Conclusion: 3D CTA with stereotactic fiducials allows surgeons to adequately estimate abdominal flap volume before surgery, potentially giving guidance in the amount of tissue that can be harvested from a patient’s lower abdomen. © 2011 Wiley-Liss, Inc. Microsurgery, 2011 “
“The present study investigates the vascular anatomy of the vastus lateralis motor nerve (VLMN) to be used as a vascularized nerve graft in facial nerve reconstruction. We evaluated the maximum length of the nerve that can be included in the flap and its vascular pedicle. In addition, we discuss its adequacy for use in early reconstruction of the facial AZD6244 supplier nerve both as ipsilateral facial nerve reconstruction and

as cross-facial nerve graft. Five fresh cadavers were used in this study. In all specimens, the VLMN and its vascular pedicle were dissected, photodocumented and measured using calipers. In addition, two vascularized

VLMN were injected with a radiopaque cAMP inhibitor contrast and underwent CT angiography and three dimensional reconstructions were scanned to illustrate the vascular supply of the nerve using OsiriX Software. The VLMN was divided into two divisions, an oblique proximal and a descending distal, in 70% of the dissections with a mean maximal length of 8.4 ± 4.5 cm for the oblique division and 15.03 ± 3.87 cm for the descending division. The length of the oblique division, when present, was shorter than the length of the descending branch in all specimens. The mean length of the pedicle was 2.93 ± 1.69 cm, and 3.27 ± 1.49 cm until crossing the oblique and the descending division of the nerve respectively.

The mean caliber of the nerve was 2.4 ± 0.62 mm. Three-dimensional computed tomography angiography demonstrated perfusion throughout the entire VLMN by branches from the descending branch of the lateral femoral circumflex artery which ran parallel to the descending division of the VLMN. Additionally, we observed that technically it was possible to preserve the Ergoloid oblique branch of the VLMN. This study confirms that VLMN presents adequate anatomic features to be used as a vascularized nerve graft for facial nerve reconstruction in terms of length, pedicle, and caliber. © 2014 Wiley Periodicals, Inc. Microsurgery, 2014. “
“Introduction: Although, the success of free flaps has increased in the last years, more details about its characteristics might improve the clinical outcome of the flaps. This study examined the thermoregulatory ability as a sign of neural re-innervation of two different types of microsurgical free flaps in the postoperative course. Methods: A total of 22 patients were examined after grafting two different flap types: The latissimus dorsi myocutaneous (LDM) flap (n = 11) and the anterolateral thigh (ALT) flap (n = 11).

MS was considered a white matter disease, but more recent studies have shown that grey matter can also

be seriously affected. MS is thought to be an autoimmune disorder, in which the immune cells enter the CNS and attack the myelin sheath covering the neurones, causing demyelination and, eventually, axonal damage. Demyelination leads to a variety of sensory and motor symptoms, such as optic neuritis, numbness, fatigue, spasticity, muscle weakness and cognitive impairment [2]. An autoimmune basis is supported by the mouse model experimental autoimmune encephalomyelitis (EAE), evoked by immunization with myelin antigens (e.g. spinal cord homogenate) in Freund’s adjuvant. EAE is a T cell-driven Endocrinology antagonist disease. Work on the resulting MS-like disease in the mouse model has suggested novel potential pathogenetic pathways and therapeutic agents, but these could not always be translated to the human disease [3]. The pleiotropic function of B cells (Fig. 1) and their potential involvement in MS pathogenesis has been overshadowed by the emphasis on T cell research in the last decade. However, recent exciting results with B cell-depleting agents highlight the pathogenetic roles for key players other than T cells. MS research is complicated by the inaccessibility of its target organ during life. Much of

the work, therefore, has selleck products focused on post-mortem brains. It has been helped by the typical mixture of old and new white matter lesions in affected MS brains. Peripheral B and T cells are numerous in white matter lesions, being frequent in acute lesions and the active margins of chronic active lesions, rather than in inactive lesions [4–7]. The characteristic inflammatory infiltrates of B, T, dendritic and plasma cells are primarily perivascular [8–11]; Tolmetin however, CD8+ T cells, in particular, tend to invade into the surrounding parenchyma. T helper type 1 (Th1) and CD4+ and CD8+ T cells expressing interleukin (IL)-17 are found in perivascular areas [6,12]. CD4+ cells were found mainly in perivascular spaces and the meninges, where B cells were also detected [5,8,13–15]. Much information has come from analysing cerebrospinal fluid (CSF); it occupies the subarachnoid

