Results were compared with phenotypic DST data. Nineteen different

mutation types to at least one of the drugs were found; six isolates (6%) were classified as MDR-TB, defined as resistance to at least rifampicin and isoniazid. The rates of concordance of the PCR with the phenotypic susceptibility test were 71.4, 54.5, and 44.4 for isoniazid, rifampicin, and ethambutol, respectively. These results highlight the importance of molecular epidemiology studies of tuberculosis in understudied regions with a tuberculosis burden to uncover the true prevalence of the CP-673451 MDR-TB. The spread of multidrug-resistant tuberculosis (MDR-TB) due to emergence of multidrug-resistant Mycobacterium tuberculosis isolates has increased worldwide and reached epidemic proportions in many countries (Mokrousov et al., 2003). The increasing number of multidrug-resistant isolates over the years has complicated the control of several outbreaks of the disease (WHO, 2000a, b). MDR-TB is defined as resistant to at least rifampicin and isoniazid, which are the backbone of short-course chemotherapy for tuberculosis (Herrera-León et al., 2005). Therefore, immediate identification of these resistant isolates is very important for adjustments in treatment (Herrera-León et al., 2005;

Abe et al., 2008). Rifampicin was introduced in 1972 as an antituberculosis drug and has excellent https://www.selleckchem.com/products/dinaciclib-sch727965.html sterilizing activity. Rifampicin acts by binding to the β-subunit of RNA polymerase (rpoB) (Ramaswamy & Musser, Miconazole 1998), the enzyme responsible for transcription and expression of mycobacterial genes, resulting in inhibition of the bacterial transcription activity and thereby killing the

organism. Mutations in the 81-bp core region of rpoB were reported to be responsible for resistance in at least 95% of isolates (Sekiguchi et al., 2007). This region is located between codons 507 and 533, with the most common changes in codons Ser531Leu, His526Tyr, and Asp516Val (González et al., 1999). Isoniazid enters the bacterial cell as a prodrug; it is then activated to a toxic substance in the cell by a catalase peroxidase encoded by the katG gene (Wang et al., 1998) and subsequently affects intracellular targets such as mycolic acid biosynthesis, an important component of the cell wall, which eventually results in loss of cellular integrity and the bacterial death. Ethambutol, a first-line-specific antituberculosis drug used in combination with other drugs, inhibits the incorporation of mycolic acids into the mycobacterial cell wall. Genetic and biochemical studies have shown that resistance to ethambutol is mediated by mutations in the embB gene, which encodes arabinosyl transferase, an integral membrane protein that is inhibited by the drug.

L. mexicana-infected cells display activation of PKCα (Figure 2b), which is confirmed by purified LPG incubated with PKCα (Figure 2a). LPG activation of PKCα then leads to enhanced oxidative burst (Figure 3a), thus reducing parasite survival, as compared with nonstimulated controls (Figure 4). It is noteworthy, that in contrast to

purified LPG, the complete parasite inhibits the respiratory burst in C57BL/6 macrophages, albeit to a lesser degree than observed for BALB/c cells. This inhibitory response in the oxidative burst induced by the whole parasite could be related to a variety of other molecules and mechanisms in addition to LPG, such as the possible recognition of opsonized parasites by CR3, a complement receptor that inhibits the oxidative burst (43). The importance of PKCα in parasite control is further strengthened by the fact that VX-770 in vivo the PKCα inhibitor Gö6976, which significantly reduced the oxidative burst in macrophages of both mouse strains, allowed an enhanced parasite survival in macrophages not only in BALB/c cells but also in C57BL/6 cells, which

were originally able to limit parasite survival. These data underscore the importance of the varying modulation of PKCα by L. mexicana LPG in regulating parasite survival within macrophages. Ceritinib solubility dmso The opposing response of macrophages from both mouse strains seems to be specifically related to L. mexicana LPG and not to alterations in the PKCα enzyme, as a nonspecific stimulus, such as PMA, modified the enzymatic activity of PKCα in an identical manner in macrophages of both mouse strains. The opposing effect of LPG on PKCα of both mouse strains is noteworthy, as to date, it has only been reported that L. donovani LPG inhibits Vorinostat PKC isolated from rat brain.

