Here we review recent evidence in support of these seemingly opposing notions gleaned from cell and animal models as well as investigations of patient samples, with particular emphasis on studies relevant to Parkinson’s disease. “
“We report a case of an infant with unique and Lenvatinib cell line unreported combinations of brain anomalies. The patient showed distinctive facial findings, severe delay in psychomotor development, cranial nerve palsy and seizures. Brain magnetic resonance imaging performed at 5 days of age revealed complex brain malformations, including heterotopia

around the mesial wall of lateral ventricles, dysmorphic cingulate gyrus, and enlarged midbrain tectum. The patient unexpectedly died at 13 months of age. Postmortem pathological findings included a polymicrogyric cingulate cortex, periventricular nodular heterotopia, basal ganglia and thalamic anomalies, and dysmorphic midbrain tectum. Potential

candidate genes showed no abnormalities by traditional PCR-based sequencing. Whole-exome sequencing confirmed the presence of novel gene variants for filamin B (FLNB), guanylate binding protein family member 6, and chromosome X open reading frame 59, which adapt to the autosomal recessive mode or X-linked recessive mode. NVP-BGJ398 chemical structure Although immunohistochemical analysis confirmed the expression of FLNB protein in the vessel walls and white matter in autopsied specimens, there may be functional relevance of the compound heterozygous FLNB variants during brain development.

“
“Niemann-Pick disease type C (NPC) is an autosomal recessive neurovisceral lipid storage disorder. Two disease-causing genes (NPC1 and NPC2) have been identified. NPC is characterized G protein-coupled receptor kinase by neuronal and glial lipid storage and NFTs. Here, we report a man with juvenile-onset progressive neurological deficits, including pyramidal signs, ataxia, bulbar palsy, vertical supranuclear ophthalmoplegia, and psychiatric symptoms; death occurred at age 37 before definitive clinical diagnosis. Post mortem gross examination revealed a unique distribution of brain atrophy, predominantly in the frontal and temporal lobes. Microscopically, lipid storage in neurons and widely distributed NFTs were observed. Lipid storage cells appeared in systemic organs and filipin staining indicated intracellular cholesterol accumulation in hepatic macrophages. Electron microscopy revealed accumulation of lipids and characteristic oligolamellar inclusions. These findings suggested an NPC diagnosis. Neuronal loss and gliosis were frequently accompanied by NFTs and occurred in the frontal and temporal cortices, hippocampus, amygdala, basal forebrain, basal ganglia, thalamus, substantia nigra and brain stem nuclei. Lewy bodies (LBs) were observed in most, but not all, regions where NFTs were evident.

VEGF expression did not reveal any correlation with necrosis or bizarre vascular patterns. Supratentorial location is an independent predictor of a poor PFS. Significant coexpression of nestin and VEGF suggests that latter possibly augments stem cell survival. Thus, anti-VEGF therapy may be a good option in future for nestin immunopositive ependymomas. “
“The chromosome 16q22.1-linked

https://www.selleckchem.com/products/ulixertinib-bvd-523-vrt752271.html autosomal-dominant cerebellar ataxia (16q-ADCA) is a form of spinocerebellar ataxia (SCA) common in Japan. It is clinically characterized by late-onset purely cerebellar ataxia. The neuropathologic hallmark of 16q-ADCA is degeneration of Purkinje cells accompanied by an eosinophilic structure which we named “halo-like amorphous materials”. By immunohistochemistry and electron microscopy, the structure has been so far found to contain two components: the somatic sprouts Navitoclax solubility dmso from the Purkinje cells and presynaptic terminals of unknown origin. As far as we are aware, this peculiar morphological change of Purkinje cells has not been previously described. Further investigations may disclose unique pathological processes in SCA. There is a considerable difference in frequencies of autosomal dominant cerebellar ataxias, also called spinocerebellar ataxia (SCA), in a small country such as Japan. However, overall, Machado-Joseph disease (MJD) and spinocerebellar