space just outside the pia mater that tightly ensheathes the brain and spinal cord and lines the ventricles. During life, tapping CSF is the most practical way of sampling the CNS milieu. In MS patients, there is evidence of persistent intrathecal B and plasma cell activation [16,17]. The characteristic oligoclonal immunoglobulin bands (OCBs) are defined as two or more independent immunoglobulin (Ig)G bands in the electrophoretic gamma region in CSF but not serum. They are found in most patients with MS and imply an immune-mediated pathology, possibly of infectious nature. However, OCBs are also present in other inflammatory diseases of the CNS, e.g. subacute sclerosing panencephalitis, where they are directed against measles virus [18].

Our data suggest that TNFRSF25 agonists, such as soluble TL1A, could potentially be used to enhance the immunogenicity of vaccines that aim to elicit human anti-tumor CD8+ T cells. The Selleck GW-572016 TNF receptor superfamily (TNFRSF) constitutes a group of structurally related cell surface glycoproteins that regulate innate and adaptive immunity 1. A subgroup of the TNFRSF

contains a conserved region within the cytoplasmic domain known as the death domain 1. Triggering of death domain-containing members of the TNFRSF can lead to the induction of apoptosis via activation of caspase-8 or stimulation of the MAP kinase and NF-κB signaling pathways. TNFRSF25, also known as death receptor 3, is most similar in sequence to TNFR1; however, unlike the widely distributed TNFR1, TNFRSF25 is expressed primarily on T cells 2, 3. The ligand for TNFRSF25 is TL1A, a TNF-like protein that exists either as a membrane-anchored protein or a soluble cytokine 4. TL1A is produced by activated DCs, monocytes, endothelial cells and T cells 4–6. TL1A costimulates T-cell production of effector cytokines in vitro 4, 6–8 and enhances the accumulation of CD4+ effector

T cells within the inflamed tissues Everolimus concentration in autoimmune and inflammatory disease models 6. TL1A also promotes Treg proliferation and attenuates Treg-mediated suppression of non-regulatory CD4+ T cells 9. In addition, TL1A has been shown to costimulate invariant NKT cells 10 and may have a role in enhancing NK cell-mediated tumor cell killing 11. In Megestrol Acetate contrast with the well-established costimulatory effects of TNFRSF25 on CD4+ T cells, little is known about its role in regulating CD8+ T-cell responses. Here we addressed the function of TNFRSF25 during CD8+ T-cell activation and in the setting of anti-tumor immunity in which CD8+ T cells play a critical role. Three transfected

J558L tumor cell lines that express relatively high levels of TL1A (Fig. 1A) were combined immediately before inoculation into mice. In T- and B-cell-deficient SCID mice TL1A-expressing J558L tumor cells grew with similar kinetics to control J558L cells transfected with the empty vector (Fig. 1B). In sharp contrast, TL1A-expressing J558L cells, but not control tumor cells, were rejected in immune competent BALB/c mice, demonstrating that tumor rejection requires an adaptive immune response (Fig. 1C). In many cases, TL1A-expressing J558L tumors grew initially following s.c. injection into BALB/c mice, but these tumors regressed and the majority of animals had no detectable tumors 70 days after initial tumor inoculation (Fig. 1C). Mice that rejected the TL1A-expressing J558L tumors were immune to a subsequent challenge with non-transfected J558L tumor cells (Fig. 1D and Supporting Information Fig. 1A). To assess the role of T-cell subsets in TL1A-mediated tumor rejection, we administered anti-CD4 or anti-CD8 depleting mAbs prior to inoculation with TL1A-expressing J558L tumor cells.

Vasomotion Becomes Less Random as Diabetes Progresses in Monkeys.