In that study, it was shown that LPG is a competitive inhibitor of diolein on the regulatory binding site C1 of PKC (44). Although the LPG binding site on PKCα has not been mapped, results suggest that LPG must bind to C1 region of PKC. Comparison of the primary sequence of PKCα C1 site between the two mice strains used in our study (data not shown) showed no differences between them. As post-translational modification represents a ubiquitous and essential device for control of PKC activity, localization, stability and protein–protein interaction, it would be possible that the opposite effect exhibited by LPG may be as a result of differences in post-translational modifications found in PKCα at or near this site en each mouse strain (45). In addition, it has been proposed that differences in specificities of high and low affinity phorbol ester-binding sites may partially contribute to distinct effects on PKC-regulated cellular processes (46).

[2] Partial flap necrosis frequently affects the radial and ulnar flap borders, which are both directly involved in the formation of the neo-urethra in the Chang-design. This may lead to a necrotic or exposed neo-urethra and consequently to urethral dysfunction. Possible contributing

factors to partial flap necrosis in a tube-in-tube setting are the flap width and the need for double bending of the flap. Additionally, postoperative flap-swelling may cause venous congestion. In the presented cases, additional risk factors which may have contributed to the occurrence of the partial flap necrosis are a heavy smoking history in both cases, as well as an osteogenesis imperfecta and arterial hypertension in the second case. In the first case, the simultaneously performed vaginectomy led to an increased operation time and blood loss, which might LY2109761 solubility dmso have further increased the risks. This led us to modify our approach by performing vaginectomy together with hysterectomy and adnexectomy. The partial flap necrosis resulted in a complete loss of the neo-urethra and a partial loss of the outer lining of

the neo-phallus on the ventral side. A second free RFF in a modified, shortened Chang-design provided well-vascularized tissue for reconstruction of both elements. Instead of a second free flap for FDA-approved Drug Library solubility dmso immediate neo-urethra-reconstruction, a tubed skin graft could be used, although the risk for urethral strictures due to graft contracture may be increased compared to vascularized tissue. Moreover, the decreased circumference due to partial loss of the outer lining and the loss of flap volume is not

addressed. If no immediate neo-urethra-reconstruction is considered, a primary urethrostomy has to be performed. To our knowledge, no data concerning the specific problem of total loss of the neo-urethra and its treatment after RFF-phalloplasty in sex reassignment surgery is available in the literature. Harrison initially described the usage of the free RFF for urethral reconstruction Gefitinib in vivo in hypospadia.[13] Dabernig et al. presented a series of nine patients who underwent urethral reconstruction and in some cases simultaneous glans penis reconstruction with a tubed RFF: three patients after subcutaneous penectomy for penile cancer and six patients after failure of primary urethra-construction in phalloplasty for sex reassignment surgery. Of these six phalloplasties, three were bilateral groin flaps and three abdominal flaps. The indication was recurrent strictures after multiple corrective procedures. All patients had satisfactory skin envelope of the neo-phallus. Two patients suffered strictures at the site of urethral anastomosis, requiring revision procedures with local flaps. At 6 months, all patients were able to urinate while standing.[14] In order to prevent partial flap necrosis in RFF-phalloplasty, alternatives to the Chang-design may be considered.

Although IL-27 was extensively investigated in conventional T cells [[2, 5]], its role on TCRγδ+ T lymphocytes remains unexplored. The latter cells, which are mainly Vγ9Vδ2+ in

human peripheral blood and poorly represented in physiological conditions (1–5% of circulating lymphocytes), may be strongly activated and expanded by nonpeptide phosphoantigens expressed by transformed or pathogen-infected cells [[6-9]]. In this context, we recently demonstrated that IL-27 acts as Decitabine chemical structure antitumor agent by targeting directly human hematological tumors including multiple myeloma, B-acute lymphoblastic leukemia, and B-cell lymphoma of germinal center origin [[10, 23, 24]]. However, it has been reported that TCRγδ+ T lymphocytes kill a vast repertoire of tumor cell lines and primary samples in vitro including leukemia, lymphoma, melanoma, neuroblastoma,

and different check details types of carcinoma, thus raising great interest in targeting TCRγδ+ T cells for cancer immunotherapy. In addition, TCRγδ+ T lymphocytes interplay with conventional T cells, B cells, NK cells and dendritic cells, neutrophils, and macrophages, thus representing a T-cell population with a critical role in both innate and adaptive immunity [[6, 11-22]]. With this in mind, we investigated the functional role of IL-27 on human TCRγδ+ T lymphocytes, either freshly isolated from peripheral blood of normal subjects or expanded in vitro upon PBMC stimulation with zoledronic acid, and asked whether IL-27 could modulate the functional properties of TCRγδ+ T cells. Resting and activated Vγ9Vδ2+ T cells expressed WSX-1 (mean relative of fluorescence intensity (MRFI) ± SD: resting 1.76 ± 0.005, activated 3.97 ± 0.56, Thiamet G Fig. 1A and B) and gp130 (MRFI ± SD: resting 3.11 ± 0.15, activated 2.63 ± 0.02, Fig. 1A and B) chains, thus indicating that both cell populations may be responsive to IL-27.

