are also other PRRs that were found to recognize chlamydial PAMPs, such as CD14 (Kol et al., 2000; Bas et al., 2008) or NOD1 (Welter-Stahl et al., 2006; Buchholz & Stephens, 2008; Shimada et al., 2009).

Determining trough levels and blood screening at least once a year for stable patients, and more often for those with complications, is medically important. Physicians

in other specialities who see patients on Ig replacement not infrequently order antibody-based tests that lead to incorrect conclusions; the most common findings that cause concern are antibodies to hepatitis B, Epstein–Barr virus or cytomegalovirus and Coomb’s test or anti-thyroid LY2157299 supplier antibodies, among others [16]. Because these antibodies are found commonly in polyclonal Ig, mistaken diagnoses can occur. With continued contact with the physician ordering the Ig therapy, these errors can be avoided. Routines to monitor subjects with chronic lung disease have been controversial; there is no current consensus. High-resolution computed tomography (HRCT) of the lungs at baseline and to monitor therapy at 3–4-year intervals would be reasonable. Immunoglobulin therapy provides the mainstay of all treatment protocols for the majority of subjects with primary immune deficiency. However, adherence to

basic principles of evaluation, prescribing and ongoing care and attention by physicians familiar with this treatment are required to derive the most benefit from this therapy. This paper is part of a supplement supported by an unrestricted grant from Grifols. The author received payment for the preparation of this article PD-0332991 cost and attendance at the

symposium in which it was presented. We thank Christopher Scalchunes and Marcia Boyle of the Immune Deficiency Foundation and Mr. Keith Crawford of Coram Clinical Trials who supplied information regarding use of Ig products in the United States. This work was supported by grants from the National Institutes of Health, AI 101093, AI-467320, and AI-48693. “
“Earlier iterations of the ‘hygiene hypothesis’, in which infections during childhood protect against allergic disease by stimulation of the T helper type 2 (Th2)-antagonistic Th1 immunity, have been supplanted progressively by a broader understanding of the complexities of the underlying cellular and molecular interactions. Most GABA Receptor notably, it is now clear that whole certain types of microbial exposure, in particular from normal gastrointestinal flora, may provide key signals driving postnatal development of immune competence, including mechanisms responsible for natural resistance to allergic sensitization. Other types of infections can exert converse effects and promote allergic disease. We review below recent findings relating to both sides of this complex picture. Until the late 1980s, interest in the role of infections in allergic diseases focused principally upon the process of primary allergic sensitization.

IL-35 is

a novel inhibitory cytokine, a member of IL-12 family, which is comprised of Ebi3 (IL-27β) and IL-12a/p35 (IL-12β). Ebi3 gene was found in mean 27% of our samples. Our results are in contrast with Bardel et al. [28], who did not detected Ebi3 in human T regulatory cells. IL-27 can promote both anti- and pro-inflammatory immune responses (reviewed in [29]). It has inhibitory effect on Th1, Th2 and Th17 subpopulations, but it also inhibits the development of Tregs via the influence on STAT3 [30]. The diminished IL-27 expression in Tregs found in our study could also confirm the role of this cytokine in disturbances of immune balance observed in the MS. The production of TGF-β by Tregs is involved in their regulatory activity BGB324 in vitro in intestinal inflammation and diabetes

[31, 32]. However, some data demonstrate that in inflammatory bowel disease, Treg-mediated suppression is not TGF-β1 dependent [33]. Thus, a diminished TGF-β expression in Tregs can lead to the appearance of low-grade inflammatory process accompanying MS. In our samples, the expression of TGF-β receptors was only a little bit different between study and control group. One of the cytokines with multifarious functions is interferon gamma. Usually regarded as proinflammatory cytokine, it is also produced by Tregs and plays some role in their activation (discussed in [34]). The immunoregulatory role of FoxP3+/IFN-γ+ cells was PLX3397 clinical trial confirmed in patients after kidney transplantation [35]. The reduced expression of this cytokine in Tregs separated from children with MS could indicate the Pyruvate dehydrogenase dysfunction of these cells. ICOS, GITR, CTLA-4, 4-1BB and OX40 belong to the most important molecules in keeping proper Treg function. We found only minimal changes in the expression of ICOS, GITR and CTLA-4, but the amounts mRNA for 4-1BB and OX40 were higher in