Microcirculation 18(6), 429–439. Objective:  Changes in vasomotion may precede other global indices of autonomic dysfunction that track the AZD9291 nmr onset and progression of diabetes. Recently, we showed that baseline spectral properties of vasomotion can discriminate among N, PreDM, and T2DM nonhuman primates. In this study, our aims were to: (i) determine the time dependence and complexity of the spectral properties of vasomotion in three metabolic groups of monkeys; (ii) examine the effects of heat-provoked vasodilatation on the power spectrum; and (iii) compare the effects of exogenous insulin on the vasomotion. Materials and Methods:  Laser Doppler flow rates were measured from the foot in 9 N, 11 PreDM, and 7 T2DM monkeys. Baseline flow was measured at 34°C, and under heat stimulation at 44°C. Euglycemic–hyperinsulinemic clamps

were performed to produce acute hyperinsulinemia. The Lempel–Ziv complexity, prediction error, and covariance complexity of five-dimensional embeddings were calculated as measures of randomness. Results and Conclusions:  With progression of diabetes, measures of randomness of the vasomotion progressively decreased, suggesting a progressive loss of the homeostatic capacity Ku-0059436 datasheet of the peripheral circulation to respond to environmental changes. Power spectral density among T2DM animals resided mostly in the 0- to 1.45-Hz range, which excluded the cardiac

component, suggesting that with progression of the disease, regulation of flow shifts toward local rather than central (autonomic) mechanisms. Heating increased all components of the spectral power in all groups. In N, insulin increased the vasomotion contributed by endothelial, neurogenic, vascular myogenic, and respiratory processes, but Avelestat (AZD9668) diminished that due to heart rate. In contrast, in T2DM, insulin failed to stimulate the vascular myogenic and respiratory activities, but increased the neural/endothelial and heart rate components. Interestingly, acute hyperinsulinemia resulted in no significant vasomotion changes in the chronically hyperinsulinemic PreDM, suggesting yet another form of “insulin resistance” during this stage of the disease. “
“Please cite this paper as: Drummond GB, Vowler SL. Analysis of variance: variably complex. Microcirculation 19: 280–283, 2012. “
“Please cite this paper as: Flouris and Cheung (2011). Thermal Basis of Finger Blood Flow Adaptations During Abrupt Perturbations in Thermal Homeostasis. Microcirculation18(1), 56–62. The objective of this experiment was to assess whether reflex alterations in finger blood flow during repetitive hot and cold water immersion are associated with changes in rectal, tympanic, mean body temperature or heat storage. Fifteen healthy adults (eight males) volunteered.

89 Resistance is much less common than with lamivudine: 0% at one year and 29% at 5 years.90 This makes adefovir an option as add-on therapy in patients who have developed lamivudine resistance.91 Adefovir has not been well examined in patients with renal failure. A French study used adefovir in a composite series of 12 patients with CKD,92 all of whom had lamivudine-resistant HBV. There was a significant fall in HBV DNA levels after a median of 15 months of therapy. Only one of these patients was actually receiving dialysis during the study. A case report described successful treatment of HBV infection in

a dialysis-dependent liver transplant recipient who had lamivudine-resistant infection and cirrhosis of the allograft.93 Entecavir is a promising drug in the management click here of HBV infection. In patients with normal renal function, entecavir has been shown to be superior to lamivudine94 and adefovir95 in reducing HBV DNA levels. Although there are not the long-term data that exist for lamivudine, resistance

rates appear to be low. Entecavir has not been studied in dialysis patients, although the dose should be reduced in renal failure.79 Tenofovir, a nucleotide reverse transcriptase inhibitor, is recommended as a Selleck Dorsomorphin first-line oral antiviral in HBV patients with normal renal function.96 Although larger series have not found tenofovir to be culpable in HIV patients with G protein-coupled receptor kinase renal failure,97 there have been a number of case reports of tubular toxicity and acute kidney injury98–100 with tenofovir use. This raises concern regarding the potential for nephrotoxicity in dialysis patients with residual renal function. A case report showed that tenofovir was effective in a single HBV-infected HD patient. This paper also assessed tenofovir pharmacokinetics,101 and recommended

a dose of 300 mg once a week to prevent accumulation. This was endorsed by the manufacturers in a study of nine HD patients.102 In summary, lamivudine has the most solid body of experience to support its use. Tenofovir and entecavir are likely to be more effective, and tenofovir has been shown to be safe in HD patients, but neither drug has any significant evidence base from this patient group. Determining which dialysis patients with chronic HBV infection to treat is a matter of controversy. In the case of patients with normal renal function, treatment is recommended for those with active HBV replication (HBeAg positive and/or HBV DNA positive) and raised alanine transaminase (ALT) levels.103 It is clear that patients with ESRD exhibit a different clinical and biochemical picture in chronic HBV infection.104 HD patients with HBV infection are less likely to have a symptomatic acute illness, and are more likely to develop chronic carrier status.

