We have previously demonstrated that Bordetella pertussis toxin-induced HA sensitization (Bphs) is a shared autoimmune disease susceptibility gene in EAE and experimental allergic orchitis, and positional candidate gene cloning identified Bphs to be Hrh1 [[27]]. In addition, gene targeting ABC294640 in vivo studies from our lab and other groups demonstrated that HA, H1R, H2R, H3R, and H4R play important roles in EAE susceptibility and pathogenesis, either by regulating

encephalitogenic T-cell responses, cytokine production by antigen-presenting cells (APCs), BBB permeability, or T regulatory (Treg)-cell activity [[27, 30-34]]. The current therapeutic mainstays for MS include IFN-β and glatiramer acetate; however, in most instances, these Selleck Decitabine drugs are of limited efficacy [[35]]. Consequently, research efforts have been increasingly directed toward identifying new therapeutic modalities and disease-modifying therapies (DMTs). Previously, using individual H1R-H4RKO mice, we showed that H1R and H2R are propathogenic, whereas H3R and H4R are antipathogenic. This

suggests that combinatorial pharmacological targeting of HRs may be an effective DMT in MS. To test this hypothesis, we generated H1H2RKO and H3H4RKO mice on the C57BL/6J (B6) background and studied them for susceptibility to EAE elicited by immunization with myelin oligodendrocyte glycoprotein peptide 35–55 (MOG35–55). The results of our study show that compared to B6 mice, H1H2RKO

mice exhibit decreased susceptibility to EAE, whereas H3H4RKO mice develop more severe disease. The findings of our study support the concept that combined pharmacological targeting of HRs may be an appropriate DMT in the treatment of MS and other immunopathologic diseases, particularly given the recent development of highly selective agonists and antagonists for H3R and H4R [[36]]. EAE was induced in B6, H1H2RKO, and H3H4RKO mice by immunization using a 2× MOG35–55-CFA protocol [[37, 38]]. The severity of the clinical disease courses differed significantly among the three strains (F = 28.5; p < 0.0001) (Fig. 1A), with H1H2RKO mice exhibiting significantly less severe disease than both B6 (F = 17.3; p < 0.0001) and H3H4RKO ADAMTS5 (F = 57.3; p < 0.0001) mice. In contrast, the severity of the clinical disease course of H3H4RKO mice was significantly greater than B6 (F = 8.2; p < 0.0001) and H1H2RKO (F = 57.3; p < 0.0001) mice. Analysis of EAE-associated clinical quantitative trait variables [[31]] revealed that the percentage of animals affected, cumulative disease score, and days affected were significantly greater in H3H4RKO compared with B6 mice. In contrast, percentage of animals affected, cumulative disease score, and days affected were significantly less in H1H2RKO compared with B6 mice (Table 1).

The FYVE and coiled-coil domain-containing protein FYCO1 functions as a Rab7 effector, binding to LC3 and PI3P and mediating microtubule plus

end-directed vesicle transport (74). The fusion of autophagosomes and lysosomes is positively regulated by the UVRAG-Vps34-beclin1 PI3-kinase complex and negatively regulated by the Rubicon-UVRAG-Vps34-beclin1 PI3-kinase complex (Fig. 1, Autophagosome-lysosome fusion) (26–29, 38). Following autolysosome formation, the lysosomal hydrolases, including cathepsins, lysosomal glycolytic enzymes, and lipases, degrade the intra-autophagosomal contents. In this step cathepsins degrade LC3-II on the intra-autophagosomal GPCR Compound Library cost surface (Fig. 1, Degradation) (75, 76). In yeasts, Atg15, a vacuolar lipase, and Atg22, a vacuolar membrane protein, are indispensable for the specific degradation of autophagic bodies (77–79). No mammalian homologs of yeast Atg15 and Atg22 have

yet been identified. During conversion by Atg4B of LC3-II to LC3-I on the cytoplasmic face of the autophagosome and degradation by lysosomal hydrolases of LC3-II on the luminal learn more face of autophagosome, LC3-II decreases. After digestion of intra-autophagosomal contents, a lysosomal-associated membrane protein 1 -positive and LC3-negative tubular structure, the protolysosome, is elongated from the autolysosome (Fig. 1, Protolysosome) (80). The protolysosome finally forms a vesicle, and matures into the lysosome by accumulating of lysosomal hydrolases. It is necessary to estimate autophagic activity accurately and quantitatively when studying autophagy