Tregs separated from children with MS when compared to reference children. CTLA-4 controls T regulatory cells’ function and is required for the suppression of autoimmune response in diabetes [36]. ICOS contributes to the role of Tregs in the pathogenesis of atherosclerosis, but its role in obesity and MS is not yet elucidated [37]. Although the signalling of TNF receptor family members, OX40/4-1BB seems to be important for Treg function, their role is largely unknown. OX40 is regarded as negative regulator of FoxP3 and antagonizer of Tregs [38]. In contrast to our findings, Liu et al. found decreased 4-1BB expression on Tregs in patients with multiple sclerosis [39]. It is possible that 4-1BB and OX40 regulate Treg function in both positive and negative manners (reviewed in [40]). The cytotoxic activity of T regulatory cells is contentious. In our samples (both study and control groups), we didn’t find any mRNA for granzyme A. This confirms our previous findings, and other authors usually examined granzyme B expression in Tregs [41, 42]. In contrast, Grossman et al.

Changes in protein antigen processing and T-cell activation have also been reported in CGD 35, while studies using human cells have reported increased pro-inflammatory and decreased anti-inflammatory mediators when compared with healthy controls 34, 36–38. We focused upon a recently described family of GlyAgs expressed by commensal and pathogenic bacteria (e.g. S. aureus, INCB024360 S. pneumoniae, and B. fragilis) that have been shown to induce abscess formation via CD4+ T-cell activation 12, 16, 20, 23, 39. Lack of intact αβ T-cell receptor expression or

blockade of co-stimulatory pathways in mice translates into a failure to develop abscesses in response to GlyAg 24. GlyAgs require processing via NO-dependent oxidation 20, 21, 23 and presentation on MHCII molecules

16, 20, 23, providing an unexpected link to oxidative disorders. Our results reveal that CGD mice showed a dramatically increased immune response against GlyAgs, resulting in more frequent and severe abscesses. This differential response was mediated by APCs rather than neutrophils as might be expected and appears to be a result of increased NO and more efficient GlyAg processing. Likewise, the CGD phenotype was transferrable to WT animals via APC transfer, which indicates that the difference in T-cell activation is due to changes in the APC and not the responding T cells. Although we cannot completely rule out direct NO effects on responding T cells, it is clear that NO is required for processing 20, 23 and that Florfenicol CGD APCs are better Lenvatinib concentration GlyAg processors than their WT counterparts. The NADPH oxidase complex is also known to maintain a neutral pH environment within endo/lysosomes 35, and thus changes impact acid-dependent

protein antigen processing. In fact, CGD favors vesicular acidification and increased conventional antigen proteolysis 35. In sharp contrast, GlyAg processing is dependent upon a neutral pH and acidification stops GlyAg processing in cells 40. As a result, one might expect the CGD cells to process GlyAg less than the WT counterparts due to increased acidification, yet we observed the opposite. With the role of NO firmly established within this pathway 20, 23 and together with the ability to ameliorate the CGD effect by iNOS inhibition and the effectiveness of APC transfer into WT animals, we conclude that CGD results in GlyAg hyperresponsiveness because of increased GlyAg processing by resident APCs via increased NO levels, resulting in greater T-cell activation and downstream sequelae. Another unexpected observation was that the level of IL-1β, used as a crude measure of inflammation, was not altered in CGD cells. While this may seem counterintuitive, recent evidence in humans has indicated that asymptomatic CGD patients do not make more IL-1β in response to a number of stimuli compared with healthy controls 41.