We observed that while PD0325901 NKT cells from mice administered with α-GalCer by the intravenous route exhibited high levels of PD-1 expression at day 1 post-immunization, those in mice where α-GalCer was delivered by the intranasal route did not (Fig. 5). Furthermore, PD-1 expression on NKT cells coincided with functional exhaustion and unresponsiveness at 24 h after a second dose of α-GalCer by the intravenous route but not when α-GalCer was delivered by the

intranasal route where NKT cells were fully functional in terms of IFN-γ production and expansion (Figs 1 and 3). Thus, in addition to the cell type mediating α-GalCer presentation

(i.e. DCs versus B cells), the phenotype of NKT cells in terms of PD-1 expression could be another important factor for the avoidance of NKT cell anergy resulting from mucosal α-GalCer delivery Navitoclax (e.g. intranasal route), as opposed to systemic delivery (e.g. intravenous route). These observed differences between intravenous versus intranasal route of α-GalCer delivery may enable the repeated activation of NKT cells to aid in promoting DC activation which allows α-GalCer to serve as an efficient mucosal adjuvant for inducing immune responses to co-administered antigens. In fact, as shown in Fig. 2 a booster dose

of α-GalCer administered by the intranasal route resulted in a subsequent increase in antigen-specific immune responses, while a booster dose of α-GalCer administered by the intravenous route did not correspond to an increase in antigen-specific immune responses. In addition to the differences in terms of NKT cell anergy induction FAD or the lack thereof, our investigation revealed several other differences for NKT cell activation after intravenous versus intranasal administration of α-GalCer. First, the timing of NKT cell activation and expansion appeared to be prolonged after intranasal administration of α-GalCer because the peak levels of NKT cell expansion were observed at day 5 post-immunization in the lung, the main responding tissue for this route of immunization. These results differ from that seen after the intravenous immunization where the NKT cell population peaked at day 3 in all tissues tested. In this regard, Fujii et al. 8 reported that intravenous administration of DCs pulsed ex vivo with α-GalCer, as opposed to free α-GalCer, which is shown to be a potential approach to avoid anergy to NKT cells, resulted in a prolonged NKT cell response, as measured by IFN-γ production.

1b). Using multiple regression analysis, we evaluated independent effects of genetic and non-genetic factors on the development of thyroid autoantibodies. The reference categories for the analysis were CT60 CTLA-4 genotype, age, family history of AITD and cigarette smoking. In the case of thyroid peroxidase antibodies, MI-503 chemical structure we confirmed a significant contribution of CT60 CTLA-4 genotype (P < 0·007) and younger age (P < 0·05), while family history and cigarette smoking did not prove to have any effect. In thyroglobulin antibodies, no contribution of either genotype or non-genetic factors

was confirmed. The genotyping in the group of 75 PPT patients revealed the AA genotype in 17 (22·7%) patients, the AG genotype in 36 (48%) and the GG genotype in 22 (29·3%) patients, showing no deviation from HWE (χ2 0·096, P = 0·757). As presented in Table 2, the patients with different genotypes did not differ in age, number of pregnancies, family history of AITD and smoking status. However, females with the G-allele carrying genotypes presented significantly more often with positive values of thyroid peroxidase antibodies (P < 0·04), while

the proportion of thyroglobulin antibody-positive patients did not differ significantly between the three genotypes. Similarly, more patients with the G-allele carrying genotypes had at least one type of thyroid autoantibody elevated compared

to the AA genotype (P < 0·04) (Table 2). Furthermore, the median value of thyroid peroxidase antibodies was Staurosporine clinical trial significantly lower in the AA genotype compared to the AG and GG genotypes (median, 12, 130 and 423 U/ml, respectively, P < 0·006) (Fig. 2a). In contrast to thyroid peroxidase antibodies, the median values of thyroglobulin antibodies did not differ significantly between the three genotypes (Fig. 2b). For the evaluation of thyroid autoantibody Urocanase development with multiple regression analysis, the reference categories were CT60 CTLA-4 genotype, age, number of pregnancies, family history of AITD and cigarette smoking. For thyroid peroxidase antibodies, we established a significant contribution of CT60 CTLA-4 genotype (P < 0·04), while the effect of other factors was not confirmed. In thyroglobulin antibodies, no significant contribution of genetic or non-genetic factors was found. In PPT patients, 41 (54·7%) were hyperthyroid at presentation, while hypothyroidism was established in 34 (45·3%) patients. As presented in Table 3, the median value of thyroid peroxidase antibodies was significantly higher in the hypothyroid form of disease (P < 0·0001). Similarly, the median value of thyroglobulin antibodies was higher, although the difference was statistically insignificant.