in infection and immune responses. LC3-II and LC3-positive puncta are recognized as promising autophagosome and autolysosome markers (but not “autophagy” markers). However, autophagosomes and autolysosomes are transient structures during autophagy. Therefore, the amount of LC3-II (or number of LC3-positive puncta) alone does Methane monooxygenase not always reflect autophagic activity. Production of LC3-II is increased when autophagy is activated (Fig. 1, Maturation), in addition lysosomal degradation of LC3-II and delipidation of LC3-II by Atg4B are simultaneously activated (Fig. 1, Autophagosome-lysosome fusion). Many methods for monitoring autophagy, including GFP-LC3, tf-LC3, and LC3-II turnover assay, have been proposed, these have both advantages and disadvantages. Recently, critical issues and guidelines for monitoring autophagy have been described (81–83). LC3 fused to green fluorescent protein is useful for in vivo imaging of autophagosome formation (84, 85). However, caution must be exercised due to the limitations of GFP-LC3 (86, 87). GFP-LC3 tends to form puncta in cells independent of autophagy, and GFP fluorescence in lysosomes may occur even after degradation of the LC3 moiety. Therefore, this method tends to overestimate the number of autophagosomes. These problems may be avoided by using a mutant, GFP-LC3ΔG which lacks the essential carboxy-terminal Gly of LC3, as a negative control (Fig. 2, LC3ΔG).

Urinary Emmprin, MMP-9 and TIMP-1 may be noninvasive potential biomarkers that could be used for long-term follow-up of children with UPJ narrowing on conservative Selleck AZD2281 treatment to determine those who might develop

obstruction. “
“151 CLASS II EXPRESSING RENAL TUBULAR CELLS LEAD TO RECONSTITUTION OF CD4 T CELLS IN CLASS II DEFICIENT MICE Y M WANG1, GY ZHANG1, A SAWYER1, JH ZHOU1, M HU2, G ZHENG2, Y WANG2, DC HARRIS2, SI ALEXANDER1 1Centre for Kidney Research, Children’s Hospital at Westmead, Sydney, NSW; 2Centre for Transplantation and Renal Research, University of Sydney, Westmead Millennium Institute, Sydney, NSW, Australia Aims: To identify whether reconstitution of Class II expression in thymus by Class II expressing renal tubular cells may lead R788 mw to reconstitution of kidney specific CD4 T cells in Class II deficient mice. Background: Regulatory T cells (Tregs) are generated

in thymus and are of the CD4 subset. Tregs require MHC Class II to be selected in the thymus. MHC Class II knockout (Class II−/−) mice are deficient in CD4 T cells. Studies have shown that renal tubular cells can express MHC class II. This study identifies the induction of CD4 T cells and Tregs by reconstitution of Class II expressing tubular cells into thymus. Methods: Renal tubular cells were isolated from C57BL/6 Ly5.1 mice and were cultured with IFN-γ. The cultured tubular cells were assessed for Class II expression and

then injected into the thymus of Class II−/− mice. CD4, CD8 and Tregs were assessed by flow cytometry prior and after tubular cell injection. Two months after thymus injection, CD4 T cells and Tregs were assessed Cell press in kidney and spleen by immunohistochemical staining. Results: 30% of tubular cells expressed MHC Class II after ten-day co-culture with IFN-γ. CD4+ T cells in Class II−/− mice increased from less than 1% of total CD3+ T cells before tubular cell injection to 1.4% at week four and 7% at two months after tubular cell thymic injection. Immunohistochemical staining showed that there were increased CD4+ T cells and Tregs in spleen and kidney for these class II deficient mice. Conclusions: Reconstitution of Class II expression in thymus by class II expressing renal tubular cells lead to reconstitution of CD4 T cells including Tregs in Class II deficient mice.