The complete IL-27R was functional in these cells, as witnessed by the ability of IL-27 to significantly induce STAT1 (MRFI ± SD: medium 1.87 ± 0.02, IL-27 13.99 ± 0.24, p < 0.0001), STAT3 (MRFI ± SD: medium 1.56 ± 0.32, IL-27 2.97 ± 0.11, p = 0.006), but not STAT5 (MRFI ± SD: medium 1.25 ± 0.01, IL-27 1.3 ± 0.02) (Fig. 1C and D) phosphorylation. Thus, TCRγδ+ T cells show a similar behavior to classical T lymphocytes in terms of IL-27R expression and IL-27-driven signaling pathway [[1, 2]]. Finally, the significant differences in WSX-1 (p = 0.03) and gp130 (p = 0.05) expression between resting and activated Vγ9Vδ2+ T cells may be conceivably related to the different experimental conditions used, that is, in vitro expansion by zoledronic acid versus direct isolation of TCRγδ+ T cells from peripheral blood (PB). However, such differences did not significantly impact on STAT-1, STAT-3, or STAT-5 activation (not shown) or other functional responses to IL-27 (i.e. cytotoxicity, see below).

[23] When positive appendices in these studies have been tested their codon 129 genotype has not been found to be restricted to the MM genotype.[24] Whether individuals of these non-MM genotypes would go on to develop clinical vCJD is unclear; however, it is now clear that blood transfusion can transmit vCJD from asymptomatic donors who subsequently developed vCJD.[25, 26] Interestingly the clinicopathological phenotype of secondary (transfusion-related) vCJD is indistinguishable from that of primary (BSE-related) vCJD, indicating that distinguishing between these two etiologies depends upon epidemiological studies such as the Transfusion Medicine Epidemiology

Belnacasan clinical trial Review.[27, 28] Additionally, an individual of the MV genotype has been found to be susceptible to vCJD infection by blood transfusion as judged by peripheral infection.[29] Evidence of a pre- or sub-clinical state existing in a hemophiliac patient who died of other causes, suggests that plasma products may also be a risk for vCJD transmission.[30] Although modeling exercises indicate that blood-borne vCJD transmission is unlikely to be self-sustaining in the UK population,[31] it may yet be premature to consider BSE and vCJD as things entirely of the past. Scrapie is endemic in many countries around

the world, yet there is no evidence to suggest that it is pathogenic for humans. The intense investigations of ruminant TSEs that followed the BSE epidemic have resulted in the identification click here of several distinct animal prion diseases, atypical or Nor98 scrapie in sheep and H-type and L-type BSE in cattle.[32] Moreover, BSE is experimentally transmissible to sheep and there

are concerns that if BSE were to have infected the national flock in the UK its presence might be masked by endemic scrapie, but it might retain its pathogenicity for humans.[33, 34] Another concern, particularly for the North American countries, is the spread of chronic wasting disease in farmed and free-ranging deer and elk.[35] There isothipendyl is no known epidemiological link between any of these animal prion diseases and human disease, but there are active efforts to try to quantify strain-related species barriers between the diseases known to be a risk (BSE/vCJD), those thought not to represent a risk (scrapie) and those for which data is lacking (atypical scrapie, H- and L-type BSE and BSE in sheep).[36] In assessing whether or not human prion diseases might have an animal origin, it is important to have a proper understanding of the clinicopathological heterogeneity of the sporadic human prion diseases, because it is against this backdrop that any new acquired forms of the disease will be seen and from which it will need to be distinguished. Sporadic CJD is the most commonly occurring human prion disease; it occurs world-wide and it has long been known to be clinically and pathologically heterogeneous.