PR-171 research buy ataxia type 6 (SCA6) are the two most prevalent SCAs in Japan. SCA1, SCA2 and dentatorubral-pallidoluysian atrophy (DRPLA), a form of SCA originally identified in Japan, are also present. These SCAs, caused by trinucleotide (CAG) repeat expansions, are diagnosed with relatively simple molecular genetic tests. While these SCAs with CAG repeat expansions are the major fraction of SCA, approximately 10–40% of all SCAs account

for diseases for which mutations have not yet been identified.1 We have been pursuing a form of SCA in which any of the known CAG repeat expansions are excluded from its cause. We started investigation on six such families which showed slowly progressive, seemingly purely cerebellar, ataxia in every generation.2 We embarked on a genome-wide linkage analysis using approximately 300 microsatellite DNA markers to discover in which chromosome the mutation is located. After screening all autosomal chromosomes, we found a significant evidence of linkage to the long arm of chromosome 16 (16q22.1).2 Surprisingly, this locus had been already known for SCA4, a SCA with prominent sensory axonal neuropathy associated with pyramidal tract signs.3 While every SCA4 patient showed prominent sensory axonal neuropathy, none of our patients presented such a remarkable “extracerebellar” dysfunction. In addition, ages of onset were earlier in SCA4 than in our families.

During surgery all not-viable tissues of the pectoralis major muscle were removed. Thoracentesis and drainage of the left pleural cavity were performed. In histopathology of operative material wide non-septate, non-pigmented hyphae were found (Fig. 1). The culture was identified selleck inhibitor as Lichtheimia corymbifera. On October 23, neutrophil count was restored (2.4 × 109/l). The total duration of severe neutropenia was more than 70 days. Despite the antifungal therapy the necrosis of soft tissue progressed (Fig. 2). Caspofungin 70 mg d−1, subsequently 50 mg d−1 was

added to the therapy. On November 2, a second surgical debridement was performed of the soft tissues of the frontal chest wall and subperiostal resection of the IV, V ribs with the cartilages in the area from the sternum to the anterior axillary line. Histopathology confirmed the presence of fungal structures in the cartilage. Combined antimycotic therapy was continued in the same mode with a positive effect (Fig. 3). Repeated cultures from affected area were negative. During the same period clinical and laboratory remission AML was achieved. On chest CT scan signs of pulmonary fibrosis were found. Plastic surgery of the wound with a skin

graft from the front surface of the left thigh was performed on December 1 (Fig. 4). On December 15, the combination antifungal therapy had been completed. Total duration of amphotericin B and caspofungin treatment was 52 days. Further antimycotic therapy was continued with posaconazole (800 mg d−1). Three courses of cytostatic chemotherapy Daporinad nmr for consolidation of AML remission were performed. Each course had been followed by a period of severe neutropenia for 10–14 days. The patient

continued to receive posaconazole, and total duration of antimycotic therapy was 210 days. At present, the patient is in good condition with complete remission of AML and mucormycosis. The study was prospective, multicentre and observational. Mucormycosis Loperamide was diagnosed and antifungal treatment was evaluated according to the criteria of European Organization for Research and Treatment of Cancer (EORTC) and National Institute of Allergy and Infectious Diseases Mycoses Study Group (NIAID-MSG), USA.[3, 4] Species identification of mycormycetes was confirmed by sequencing of ITS/D1-D2 fragments of fungal ribosomal DNA.[5] During the period 2004–2013, we observed 36 haematological patients aged 5–74 years (mean age 23 ± 12 years) from nine hospitals of St. Petersburg. Among them 14 were children (38%, median age 11 ± 3 years), and 22 adults (62%, median age 28 ± 14 years): 18 males (53%), 16 females (47%). Almost all cases of mucormycosis developed after a long stay in the hospital (97%) with a median of 36 days. One case developed during outpatient follow-up after undergoing allogeneic haematopoietic stem cell transplantation (allo-HSCT).

It arose in the left anterior cingulate cortex with a pseudo-polycystic appearance on neuroimaging. Histological features contained the “specific glioneuronal element” mimicking DNT FK506 solubility dmso and the components of distinct neurocytic rosettes with a center of neuropil islands and pilocytic astrocytoma resembling RGNT. Although the mechanisms of mixed glioneuronal tumor are far from being well-known, their co-existence might suggest a possible etiologic relationship between DNT and RGNT. “
“C. Soler-Martín, Ú. Vilardosa, S. Saldaña-Ruíz, N. Garcia and J. Llorens (2012) Neuropathology and Applied Neurobiology38, 61–71 Loss of neurofilaments in the neuromuscular junction