Similarly to the tolDC trial in type I diabetes, Rheumavax was well tolerated; no major adverse effects were observed, and treatment did not appear to enhance the autoinflammatory response. Further assessments on how Rheumavax treatment has modulated anti-citrullinated peptide-specific immunity will be highly informative for understanding how tolDC affect antigen-specific

T cell responses. The main conclusion that can be drawn from these trials is that intradermal injection of autologous tolDC that are maturation-resistant appears to be safe – the autoimmune response was not enhanced. Although these trials were primarily safety trials, not designed to measure efficacy, they represent an important step Smoothened Agonist chemical structure forward in the field, and will pave the way for future tolDC trials. We have developed a protocol to produce tolDC for the treatment of RA (Fig. 1) by pharmacological modulation

of monocyte-derived DC with the immunosuppressive agents dexamethasone (Dex) and vitamin D3 [1,25 dihydroxyvitamin D3 (VitD3)], together with a Toll-like receptor (TLR)-4 agonist [Escherichia coli LPS or monophosphoryl lipid A (MPLA); see below]. Compared to mature DC, our tolDC are characterized by (i) high expression of MHC class II (i.e. similar levels as mature DC); (ii) intermediate expression of co-stimulatory molecules CD80 and CD86 and low expression BGB324 supplier of CD40 and CD83; and (iii) an anti-inflammatory cytokine production profile with high levels of IL-10 and TGF-β and low or undetectable levels of IL-12, IL-23 and TNF ([55, 82, 83] and unpublished data). There PI-1840 are two reasons for including a TLR-4 ligand in the tolDC generation protocol. First, activation through TLR-4 is required for tolDC to process and present

exogenous antigen efficiently on MHC class II [82]; a similar observation has been reported for immunogenic DC [84]. Thus, MHC class II–peptide complexes do not form efficiently unless the (tol)DC also receives a proinflammatory signal (e.g. LPS) during antigen uptake [82, 84]. The ability of tolDC to present antigens is clearly critical to the success of tolDC therapy, because the main goal of tolDC therapy is to induce T cell tolerance to relevant autoantigens. Secondly, TLR-4-mediated activation is also required for tolDC to acquire the ability to migrate in a CCR7-dependent manner [82], thus enabling them to migrate to secondary lymphoid tissues, where they can interact with T cells. Whether this migratory capacity is required for tolDC therapy to be successful in RA is not entirely clear, but there is evidence from the transplant setting that CCR7 expression by tolDC is required to prolong the survival of allografts in an animal model [85]. These data fit the paradigm that secondary lymphoid tissues are an important site for the induction of immune tolerance [86, 87], at least under normal, steady state conditions.

Stimulatory effects of progesterone and estrogen hormones together with a higher basal metabolic rate increase maternal ventilatory sensitivity to chemosensory stimuli and raise MLN8237 concentration ventilation by 25% [53]. The greatest changes, however, are those occurring in the uteroplacental circulation, where an even greater fall in vascular resistance preferentially directs some 20% of total cardiac output to this vascular bed by term, amounting to a >10-fold or greater increase over levels present in the nonpregnant state such that, by term, uteroplacental flow may approach 1 L/min [61]. Many of these changes are complex, distinctive,

and subject to particular, local control. The purpose of this review is to describe the remodeling process that enables the progressive and substantial increase in uteroplacental blood flow required for normal fetal growth and development. Most broadly, the remodeling process can be viewed as a combination of changes in vascular structure, which result in increased vessel diameter and length, and concurrent changes in vascular function, i.e., altered vasoreactivity (including Adriamycin clinical trial myogenic tone). Ultimately, this combination of passive structure and superimposed

active tone regulate arterial lumen diameter, the primary physiological determinant of vascular resistance and, hence, blood flow to the uteroplacental circulation. With the exception of the endometrium, the vascular system of the adult is largely quiescent. Structural changes that do occur with age, such as arterial stiffening and plaque formation, are generally pathological in nature as they may lead to the development of hypertension and atherosclerosis, respectively. Endometrial changes are cyclic with each menstrual cycle and involve only the microcirculation. Hence, the significant growth of the maternal vessels

during pregnancy represents a unique physiological event whose understanding can be approached from the standpoint of underlying processes and associated events, signals and pathways (Figure 1). Much of this review is focused on the structural changes that occur in arteries and veins, i.e., true structural oxyclozanide remodeling, whose pattern is most often referred to as being outward (or expansive) and hypertrophic [59]. The latter term derives from the fact that the most common pattern is one of luminal enlargement with little or no change in wall thickness (with the exception of the mouse [81, 82]). Without any change in wall thickness, cross-sectional area will increase secondary to the larger lumen and result in a greater overall tissue mass. Put differently, eutrophic lumenal expansion requires a reduction in wall thickness to maintain a constant cross-sectional area whereas hypertrophic expansion accomplishes an increase in diameter without any change in wall thickness (although total cross-sectional area is still increased).