In this system, DDA targets the vaccine antigen to APCs while TDB provides proinflammatory stimuli, triggering a Th-1 cytokine response via a TLR-independent pathway (Agger et al., 2008). CAF01 has proven to be highly efficacious, inducing cellular and humoral responses simultaneously in animal models more effectively than the single antigens administered alone. In addition to its priming activity, this vaccine has also been demonstrated to have a BCG booster effect (Doherty et al., 2004; Davidsen et al., 2005). AS01B, developed by Corixa

and GlaxoSmithKline Lumacaftor in vivo Biologicals, contains the TLR4 ligand MPL and the saponin derivative QS-21 in a liposomal formulation including the fusion molecule Mtb72F. The Mtb72F antigen is comprised of the PPE family member Rv1196 inserted into the middle HSP signaling pathway of the putative serine protease Rv0125, which is thus present as two fragments (Mtb32C–Mtb39–Mtb32N) (Skeiky et al., 2004). In the AS01B or AS02A formulations, this vaccine has also been demonstrated to have priming and BCG booster effects (Brandt et al.,

2004). IC31, also developed by the Statens Serum Institute, consists of a vehicle combining the synthetic antimicrobial peptide KLKL5KLK, which actively loads APCs with antigen, and the immunostimulatory TLR9 ligand ODN1a, with the fusion proteins H1 and Ag85B–TB10.4 (Agger et al., 2006; Lingnau et al., 2007). This vaccine confers protective immunity in murine tuberculosis models and was recently shown to safely induce strong T-cell responses with a mixed Th-1/Th-2 cytokine profile in both neonates and adults (Kamath et al., 2008). CAF01, AS01B and IC31 are currently undergoing clinical Phase I/II trials. Mtb72F/AS01B is being tested in Lausanne, Switzerland, in individuals previously check details exposed to BCG or previously treated individuals

currently infected with Mtb. H1 in IC31 and CAF01 are being tested in Leiden, the Netherlands, in purified protein derivative (PPD)-negative subjects. These adjuvants share the same basic combination of a delivery vehicle and a Th-1-skewing immunomodulator, conferring more potent protection against tuberculosis infection than single immunomodulators (CpG or MPL) or delivery vehicles lacking immunomodulators (liposomes or niosomes) (Agger et al., 2006). LTK63, a modified and detoxified heat-labile toxin derived from E. coli, has been combined with the fusion protein H1 for nasal immunization and has passed Phase I clinical trials (in London, UK, with PPD-negative subjects). A strong and sustained Th-1 response mediated by IFN-γ-secreting CD4+ T cells was observed, leading to long-lasting protection against tuberculosis and boosting prior BCG-induced immunity (Dietrich et al., 2006; Badell et al., 2009).

19). Among patients receiving cinacalcet, the average carotid-femoral pulse wave velocity increased from 10.46 ± 2.12 m/s at baseline to 11.41 ± 2.79 m/s at 52 weeks (P = 0.001). The change in carotid-femoral pulse wave velocity over 1 year had no significant correlation with the final parathyroid hormone level or change in parathyroid hormone level. Among prevalent patients receiving peritoneal dialysis and with hyperparathyroidism, a reduction of 60.6% parathyroid hormone level after cinacalcet treatment for one year did not reduce the carotid-femoral pulse wave velocity. “
“Sudden cardiac MK-2206 mw death (SCD) is the most common cause of death

in haemodialysis patients, accounting for 25% of all-cause mortality. There are many potential pathological precipitants as most patients with end-stage renal disease have structurally or functionally abnormal hearts. For example, at initiation of dialysis, 74% of patients have left ventricular hypertrophy. The pathophysiological and metabolic milieu of patients with end-stage renal disease, allied to the regular stresses of dialysis, may provide

the trigger to a fatal cardiac event. Prevention of SCD can be seen as a legitimate target to improve survival in this patient group. In the general population, this is most effective by reducing the burden of ischaemic heart disease. However, selleck screening library the aetiology of SCD in haemodialysis patients appears to be different, with myocardial fibrosis, vascular calcification and autonomic

dysfunction implicated as possible causes. Thus, the range of therapies is different to the general population. There are potential preventative measures emerging as our understanding of the underlying mechanisms progresses. This article aims to review the evidence for therapies to prevent SCD effective in the general population when applied to dialysis Liothyronine Sodium patients, as well as promising new treatments specific to this population group. The most widely agreed definition of sudden cardiac death (SCD) is unexpected cardiac death that occurs within 1 h of onset of symptoms in a person without a prior condition that would appear fatal.[1] In end stage kidney disease (CKD-5D) patients undergoing haemodialysis, SCD is common. The United States Renal Data System (USRDS) reports that ‘cardiac death, cause unknown’ and arrhythmia account for 25% of all-cause mortality at a rate of 90–200 events/1000 patient-years.[2] This compares with 1–2 events/1000 patient-years in the general population. However, epidemiological data pertaining to the fatal rhythm in dialysis patients who suffer SCD are lacking. Cardiac structure and function are frequently abnormal in CKD-5D; findings associated with vulnerability to malignant arrhythmia. It is likely that SCD is a result of various triggers on an already abnormal myocardium (Fig. 1). For example, dialysis itself is likely to play a prominent role.