in a rat model of proximal axonopathy Aims: Rodents exposed to 3,3′-iminodipropionitrile (IDPN) develop an axonopathy similar to that observed in amyotrophic lateral sclerosis motor neurones, in which neurofilaments accumulate in swollen proximal axon segments. This study addressed the hypotheses that this proximal axonopathy is associated with loss of neurofilament proteins in the neuromuscular BYL719 order junctions and a progressive loss of neurofilaments

advancing in a distal-proximal direction from the distal motor nerve. Methods: Adult male Long-Evans rats were exposed to 0 or 15 mM of IDPN in drinking water for 1, 3 or 5 weeks, and their distal axons and neuromuscular junction organization studied by immunohistochemistry. Quantitative data were obtained by confocal microscopy on whole mounts of the Levator auris longus. Results: PDK4 Muscles showed no change in the distribution of acetylcholine receptor

labelling in the neuromuscular junctions after IDPN. In contrast, the amount of neurofilament labelling in the junctions was significantly reduced by IDPN, assessed with two different anti-neurofilament antibodies. In preterminal axons and in more proximal axon levels, no statistically significant reductions in neurofilament content were observed. Conclusions: The proximal neurofilamentous axonopathy induced by IDPN is associated with an abnormally low content of neurofilaments in the motor terminals, with a potential impact in the function or stability of the neuromuscular junction. In contrast, neurofilaments are significantly maintained in the distal axon. “
“We report clinicopathological features of a 23-year-old woman with Down syndrome (DS) presenting with subacute myelopathy treated with chemotherapy, including intravenous and intrathecal administration of methotrexate (MTX), and with allogenic bone-marrow transplantation for B lymphoblastic leukemia. Autopsy revealed severe demyelinating vacuolar myelopathy in the posterior and lateral columns of the spinal cord, associated with macrophage infiltration, marked axonal loss and some swollen axons.

Inguinal lymphocele nonresponsive to conservative treatment can be advantageously studied by LS and successfully treated by microsurgical reconstructive procedures, above all if associated to LL. © 2013 Wiley Periodicals, Inc. Microsurgery 34:10–13, 2014. Groin lymphocele (GL) is an important complication after inguinal lymph node dissection, for skin melanoma, vulvar cancer, and venous surgery,

with an incidence varying from 1.3 to 18.9%.[1-3] Conservative resolution is possible through Protease Inhibitor Library several needle aspirations and compression bandaging, but it usually takes several months to show the risk of infections and other late complications. Recently, the use of intraoperative Isosulfan Blue,[4] modified technique of radical inguinal lymphadenectomy[5]and laparoscopic lymphnode resection,[6] have reduced the incidence of postoperative lymphatic morbidities such as wound dehiscence, infections, lymphorrhoea, and lymphedema. However, the incidence of lymphocele remains significant.[7] Nonoperative treatment of lymphocele arising from lymphatics injured during groin dissection

is not rarely unsuccessful. Different surgical NVP-BGJ398 price methods have been proposed,[8] but all involve the closure of lymphatics merging at the lymphocele, increasing the risk of postoperative lower limb lymphedema or of worsening lymphedema if already clinically evident. In this report, we assessed the efficacy of a diagnostic and therapeutic protocol to manage inguinal lymphocele using lymphoscintigraphy (LS) and microsurgical procedures. Sixteen patients with unilateral GL were included in this report. Lymphocele was present for a mean period of 5.7 months (3–8 months) before surgical treatment. None of the patients had responded to

conservative treatment, including needle aspiration, sclerosing therapy, and compression. Infection occurred in three patients, with lymphangitis and fever. The mean age of the patients was 53.4 years (42–63 years). The size of lymphoceles varied from 7 to 12 cm in diameter. Seven of them presented also clinically evident leg lymphedema (LL) at the same side of the lymphocele. All of them had been previously treated nonoperatively by needle aspiration, Vildagliptin sclerosing agents, and compression bandaging without healing of the pathology and relapse of lymphocele. Diagnostic investigations included venous ultrasound and superficial and deep LS of lower limbs. The patients’ information is shown in Table 1. To quantify visual findings in LS, the Kleinhans transport index (T.I.) was used. In this index, five parameters describe the lymph flow: lymphatic transport kinetics (K), distribution pattern (D), time lapse to appearance of lymph nodes (T in minutes, multiplied by 0.04), assessment of lymph nodes (N), and assessment of lymph vessels (V).