2D). Importantly, all vaccinated mice rapidly lost weight and succumbed to LCMV infection while nonvaccinated mice exhibited less weight loss and survived (Fig. 2E and F). In order to further decrease the number of memory CD8+ T cells we performed adoptive transfer of different numbers of NP118-specific memory CD8+ T cells (ranging from 8 × 102 cells to 8 × 105 cells per mouse) into naïve PKO hosts. The NP118-specific population of memory CD8+ T cells transferred exhibited a late memory phenotype (CD127hi, LDE225 order CD62Lhi, KLRG-1lo, CD27hi) and function (IL-2 and TNF cytokine production upon restimulation with NP118 peptide; Fig. 3A). All recipient

mice and a group that did not receive memory CD8+ T cells were challenged with LCMV-Arm. Mice receiving 8 × 105 and 8 × 104 NP118-specific memory CD8+ T cells rapidly lost weight and succumbed following LCMV infection (Fig. 3B and C). Interestingly, mice receiving 8 × 103 NP118-specific memory CD8+ T cells lost weight during the first week after LCMV infection but recovered without any mortality. On the other hand, mice receiving 8 × 102 NP118-specific memory CD8+ T cells exhibited only slight weight loss and did not succumb, similar to control mice that did not receive any memory CD8+ T cells (Fig. 3B and C). Consistent with their poor outcome, mice receiving either 8 × 105 or 8 × 104 NP118-specific

memory CD8+ T cells had high numbers (>107 cells/spleen) at 5 days post-LCMV infection (Fig. 3D). Importantly, a substantial fraction of NP118-specific secondary effector CD8+ T cells in the groups receiving the highest numbers AT9283 cell line of memory CD8+ T Protein kinase N1 cells produced IFN-γ

directly ex vivo even in the absence of exogenous peptide stimulation (Fig. 3D). Together, these results suggested that secondary CD8+ T cells expansion and mortality in PKO mice are dictated by the starting number of NP118-specific memory CD8+ T cells at the time of LCMV challenge. Naïve PKO mice survive LCMV-Arm infection by exhausting their NP118-specific CD8+ T cells [[16]]. Furthermore, more than 98% of the CD8+ T cells response to LCMV infection in BALB/c mice is directed at the dominant NP118 epitope, with subdominant responses directed to GP283 and GP96 epitopes [[34, 35]]. Previous work showed that vaccination to generate wild-type memory CD8+ T cells against subdominant epitopes may be effective at protecting from both LCMV and LM infection [[36, 37]]. However, it remains unknown whether memory CD8+ T cells specific for subdominant LCMV epitopes will also lead to vaccine-induced mortality in perforin-deficient hosts. To address this issue, we immunized naïve PKO mice with 5 × 105 DC coated with either the dominant NP118 or subdominant GP283 LCMV epitopes, while mice in the control group received DC coated with a Plasmodium berghei CS252 epitope.

Candida albicans was the predominant yeast isolated [30 patients (62.5%)], followed by C. parapsilosis [6 (12.5%)] and C. dubliniensis 5 (10.4%). Aspergillus fumigatus was the most common filamentous fungus [5 (10.4%)] and non-fumigatus Aspergillus species were isolated from four (8.3%) patients. Staphylococcus aureus was the most frequently detected bacterium in C. Hedgehog antagonist albicans

positive samples (53.57%). A. fumigatus and Pseudomonas aeruginosa or S. aureus were detected together in 75% of A. fumigatus positive samples each. No statistically significant relationship was detected between growth of yeast and moulds and age, gender, the use of inhaled corticosteroids or tobramycin. No significant correlation was found between the isolation of C. albicans, A. fumigatus and P. aeruginosa, Stenotrophomonas maltophilia selleck chemicals llc or S. aureus, and the isolation of C. albicans and Haemophilus influenzae. Other factors which may be responsible for the increased isolation of fungi in CF need to be investigated. “
“Patients with acute myelogenous leukaemia (AML) and neutropenia after chemotherapy are at high risk for life-threatening invasive fungal disease (IFD), in particular, invasive aspergillosis (IA). The aim of the study was to evaluate data on characteristics, risk factors, complications and additional

antifungal treatment of patients with AML receiving posaconazole prophylaxis (PP) after chemotherapy in an actual clinical setting. A retrospective single-centre observational study on 40 patients with AML, median age 66 years, was conducted. PP 200 mg three times daily was given routinely. After 76 cycles of remission induction chemotherapy followed by PP, median duration of 31 days (range 6–61 days), no fatal case occurred. second The majority of patients had at least one additional risk factor for IFD and during 32 cycles (42.1%), three risk factors were present. During 40 therapy cycles (52.6%), fever of unknown origin occurred. Pneumonia was diagnosed after 23 cycles