It is assumed to exert multiple functions including packaging of pre-mRNA, regulation of alternative splicing, and nucleo-cytoplasmic transport of mRNA 7. HnRNP-A2 appears to be ubiquitously expressed, although the level of expression may greatly vary between different tissues. Interestingly,

hnRNP-A2 is overexpressed in RA synovial tissue, where it is detectable not only in the nucleus but also in the cytoplasm of macrophages and fibroblast-like synoviocytes 8. Autoantibodies 5-Fluoracil datasheet to hnRNP-A2 (which are also known as anti-RA33 Ab) are present in approximately 30% of RA patients 9, but also in patients with systemic lupus erythematosus (SLE) and mixed connective tissue disease 9. Remarkably, however, epitope recognition was found to differ between the three disorders 10. Furthermore, also T cells from peripheral blood and synovial fluid of RA patients were found to

react to hnRNP-A2, in about 60% of the patients 8. Interestingly, autoimmunity to hnRNP-A2 has been observed in TNF-transgenic (Tg) mice 11, which develop arthritis spontaneously, and is a dominant immunological event in pristane-induced arthritis in rats 12. Altogether, the results suggest that this protein is an important and potentially pathogenic autoantigen in animal models of arthritis and in RA. Thus, it was the aim of the present study to characterize putative pathogenic T-cell epitopes of hnRNP-A2. To achieve this goal, we started with a comprehensive investigation of MHC binders among a library Bortezomib mw heptaminol of 15-mer peptides spanning the entire human hnRNP-A2 protein. Peptides of this length can bind directly to MHC class II molecules on the cell surface

of APC where they can stimulate peptide-specific T cells. This method allows the analysis of all possible determinants regardless of whether the peptide is dominant or cryptic following natural processing. Then, to identify hnRNP-A2-specific T-cell epitopes in patients with RA, we used a sensitive IFN-γ ELISPOT assay, which detects in vivo-generated antigen-specific T cells in a low frequency range 13. The data obtained were confirmed in proliferation assays and reveal the presence of an immunodominant T-cell epitope associated to active RA. We synthesized 280 15-mer peptides overlapping by 13 or 14 amino acids and spanning the whole hnRNP-A2 sequence. These peptides were tested by competitive ELISA for binding to the RA-associated DR*0101 and DR*0401 molecules. The results obtained show that most epitopes binding to either DR*0101 or DR*0401 were localized in the N-terminal half (first 170 amino acids) of the hnRNP-A2 sequence (Fig. 1). Presence of an MHC epitope was revealed by 4–7 consecutive binding peptides. Frequently, many more consecutive peptides were binding, indicating overlapping epitopes. Six major determinants were found to bind to both DR*0101 and DR*0401: peptides no.

“
“This study evaluated the potential of plasma treatments to modify the surface chemistry and hydrophobicity of a denture base acrylic resin to reduce the Candida glabrata adhesion. Specimens (n = 54) with smooth surfaces were made and divided into three groups (n = 18): control – non-treated;

experimental groups – submitted to plasma treatment (Ar/50 W; AAt/130 W). The effects of these treatments on chemical composition and surface topography of the acrylic resin were evaluated. Surface free energy measurements (SFE) were performed after the treatments and after 48 h of immersion in water. For each group, half (n = 9) of the specimens were preconditionated with saliva before the adhesion assay. The number of adhered C. glabrata was evaluated

STA-9090 concentration by cell counting after crystal violet staining. The Ar/50 W and AAt/130 W treatments altered the chemistry composition, hydrophobicity and topography of acrylic surface. The Ar/50 W group showed significantly lower C. glabrata BAY 80-6946 ic50 adherence than the control group, in the absence of saliva. After preconditioning with saliva, C. glabrata adherence in experimental and control groups did not differ significantly. There were significant changes in the SFE after immersion in water. The results demonstrated that Ar/50 W treated surfaces have potential for reducing C. glabrata adhesion to denture base resins and deserve isothipendyl further investigation, especially to tailor the parameters to prolong the increased wettability. “
“The respiratory tract of cystic fibrosis patients is colonised by bacteria and fungi. Although colonisation by slow growing fungi such as Pseudallescheria, Scedosporium and Exophiala species has been studied previously, the colonisation rate differs from study to study. Infections caused by these fungi have been recognised,