85–23, revised 1985) and the national laws on Protection of Animals were followed. A total of 109 female NOD mice were analysed. First, 62 female NOD mice were litter-matched and randomized after weaning into four groups (groups A1–D1; Fig. S1). As

a control group, female NOD mice in group A1 (n = 16) were not mated. In the remaining groups, female NOD were mated at age 10 weeks to male NOD mice (group B1, n = 15) representing MHC identical mating, male CByB6F1/J mice (group C1, n = 16) representing MHC haploidentical mating or male C57BL/6J mice (group D1, n = 15), representing fully MHC mismatched mating. For pairings, two male mice were used in each group. To analyse the effect of later gestation, a second set of 47 female NOD mice were litter-matched and randomized after weaning into three groups: control unmated females (n = 16, group A2); females mated at

age 13 weeks to three male Ulixertinib NOD mice (n = 16, group B2); and females mated at age 13 weeks to three male CByB6F1/J mice (n = 15, group C2). For the mating, two female and one male mouse were housed together in one cage for a median time of 14 days [interquartile range (IQR), 14–17 days]. Subsequently, 45 of 46 females mated at 10 weeks of age and 29 of 31 females mated at 13 weeks of age delivered altogether 610 pups. The number of pups per litter ranged between four and 13 (median, 9; IQR, 7–10), and the offspring numbers were distributed equally between the different mating groups (Fig. S1). All pups remained with their dam for the weaning period of median 21 days (IQR, 21–23 days). All female Adriamycin order NOD mice were followed to overt diabetes or until the age of 28 weeks. Inositol monophosphatase 1 Urine glucose levels were measured twice weekly using urine glucose sticks (Diastix, Bayer HealthCare LLC, Mishawaka, IN, USA), beginning at 10 weeks of age. The diagnosis of diabetes was defined as two consecutive urine glucose values > 5·5 mmol/l and blood glucose levels > 13·9 mmol/l (Glucometer Elite,

Bayer Diagnostics GmbH, Munich, Germany). Venous blood was obtained at age 10 weeks (prior to the mating) and 16 weeks (after weaning), and diabetes onset or 30 weeks for the measurement of insulin autoantibodies. In group C1, splenocytes from two diabetic mice at diabetes onset and two non-diabetic mice at the end of observation were collected to look for lymphocyte chimerism. Antibodies to insulin were detected using a radiobinding assay, as described previously [14]. All measurements were performed on coded samples that were operator-blinded. The upper limit of normal was determined from the 99th centile values obtained in sera from BALB/c and C57BL/6 female mice. The assay is represented as laboratory B in the animal models of Diabetes Workshop [15]. In order to analyse if cells with paternal genome alleles migrated during gestation from the fetus to the dam and persisted, staining and flow cytometry for MHC class I molecules was performed on the collected splenocytes.

The information summarized in Table 1 is indeed going to rapidly evolve with the exponential increase of community level genome-wide surveys of the microorganisms inhabiting the various microenvironments of the human body (i.e., gut, skin, oral mucosa, and urogenital tract) [23], their environmental reservoir [24], and the human populations living in different geographic regions [6, 8]. Understanding the prevalence and distribution of microbial eukaryotes in addition to prokaryotic

microorganisms in the human body may have important consequences for human health. While current studies of the human mycobiota focus mainly on pathogens or opportunistic fungi, most resident microbial eukaryotes do not cause infections, and are instead either beneficial or commensal. Elucidating community-wide changes in the human mycobiota, LDK378 nmr rather than only the presence or absence