(30.3%), thereof one case of proven IA (1.3%). PP was interrupted in 25 cycles (32.9%) and was followed by systemic antifungal therapy with different agents, with a median duration 15 days (range: 6–32 days). PP appears to be an effective and well-tolerated protection against IFD for AML patients under natural clinical conditions. “
“Data on the epidemiology of invasive Candida infections in paediatric patients in Europe are still limited. The aim of this retrospective study was to analyse the epidemiology of candidaemia in a tertiary paediatric hospital in Poland from 2000 to 2010. Using microbiological records, a total of 118 episodes of candidaemia were identified in 114 children, with an annual incidence of 0.35 episodes/1000 discharges. The highest incidences were found in the medical intensive care unit (5.28), and in neonatal intensive care (1.47). The mortality rate was 8.5%. Candida albicans and C. parapsilosis were the most prevalent species (39.8% and 35.6% respectively).

It was noted that the punctate immunostaining for MSA-1 was accompanied by sparse CD13 staining and always in juxtaposition to redistributed iDCs. We have previously shown that maturation of splenic iDC from naïve calves in vitro results in the loss of CD13 expression and gain in capacity to present antigen (12,41). Thus, similar to the P. chabaudi model in mice (23), these results

support the hypothesis that iDC mature during processing of the parasite and migrate as antigen-presenting cells to lymphocyte-rich domains. The spleen-dependent innate response of naïve selleck products calves to infection with B. bovis is also characterized by early IL-12 production with subsequent IL-10 modulation (6), the major sources of which in cattle are iDCs and monocytes/macrophages, respectively (8,14,42). We have also shown that monocytes/macrophages of cattle can produce NO with direct babesiacidal activity (14,27,43). It was interesting to note that following haemoparasitic infection, intense acute hyperplasia of monocytes/macrophages is restricted to the red pulp of both mice (23) and calves (present study). Thus, in addition to regulatory function through cytokine production, our collective findings are consistent with monocytes/macrophages acting as effector cells in close juxtaposition with infected erythrocytes as they enter

the splenic sinuses. Regarding the distribution of small leucocytes, dual-labelling experiments demonstrated acute progressive accumulation of numerous CD3+ CD4− cells and TcR1+ WC1− cells within the red Quizartinib pulp. Thus, it is likely that at least a portion of these accumulated Cytidine deaminase lymphocytes were WC1−γδ T cells. The role of these cells is still not clear but as bovine WC1−γδ T cells express CD2 and CD8, can produce

IFN-γ in response to cytokine stimulation, and are found in largest proportion in the spleen and intestine (15,16,44,45), it is intriguing to consider the possibility that cells with this phenotype might be the bovine functional equivalent of NKT cells (46–48). If so, then the observed accumulation of these cells in the red pulp of naïve calves infected with B. bovis is consistent with their expected role in the transition from innate to acquired immunity. Our results are in agreement with previous reports (49,50) that demonstrate relatively small accumulations of WC1+γδ T cells within the splenic marginal zones of uninfected calves. The splenic decrease in WC1+γδ T cells during the acute response of calves to B. bovis infection may indicate their activation within the marginal zone is followed by redistribution to effector sites outside of the spleen. Indeed, several reports indicate WC1+γδ T cells are most numerous and reactive within the blood of young calves (45,49,51–53).

Early in the disease process systemic mRNA expression of T-bet and Rorγ was increased in STAT6–/– mice. We conclude that STAT6 is required for attenuation of Th1 and Th17 nephritogenic immune responses and protection from crescentic glomerulonephritis. Glomerulonephritis (GN) is a common cause of renal disease, including end-stage renal failure. Experimental crescentic GN is the murine homologue of rapidly progressive