especially after lung transplants. Monitoring of respiratory tract colonisation in cystic fibrosis patients includes the use of several semi-selective culture media to detect bacteria such as Pseudomonas aeruginosa and Burkholderia cepacia as well as Candida albicans. It is relevant to study whether conventional methods are sufficient for the detection of slow growing hyphomycetes or if additional semi-selective culture media should be used. In total, 589 respiratory specimens from cystic fibrosis patients were examined for the presence of slow growing hyphomycetes. For 439 samples from 81 patients, in addition to conventional methods, erythritol–chloramphenicol agar was used for the selective isolation of Exophiala dermatitidis and paraffin-covered liquid Sabouraud media for the detection of phaeohyphomycetes. For 150 subsequent samples from 42 patients, SceSel+ agar was used for selective isolation of Pseudallescheria and Scedosporium species,and brain–heart infusion bouillon containing a wooden stick for hyphomycete detection.

Further study is needed to clarify the long term impacts of ADMA elevation in CIN patients on future of organ damage. LEE YU JI, CHO SEONG, KIM SUNG ROK Department of Medicine, Samsung Changwon Hospital, Sungkyunkwan University School of Medicine, Changwon Introduction: Although colistin has recently reintroduced as a therapeutic agent for the treatment

of multidrug-resistant organisms, concerns about nephrotoxicity associated with colistin allow the limited use of colistin. The objective of this study was to evaluate the association between colistin doses and the development of nephrotoxicity. Methods: A retrospective cohort study of all patients received intravenous colistin to treat infections caused by multidrug-resistant Gram-negative rods at Samsung Changwon CT99021 nmr Hospital was conducted. From FK506 chemical structure 2010 to 2013, adult patients receiving colistin for 72 hr or longer were included in this study. The patients with a glomerular filtration rate <50 ml/min/1.73 m2 at baseline were excluded. Nephrotoxicity was defined as doubling of baseline serum creatinine. Colistin dosing was evaluated based on both actual body weight (ABW) and ideal body weight (IBW). Results: One hundred fifty-six patients met inclusion criteria and were included in the analysis. The mean age of the patients was 64.2 ± 15.2 years. Seventy-five patients (48.1%) experienced nephrotoxicity during colistin treatment. The mean onset time of

nephrotoxicity was 10.2 ± 6.3 days. The mean daily dose of colistin based on IBW and ABW was 4.8 ± 1.5 and 5.0 ± 1.6 mg/kg/day, respectively. In logistic regression analysis using backward stepwise selection method to identify predictors of nephrotoxicity, daily colistin dose based on ABW (mg/kg/day) [Odds Ratio (OR) = 1.28, 95% confidence interval (CI), 1.03–1.58] was associated with the development Aurora Kinase of nephrotoxicity with concominant use of diuretics (OR = 2.21, 95% CI 1.099–4.458) and serum albumin level (OR = 0.27, 95% CI, 0.11–0.68) after adjusting for concominant uses of inotropics and glycopeptides, age and hematocrit.

However, when colistin dose based on IBW instead of ABW was added in logistic model, colistin dose was no longer a risk factor of nephrotoxicity. Conclusion: Colistin doses based on IBW was not associated with the development of nephrotoxicity during colistin treatment. Colistin dosing based on IBW may be relatively safe from colistin-associated nephrotoxicity. PARAPIBOON WATANYU, SATHITTRAKOOL SUPHASIT, TAWEESAK PANAWAN, CHOEIKAMHAENG LADDAPORN Department of Medicine, Maharat Nakhonratchasima Hospital Introduction: Intermittent hemodialysis (IHD) and Continuous renal replacement therapy (CRRT) have been widely used in acute kidney injury (AKI). However, acute peritoneal dialysis (APD) is still commonly used in AKI especially in hemodynamically unstable patients and unavailable IHD or CRRT. Therefore, outcomes of IHD and APD in treatment of AKI patients need to be clarified.