T cell proliferation: Heparin anticoagulated blood (50 ml) was obtained from 10 randomly selected members of each of the three subject groups and centrifuged at 850 g for

20 min. Plasma was removed, and cells were suspended Vismodegib purchase in D-Hanks solution. This was layered onto Ficoll separation medium in a tube followed by centrifugation at 850 g for 20 min. Cells in the middle layer were carefully collected, which were peripheral blood mononuclear cells (PBMCs). PBMCs were washed 3 times in RPMI-1640 by centrifugation at 450 g for 10 min and then re-suspended in RPMI-1640 to a density of 1 × 108/ml. A fraction of this cell suspension was loaded onto a prewarmed Nylon Fiber column T (37 °C) with RPMI-1640 medium containing 10% FBS; the volume of the cell suspension was one-third that of the column. After sealing,

MAPK Inhibitor Library cell assay the column was kept warm at 37 °C for 1 h, after which prewarmed RPMI-1640 (37 °C) was added at a flow rate of 3–4 ml/min. The opaque medium was collected, which contained T lymphocytes. T lymphocytes were re-suspended in RPMI-1640 containing 10% FBS at a density of 1 × 106/ml. Cell suspensions were added to a 96-well plate (100 μl/well) followed by adding PHA (final concentration: 20 μg/ml; and final volume in each well: 200 μl). As controls, cells without PHA were also included, and three wells were included for each group. Plates were incubated at 37 °C in a 5% CO2 atmosphere for 48 h. At 4 h before the end of incubation, MTT (20 μl; 5 g/l) was added and incubation was continued at 37 °C for the remaining 4 h. The plate was centrifuged, the supernatant was removed, and DMSO (100 μl/well) was added to dissolve the crystals followed by incubation for 15 min. Optical

density (OD) was measured with a Progesterone microplate reader (detection wavelength: 570 nm; reference wavelength: 630 nm), and a stimulation index (SI) was calculated: SI = ODexperiment/ODcontrol. Cytokine-induced killer (CIK) cell culture and assessment of tumouricidal activity: PBMCs were suspended in RPMI-1640 at a density of 1 × 106/ml. On day 0, γ-INF (1000 U/ml) was added followed by incubation at 37 °C in a 5% CO2 atmosphere for 24 h. On day 1, IL-1 (100 U/ml), CD3 mAb (50 ng/ml) and IL-2 (500 U/ml) were added followed by further incubation; half of the medium was refreshed every 3 day during which IL-2 was added. On day 6, CD3 mAb (50 ng/ml) was added again. On day 15, cells (CIK cells) were harvested and re-suspended in RPMI-1640 at a density of 1 × 106/ml; these were used as effector cells. K562 cells were used as target cells. Effector cells were mixed with target cells at a ratio of 10:1 and then added to a 96-well plate. As controls, effector cells or target cells alone were also added to three wells for each group. MTT (20 μl; 5 g/l) was added, and plates were incubated at 37 °C in a 5% CO2 atmosphere for 4 h followed by centrifugation.

0008 [.0011], z = −.71, p = .4761). Turning to interdyadic

differences (random effects, Table 2), affect and language patterns showed significant values. With respect to affect, the covariance between intercept and linear effect of age was significant (χ2[1] = 4.51, p < .05), with the variability decreasing nonlinearly toward the end of the second year of life. As regards language, significant differences between dyads were found for the intercept (σ2u0), the slopes (σ2u1), and the covariance between intercept and slopes (σ2u01) for the linear trend (respectively, χ2[1] = 4.27, p < .05; χ2[1] = 4.13, p < .05; χ2[1] = 4.21, p < .05). As shown in Figure 6, three of 10 dyads (dyads 8–10) started to increase the proportional duration of language patterns from about 14 months (65 weeks), whereas the others remained quite low until 18 months (80 weeks). selleck Only at that age did these latter dyads begin to accelerate,

although at a slower rate than the former. Finally, the covariance effect signals that differences among dyads in the use of language become more this website and more evident over time. Finally, intradyadic variance for the affect and language patterns showed a systematic time-dependent pattern. As to affect, the covariance between the intercept and the linear effect of age was significant (σ2e01 =.00004, χ2[1] = 3.73, p < .05), meaning that variability among sessions increased at the end of the observational period. As to language, the difference in proportional duration of these frames