GN, the most severe form of GN. Severe injury in this model is mediated by cellular immunity and CD4+ T cells are key components of renal injury [1,2]. Upon activation, naive CD4+ cells tend to differentiate into subsets (T helper cells – Th1, Th2 and Th17) that engage immune effectors in different ways. In proliferative forms of Proteasome inhibition GN, T cells direct adaptive immune responses that drive glomerular disease, but also, in rapidly progressive GN, CD4+ cells themselves accumulate in glomeruli as effectors. These effector Selleck BMN-673 T helper cells activate innate immune effector cells, predominantly neutrophils and macrophages, which activate and damage intrinsic renal cells. While humoral immunity influences the patterns and severity of some forms of GN, in this model severe renal injury is driven by cell-mediated immunity [3] and occurs independently

of autologous antibodies [4]. There is evidence that both Th1 [5] and Th17 [6] responses are pathogenic in experimental crescentic GN. Deficiencies in the key transcription factors, T-bet for Th1 cells [7] and retinoic acid-related orphan receptor-γt (Rorγt) for Th17

cells [8], result in significantly attenuated renal injury. Traditionally, Th2 cells have been considered essential for host protection from parasitic infections, while Tobramycin aberrant Th2 responses have been associated with allergy and asthma. In experimental crescentic GN, some Th2-associated cytokines are reno-protective [9]. The signal transducer and activation of transcription (STAT) proteins provide a direct link between cytokine receptors and cytokine induced gene transcription [10]. Activation of the interleukin (IL)-4 receptor on undifferentiated T cells results in the activation of STAT6 with expression of IL-4 related genes [11]. STAT6 is considered central to mounting effective Th2 responses, including the production of Th2 cytokines IL-4 and IL-5, and the key transcription factor GATA binding protein 3 (GATA3) [12]. STAT6-deficient mice have impaired Th2 immune responses, but otherwise are phenotypically normal and produce normal numbers of CD4+ T cells [13]. While early studies suggested that STAT6 was an absolute requirement for IL-4 production [14,15], subsequently it was demonstrated that STAT6-deficient mice can produce IL-4 in response to parasitic infection [16,17]. STAT6 deficiency is protective in several Th2-associated disease models, including allergic asthma [18,19] and eosinophilia with airway hypersensitivity [20].

Renal transplantation improves survival of patients with end-stage kidney disease (ESKD).1 However, there continues to be a disparity between availability of deceased donor kidneys and potential recipients. In Australia, acceptance of ESKD patients aged 70–74 years for renal replacement therapy increased from 390 per million population (pmp) in 2004, to 469 pmp in 2008.2 In addition, Rapamycin the proportion of potential recipients aged 65 years and

over awaiting renal transplantation has increased by 21% between 2005 to 2008.3,4 The Scientific Registry of Transplant Patients (SRTR; i.e. US transplant registry data) has recorded a similar increase of prevalent potential recipients aged ≥70 years on the deceased donor waiting

list, from 114 in 1990 to 2544 in 2004.5 Deceased donor rates in Australia have remained low at 11 donors pmp in 2009 (10 pmp in 2005), compared with 34 pmp in Spain, 24 pmp in the USA and 17 pmp in the UK.6,7 However, there has been an increase in acceptance of older donor kidneys in Australia, with the number of deceased donors aged ≥55 years increasing 1.8-fold between 2001–2003 to 2007–2009.7 Kidneys from older donors are associated with inferior graft outcomes including late graft loss, chronic allograft nephropathy and higher risk of cardiovascular mortality;8,9 this is partially offset by the reduction in mortality associated with reduced wait-list time. Between 2005 and 2009 in Australia, there was a 1.3-fold increase in the number of expanded criteria donors (ECD),7,14 defined as any learn more donor aged ≥60 years, or any donor aged 50–59 years, with two of the following three criteria: cerebrovascular accident (CVA) death, terminal creatinine > 133 µmol/L or hypertension.15 Although the concept of ECD focuses primarily on advanced donor age, other risk factors such as CVA, hypertension, diabetes and high serum creatinine are also taken into account.16,17 Gaber et al. reported an

increase in glomerulosclerosis with increasing donor age, which correlated with a similar increased risk of delayed graft CYTH4 function (DGF), graft loss and poorer graft function in kidneys transplanted from older donors.18 Multiple studies have demonstrated that recipients of ECD kidneys have better survival compared with potential recipients on the waiting list but long-term outcomes associated with ECD grafts remains unclear.19,20 In a retrospective study of 2845 French transplant recipients aged ≥60 years, ECD grafts were associated with poorer graft survival compared with non-ECD grafts.12 The difference in graft survival was 6.2% at 12 months and 14.2% at 5 years (adjusted relative risk of graft failure associated with ECD grafts compared with non-ECD grafts was 1.98, P < 0.01).