To investigate whether the expression of this gene was related to JC virus (JCV)

infection, we examined brains of four progressive multifocal leukoencephalopathy (PML) patients. JCV infection was confirmed by immunohistochemical labeling with antibodies against JCV VP1, agnoprotein and large T antigen. MeCP2 expression was examined by immunohistochemistry using a specific polyclonal antibody against MeCP2. In normal brains and uninfected cortices of PML brains, MeCP2 expression was observed in the nuclei of neurons, but not observed in glial and endothelial cell nuclei. However, in PML brains intense immunolabeling was observed in abnormally enlarged glial nuclei of JCV-infected cells. Double immunolabeling using antibodies against large T antigen (visualized as blue) and MeCP2 (visualised as red) revealed dark red JCV-infected nuclei, which confirmed that the JCV infected Erastin nmr nuclei expressed MeCP2. We conclude that MeCP2 is highly expressed

in the JCV-infected nuclei of PML brain and these results may provide a new insight into the mechanism which regulates the MeCP2 expression in glial cells by the infection of JCV. “
“Human cytomegalovirus (HCMV) is an ubiquitous beta human herpesvirus able to influence infected cell survival and proliferation and to modulate the host immune response. As there is accumulating evidence that HCMV is detected in primary intracranial astrocytic tumors, in this study we looked for the presence https://www.selleckchem.com/products/LBH-589.html of HCMV in intracranial tumors and tried to correlate this eventual presence with the anti-HCMV systemic immunoreactivity and with the detection of HCMV in peripheral blood. In this study, we analyzed 43 glioblastomas (GBM), 14 oligodendrogliomas (OL) and 20 meningiomas (MG) by immunofluorescence

(IF) targeting HCMV immediate early antigen (IE1) and by nested PCR (nPCR) amplifying HCMV glycoprotein B (gB). Detection of IE1 by IF showed the presence of HCMV in 70% of GBM, 57% of OL and 85% of MG, in BCKDHA contrast to gB nPCR, which detected HCMV in only 50% of GBM, 38% of OL and 46% of MG. Unexpectedly, HCMV DNA and antigens were detected within GBM, OL and MG of patients that exhibit negative viral serology. More surprisingly, PCR on the peripheral blood did not detect HCMV in patients with a HCMV positive tumor. Our results are in agreement with previous observations demonstrating HCMV in glial tumors and highlight the presence of HCMV in meningiomas. We also showed that anti-HCMV specific systemic immunoreactivity and detection of HCMV in peripheral blood are not predictive of HCMV presence in primary intracranial tumors. “
“This study explores the neuroprotective effects and mechanisms of N-acetyl-L-cysteine (NAC) in mice exposed to cadmium (Cd). NAC (150 mg/kg) was intraperitoneally administered to mice exposed to Cd (10–50 mg/L) in drinking water for 6 weeks.

For use in mouse pups, optimal intranasal exposure volumes for lung deposition were determined. Volumes of 5-, 10- or 15-μl Evans Blue solution were deposited on the nostrils under isoflurane anaesthesia. After 15 min, the pups were killed by cervical dislocation. The 10-μl volume was determined to give maximal lung deposition by visual inspection of the blue-colouring

of the lungs and stomach. Selection of 30 μl as the booster volume (Table 1) was based on the estimated 300% increase in body mass from 1 to 4 weeks of age [16, 17]. Determination of OVA-specific antibodies in serum.  OVA-specific IgE antibodies were detected in a capture ELISA as previously described by Lovik et al. [18] and modified by Ormstad et al. [19]. Poly-HRP-streptavidin (Thermo-Scientific,