among sessions was time dependent (σ2e1 = .00001, χ2[1] = 22. 56, p < .00), meaning that Endonuclease this difference increased rapidly and in a nonlinear way with advancing infant age. As the covariance between the intercept and the linear component (σ2e01 =.00027, χ2[1] = 79.77, p < .00) was also significant, the sessions differed more at the end of the second year than at the beginning. Therefore, as for symmetrical patterns, language patterns also increased with a certain degree of fluctuation. This study aimed to examine mother–infant social play in the second year of life. With reference to Fogel’s (1993) model of interaction as a continuous adjustment between partners instead of a sequence of discrete acts, we focused on mother–infant interpersonal functioning during play rather than on individual behaviors. Communicative patterns were identified (Fogel, 1993) to distinguish different forms of coregulation, an intensive longitudinal design was adopted to match the developmental process as closely as possible, a multiple case study was used to make claims about the group as well as the individuals and, finally, a hierarchical linear analysis was performed to model the trajectories of different coregulation forms. We expected to find developmental transitions and individual differences.

1A and B). It should be noted that the recombination

efficiency of Cyldflx9 allele in LckCre-Cyldflx9/flx9-Ikk2flx/flx mice was comparable to its recombination efficiency in LckCre-Cyldflx9/flx9 mice (Supporting Information Fig. 1B). Moreover, the efficient recombination of the Cyldflx9 allele was further confirmed by the very low levels of full-length Cyld transcript and the expression of CyldΔ9 transcript in the thymocytes of LckCre-Cyldflx9/flx9-Ikk2flx/flx mice, which were comparable to the corresponding transcript levels in the thymocytes of LckCre-Cyldflx9/flx9 mice (Supporting Information Fig. 1C). Finally, CYLD protein was practically undetectable (Supporting Information Fig. 1D), and IKK2 was Buparlisib purchase also greatly reduced in thymocytes from LckCre-Cyldflx9/flx9-Ikk2flx/flx double mutant mice as determined by immunoblotting (Supporting Information Fig. 1D). We have previously demonstrated that LckCre-Cyldflx9/flx9 mice exhibit a dramatic decrease in the numbers of SP thymocytes. Interestingly, the concomitant inactivation of Ikk2 and Epacadostat Cyld resulted in the restoration of CD4 SP development, whereas CD8 SP cells were slightly reduced when compared with control mice but overall

their representation was within the normal range (Fig. 1A and B). Our previous data established that the demise of CyldΔ9 SP thymocytes was due to a block in positive selection. During the process of positive selection, the phenotype of DP cells changes to reflect a state of activation prior to the acquisition of a single CD4+ or CD8+ co-receptor phenotype. These changes include the increase in surface TCR expression from intermediate (TCRβint) to high (TCRβhi) levels, the transient expression of the early activation marker CD69 20 and the increase

in the expression of the TCR-associated about molecule CD5 21 marking the initiation of selection. In wild-type mice, TCR−/loCD69− cells consist of preselection DP thymocytes; TCRint CD69lo/hi are cells initiating and undergoing positive selection whereas TCRhi CD69hi and finally TCRhi CD69lo/− represent mainly postselection thymocytes 22. As shown in Fig. 1C, CyldΔ9 DP thymocytes were capable of initiating positive selection since TCRβintCD69lo/hi DP thymocytes were even more abundant in LckCre-Cyldflx9/flx9 mice compared with control mice (Fig. 1C and D). Furthermore, immature TCRhiCD69hi SP thymocytes as well as mature TCRhiCD69lo/− SP thymocytes were dramatically reduced. Interestingly, the thymocyte subpopulations in mice with mutated Cyld and Ikk2 were restored to levels that were comparable to those seen in control mice (Fig. 1C and D). As shown in the Supporting Information Fig. 2, CyldΔ9 DP cells initiated the process of positive selection as indicated by the overrepresentation of TCRloCD5int cells in comparison to control thymocytes.

After 48 hr, however, h-S100A9-stimulated cells showed almost no further increment in NF-κB activity, but LPS-stimulated cells had further increased NF-κB activity at 48 hr of stimulation (Fig. 1). During the past few years, emerging evidence showed that at least part of the effects claimed for S100A9 protein might selleck screening library have been influenced by LPS contamination.[29, 30] To avoid this problem, we ensured that highly

purified recombinant human and mouse S100A9 protein was used. To confirm that the h-S100A9 protein was LPS free, we stimulated THP-1 XBlue cells with h-S100A9 or LPS in the presence of 50 μg/ml polymyxin B. After 48 hr of incubation, the h-S100A9 effect was only slightly inhibited by polymyxin B, whereas the LPS effect was completely absent (Fig. 1). The partial inhibition of the h-S100A9 effect by polymyxin