of specific taxa, will be crucial to understanding the cause of, and potential treatment for, several multifaceted polymicrobial diseases [25]. Immune responses to fungi require PRRs, such as TLRs, C-type lectin receptors, and the galectin family of proteins [26-28] to trigger intracellular signaling cascades that initiate and direct innate and adaptive immune responses check details [29]. By sensing conserved molecular structures on fungi, namely the PAMPs, PRRs promote the activation of the immune system and the clearance of fungi, with specific immune responses generated depending on the cell type involved. In a recent review [30], we highlighted the roles and mechanisms of dectin-1, dectin-2, and DC-SIGN in orchestrating antifungal to immunity, exploring how these PRRs help maintain homeostasis between potential disease-causing organisms and resident microbial populations. Indeed, the immune system does not remain ignorant of commensal, passenger (transient), or opportunistic fungi, and sensing these different fungi through PRRs serve to ensure that

both the symbiotic host–microbial relationship and a homeostatic balance between tolerogenic and proinflammatory immune responses are maintained. In light of this, tissue homeostasis and its possible breakdown in fungal infections and diseases play a fundamental role. A number of seminal reviews have addressed the importance of both resistance — the ability to limit microbial burden — and tolerance — the ability to limit the host damage caused by an uncontrolled response — as mechanisms of immune responses to fungi and the reader is directed to these for more in-depth information about specific immune mechanisms [31-34]. Monocytes, macrophages, neutrophils as well as epithelial and endothelial cells [35], mostly contribute to the antifungal innate immune response through phagocytosis and direct pathogen killing. By contrast, uptake of fungi by DCs promotes the differentiation of naïve T cells into effector Th-cell subtypes (Fig. 1).

PTEN protein was present heterogeneously in 42 cases and homogeneously in 18

cases. In homogeneous glioblastomas, no correlation was found between PTEN protein expression and the Carfilzomib datasheet LOH of the gene. Surprisingly, in the heterogeneous glioblastomas, LOH was found significantly more frequently (P < 0.001) in PTEN-positive areas (81%) than in PTEN-negative ones (35.7%). In general, molecular results of frozen tissue were representative of the tumour. Only two cases of methylation of the PTEN promoter were identified. A significant difference was found for overall survival for LOH10q23 status (P = 0.005) and for homogeneous vs. heterogeneous tumours (P = 0.014). The expression of PTEN protein does not correlate with the abnormalities of the LOH of the gene. Interestingly, patients with glioblastomas presenting either LOH of 10q23 or heterogeneous PTEN expression have a poorer prognosis. "
“In the CNS, primary tumors with rhabdoid components are classified as atypical teratoid/rhabdoid tumor, rhabdoid meningioma or rhabdoid glioblastoma. The authors present a young adult patient with supratentorial rhabdoid tumor incidentally found after head trauma as a small pre-existing lesion

in the parahippocampal gyrus. Pembrolizumab purchase MRI demonstrated an area of hypointensity on T1-weighted images and hyperintensity on T2-weighted and fluid attenuated inversion recovery images. A serial MR scan revealed no change 3 months after the initial examination but drastic changes at 6 months. As the tumor and accompanying intratumoral hemorrhage enlarged rapidly, resection of the tumor was performed. Histopathology Org 27569 revealed that the main component of the tumor was typical rhabdoid cells with some necrotic areas. There were also pathological features consistent with oligoastrocytoma. The specimen had neither vascular

proliferation usually seen in high-grade glioma nor the meningothelial pattern that suggests meningioma. Immunohistochemical findings revealed that cells were strongly positive for vimentin, epithelial membrane antigen and INI-1 antibody throughout the specimen. Further, monosomy 22 was detected by fluorescence in situ hybridization. The tumor was finally thought to be an unclassifiable primitive rhabdoid tumor with oligoastrocytoma that arose in the CNS. The patient died within 5 months of detection of the tumor, regardless of surgical resection, radiotherapy and chemotherapy. “
“Institut de Neurociències, Department of Cell Biology, Physiology and Immunology and Centro Investigación Biomédica en Red Enfermedades Neurodegenerativas (CIBERNED), Universitat Autònoma de Barcelona, Barcelona, Spain Auditory Neurophysiology Unit, Institute of Neuroscience of Castilla y León, University of Salamanca, Salamanca, Spain Dithiocarb (diethyldithiocarbamate, DEDTC) belongs to the group of dithiocarbamates and is the main metabolite of disulphiram, a drug of choice for the treatment of alcohol dependence.