Pierce Biotechnology Inc., Rockford, IL, USA) followed by Stabilized chromogen TBM (Invitrogen, Camarillo, CA, USA) was used for detection and the reaction Hydroxychloroquine cost stopped with 2 N H2SO4 solution. OVA-specific IgG1 was measured in a capture ELISA as previously described [13]. The sera to be tested were analysed in duplicates following optimal dilution; 1:50 for IgE and 1:200 or 1:200,000 for IgG1. For both antibody assays, a standard curve was included on each plate. Standard curves were NVP-BKM120 datasheet made from duplicates of diluted IgE standard (mouse anti-OVA IgE, AbD Serotec) or serum pools from mice immunized with OVA and Al(OH)3 for IgG1. OD was measured at 450 nm on a MRX Microplate Reader (Dynatech Laboratories, Chantilly, MTMR9 VA, USA) connected to a PC using Revelation software (Thermo Labsystems, Chantilly, VA, USA). Lymph node preparation and determination of cytokine release.  Single-cell suspension of SLNs and MLNs was prepared

by forcing the lymph nodes through a 70-μm cell strainer (BD Labware, Franklin Lakes, NJ, USA). The cells were washed and then counted in a Coulter Counter Z1. After incubation in culture medium (RPMI 1640 with 10% foetal calf serum, 100 U penicillin G, and 0.1 mg/ml streptomycin) with or without 1 mg/ml OVA at 37 °C and 5% CO2 for 4 or 5 days (differed for practical reasons between the i.n. and i.p. study, respectively), the supernatants were removed and stored at −20 °C until cytokine measurements. The levels of IL-4, IL-5, IL-10, IL-13, IFN-γ, and in the i.n. study also IL-17, were determined using BD CBA Mouse Soluble Protein Flex Sets measured on a BD LSR II flowcytometer and analysed by the FCAP Array software (all from BD Biosciences, San Jose, CA, USA) according to the manufacturer’s protocol. Assessment of inflammatory cells and cytokines in BALF.  Cells in BALF were prepared and stained with the Hemacolor rapid staining of blood smear kit (Merck KGaA, Darmstad, Germany) as previously described [13]. Cell differential counting of blinded slides was performed by microscopic examination by the same investigator (JSH). In the i.n.

Background: Indigenous Australians experience significantly worse graft and patient outcomes following kidney transplantation compared with non-Indigenous Australians. It is unclear whether residential check details location might contribute to this. Methods: This study involved all adult patients from the ANZDATA registry who received a kidney transplant in Australia between January 1st 2000 and December 31st 2012. Patients’ residential locations were classified as urban (major city + inner regional) or rural (outer regional–very remote)

using the Australian Bureau of Statistics Remoteness Area Classification. Results: Of 7,826 kidney transplant recipients, 271 (3%) were Indigenous. Sixty three percent of Indigenous Australians lived in rural locations compared with 10% of non-Indigenous (P < 0.001). In adjusted analyses, the hazard ratio (HR) for graft loss for Indigenous compared with non-indigenous was 1.67 (95% CI 1.04–2.65, P = 0.031). Residential location was not associated with graft survival (HR 1.19, 95% CI 0.95–1.48, P = 0.12). Both Indigenous race and residential location influenced patient survival, with an adjusted HR for death of 1.94 (95% CI 1.23–3.05, P = 0.004) comparing Indigenous with non-indigenous and 1.26

(95% CI 1.01–1.58, P = 0.043) comparing rural with urban recipients. Five-year graft and patient survival were 70% (95%CI 60–78%) and 69% (95%CI 61–76%) in rural Indigenous recipients compared with 91% (95%CI 90–92%) find more and 92% (95%CI 91–93%) in urban non-Indigenous recipients. Conclusions: Indigenous kidney transplant

AZD9291 mouse recipients experience worse patient and graft survival compared with non-Indigenous recipients, while rural residential location is associated with patient but not graft survival. Of all groups, Indigenous recipients residing in rural locations experienced the lowest 5-year graft and patient survival. 272 RENAL TRANSPLANTATION IN NEW ZEALAND MĀORI AND PACIFIC PEOPLE: AUSTRALIA AND NEW ZEALAND B GRACE1,2, T KARA1,2, S McDONALD2,3 1ANZDATA Registry, Adelaide, South Australia; 2University of Adelaide, South Australia, Australia; 3Starship Children’s Hospital, Auckland, New Zealand Aim: To compare incidence of RRT, deceased organ donation rates, transplantation rates and outcomes in Māori and Pacific people between Australia and New Zealand. Background: Associations between country of residence and incidence and treatment for ESKD are not known for these groups. Methods: RRT patient and deceased donor records were extracted from ANZDATA and ANZOD registries for 2000–2012. Populations were derived from StatsNZ and Australian Bureau of Statistics.