B might be the result of an effect of polymyxin B on cell signalling. To address this possibility, we incubated THP-1 XBlue cells with 1 ng/ml TNF-α with or without polymyxin B and also here, we found a slight reduction of NF-&kgr;B activation (see Supplementary material, Fig. S1c), indicating that part of the inhibition mediated by polymyxin B might not be the result of LPS contaminants. Furthermore, we also treated h-S100A9 and LPS at 80° for Lenvatinib 30 min and observed that the h-S100A9 effect was almost completely abolished, whereas the LPS effect remained intact (see Supplementary material, Fig. S1b). From these results we could conclude that h-S100A9 induced NF-κB activity directly. We next investigated whether h-S100A9 would induce a similar cytokine response as did LPS. After 4 hr stimulation, both molecules induced elevated secretion of IL-1β, Terminal deoxynucleotidyl transferase TNF-α, IL-6, IL-8 and IL-10. However, despite the similar NF-κB activation after 4 hr of stimulation, h-S100A9 induced less potent cytokine secretion than LPS. After 48 hr of stimulation, LPS was still able to stimulate IL-6, IL-8 and above all IL-1β secretion, whereas h-S100A9 stimulation only induced secretion of IL-8 at this

time-point (Fig. 2). We confirmed our findings using mouse BM-DC stimulated with murine S100A9 (m-S100A9) or LPS under the same conditions as human THP-1 cells (Fig. 3a). Mouse BM-DC are considered a good model of mouse monocytes[48] and the name ‘dendritic cells’ refers mainly to their shape, which resembles dendritic cells. In this model, we chose to study cytokine secretion after 48 hr stimulation when the cytokine concentration reached the plateau even if we could observe cytokine secretion already at 4 hr (data not shown). Once again, the m-S100A9 effect was less potent than LPS. The BM-DC remained a heterogeneous population of granulocytes, macrophages and DC even after the incubation with granulocyte–macrophage colony-stimulating factor for 7 days. Hence, we confirmed our findings with isolated CD11c+ BM-DC.

The second report focused on the recently recognized disease, IgG4-related nephropathy, arising in the kidney allograft. Two special comprehensive lectures were provided after the oral session in order to help the audience gain a thorough understanding and update their knowledge. One looked at anti-HLA antibody in kidney transplantation – basic and practical management of desensitization

– and was presented by Dr. H. Ishida, from the preeminent transplant centre in Japan. Another paper on BK virus nephropathy was delivered by Dr K. Masutani, who is an authority in this field in our country. Best of all, the main topic focused on protocol kidney allograft Protease Inhibitor Library biopsy, and two doctors (Dr Y. Fukasawa and Dr T. Tanabe) from the enthusiastic institution reported the results and their implications from the pathological or clinical point of view. A selection

of nine interesting case reports and two original articles have been included in this supplement CHIR-99021 in vivo of Nephrology, and two comprehensive reviews are available in Mini Reviews. All of these were presented in the 17th Japanese Clinicopathological Conference of Renal Allograft Pathology and intensely discussed by the participants. Dr K. Morozumi, one of the editors, contributed a review article titled ‘Recurrent glomerular disease after kidney transplantation: an update of selected areas and the impact of protocol biopsy’ in Mini Reviews. We hope that readers enjoy the interesting issues and that this supplement is helpful for understanding the current concept of injury in kidney allografts and as a mediator between clinicians and pathologists of optimal treatment for patients. The guest editors would like to thank all authors and participants for their contributions. We would especially like to express our sincere appreciation

to Drs K. Morozumi and Y. Yamaguchi, organizers of the meeting acting as the general secretaries. Finally, we are eternally grateful to the editors of Nephrology for accepting the proceedings of the Japanese Clinicopathological Conference of Renal Allograft Pathology and their sincere cooperation in publishing this supplement. The author has no see more conflicts of interest to declare. “
“There is a disproportionate increase in the number of elderly patients, many with multiple co-morbidities, commencing dialysis. Predictors of survival for elderly patients on dialysis include age, comorbidity score, malnutrition, poor functional status and late referral. Patients with high co morbidity scores may not gain a survival advantage with dialysis vs a non dialysis pathway. Late referral and lack of dialysis access are independent predictors of mortality in elderly patients commencing dialysis.