[1, 4, 10] Taken together these data indicate that the duration/strength of TCR ligation check details results in a progressive reinforcement of expression programmes that are downstream of the TCR signal. Fixation of epigenetic modifications and or the expression of unique transcription factors are a likely mechanism for preserving the exhausted state in the absence of antigen (Fig. 1b). Indeed, gene expression profiling studies demonstrate the preservation of many effector transcriptional programmes including persistent down-regulation of several on-off-on genes (Fig. 1b). Consistent with this idea, we have recently reported on preservation of acquired epigenetic modifications at the PD-1 locus

regulatory regions in virus-specific

CD8 T cells during chronic viral infection.[27] Our data demonstrated that the transient up-regulation of PD-1 expression in functional virus-specific CD8 T cells Selleckchem GSK2118436 was coupled to chromatin accessibility, permissive histone modifications, and acquisition of an unmethylated transcriptional regulatory region at the peak of acute viraemia. Following clearance of the acute viral infection, the PD-1 transcriptional regulatory region regained the DNA methylation programme and became less sensitive to DNase challenge. Importantly, the repressive transcriptional programme was not reacquired in virus-specific CD8 T cells during chronic infection of mice and humans.[27] To our surprise, the permissive epigenetic transcriptional programme at the PD-1 locus was retained in PD-1lo cells following reduction in chronic viral load. Preservation of the permissive transcriptional programme facilitated enhanced re-expression of PD-1 relative to functional memory cells that contained the repressive programme at the PD-1 locus.[27] The kinetic analysis of epigenetic regulation of PD-1 during acute and chronic infections as well as analysis of effector molecule regulation during CD4 and CD8 T-cell memory cell differentiation

have set the stage for further analysis of the enzymes that catalyse the epigenetic modifications Niclosamide and their specificity determinates. Further scrutiny of gene regulatory mechanisms related to the identification and function of phenotypically distinct effector and memory T-cell subsets is necessary. Undoubtedly such studies will further clarify when memory cells are generated and how progressive changes in phenotype and function are obtained. Specifically, analysis of epigenetic modifications will provide a snapshot of the differentiation status of effector and memory T cells. Epigenetic profiling of antigen-specific CD4 and CD8 memory T cells will immediately benefit vaccine development as it will provide a novel parameter for identifying poised expression programmes aiding in the assessment of T-cell memory quality.

This technology is particularly applicable to nephrology, in which the genetic basis of multiple disorders has been identified, but single-gene testing remains impractical given broad, overlapping clinical phenotypes. We describe two cases of nephronophthisis mutations identified via whole exome sequencing. Case Report: The first, a case of a 29 year

old female Maraviroc cell line who was diagnosed with juvenile nephronophthisis on renal biopsy at 14 years old. She subsequently underwent deceased-donor kidney transplantation at 18years. She is a product of consanguineous parents. Her mother and brother also have end stage renal failure. The family underwent single-gene testing of the UMOD gene, as a possible autosomal dominant cause of their renal failure, with no pathologic mutation identified. Our patient subsequently underwent whole R788 cost exome sequencing, as part of a research cohort of Australian patients investigated for a genetic cause for their kidney disease. Sequencing revealed a novel homozygous splice-site mutation within NPHP1 (NM_000272.3:c.1884+1G>T).The second is a case of a 3 year old boy who presented with hepatosplenomegaly

and renal failure at 18 months old, and is now dialysis dependent. He had no significant family history. Whole exome sequencing tuclazepam identified a reported homozygous missense mutation within NPHP3 (NM_153240.4:c.1928C>T:p.Pro643Leu). Conclusions: We have utilised massively parallel sequencing to identify both a novel and known nephronophthisis mutation in separate cases, and importantly these findings have guided treatment, transplantation and family planning for these patients. These experiences highlight the benefits of utilising this technology to

identify a genetic diagnosis in patients with renal disease. 203 ASSESSMENT OF MEDICATION AWARENESS AND THE UTILITY OF MEDICATION CARDS IN CHRONIC HAEMODIALYSIS PATIENTS H NANDAKOBAN, YM KUANG, M SURANYI, A MAKRIS Renal Unit, Liverpool Hospital, Sydney, NSW, Australia Aim: To determine the factors contributing to medication awareness for chronic haemodialysis (HD) patients and determine the utility of medication cards in improving medication awareness. Background: Patients on HD often have several chronic health issues and are subject to polypharmacy. Errors in medication prescription and ingestion can lead to morbidity. There is little information about prescribed medication understanding in HD patients. Medication cards may improve patient understanding of their medications.