There are scanty reports of meningitis caused by Rhodurorula spp

There are scanty reports of meningitis caused by Rhodurorula spp in HIV infected patients. We Nutlin-3a manufacturer present one such case of meningitis by Rhodutorula glutinis in HIV-infected

patient. The patient also had a past history of abdominal tuberculosis. The diagnosis of Rhodotorula was confirmed by Gram staining and culture of the cerebrospinal fluid (CSF). Contamination was ruled out by repeated culturing of CSF from the same patient. Therapy with Amphotericin B showed good results. Patient was discharged from the hospital. However, in the seventh month of follow-up patient was readmitted with complaints of fever, breathlessness, altered sensorium, vomiting and succumbed to his illness. This time the CSF cultures remained negative for Rhodotorula, acid fast bacilli and other pyogenic organisms. Our last 11-year retrospective analysis of 8197 specimens received for mycological

work-up showed that this is the selleck products first report of R. glutinis isolation from our institute. “
“Chromoblastomycosis is a chronic mycosis that affects the skin and subcutaneous tissues caused by several genera of dematiaceous fungi. There is not a treatment of choice. Thus, tools that help guide clinical practice are fundamental. In this sense, antifungal activity tests in vitro could be useful. However, trials with chromoblastomycosis agents are scarce. The aim of this study was to evaluate both the in vitro susceptibility of 60 chromoblastomycosis agents to five antifungals and the combination of amphotericin B (AMB) and terbinafine (TRB). TRB, itraconazole (ITZ) and ketoconazole (KTZ) were, in this order, the drugs which showed better activity against the chromoblastomycosis agents. The less active drugs were voriconazole (VRZ) and AMB. The more differentiated group was Exophiala spinifera. Cladophialophora carrionii and Fonsecaea spp. are significantly more susceptible to KTZ than Phialophora verrucosa, whereas C. carrionii is significantly more sensitive to VRZ than P. verrucosa and E. spinifera. Assays in this direction allow

Mannose-binding protein-associated serine protease the knowledge of the susceptibility of the causative agents which may help the management of patients with this disease. This study includes the largest number of these agents and of genera found in the literature. “
“Recent studies have shown decreased susceptibility of Candida krusei to amphotericin B (AmB), in addition to its inherent resistance to fluconazole. The susceptibility of C. krusei to AmB was studied in the Parasitology–Mycology laboratory of Grenoble Teaching Hospital, France. Between 2003 and 2011, we analysed 200 C. krusei isolates from 130 patients. The isolates were mainly collected in intensive care, cardio-thoracic and cancer/haematology units. Minimum inhibitory concentrations (MICs) were determined by the E-test method. The modal MIC was 0.5 μg ml−1; the MIC50 and MIC90 (MICs encompassing 50% and 90% of all isolates tested, respectively) were 0.

30070730) “
“Foxp3+ regulatory T cells (Tregs) are essentia

30070730). “
“Foxp3+ regulatory T cells (Tregs) are essential to maintain immune homeostasis, yet controversy exists about the stability of this cell population. Bcl6-deficient (Bcl6-/-) mice develop severe and spontaneous Th2-type

inflammation and Bcl6-deficient Tregs are ineffective at controlling Th2 responses. We used a lineage INK 128 purchase tracing approach to analyze the fate of Tregs in these mice. In the periphery of Bcl6-/- mice, increased numbers of Foxp3-negative “exTreg” cells were found, particularly in the CD25+ population. ExTregs from Bcl6-/- mice expressed increased IL-17 and extremely elevated levels of Th2 cytokines compared to wild-type exTregs. While Tregs normally express only low levels of cytokines, Tregs from Bcl6-/- mice secreted higher levels of IL-4, IL-5, IL-13 and IL-17 than wild-type conventional T cells. Next, Treg-specific conditional Bcl6-deficient (Bcl6Foxp3-/-) mice were analyzed. Bcl6Foxp3-/- mice do not develop inflammatory disease, indicating a requirement for non-Treg cells for the inflammation in Bcl6-/- mice, and have normal

numbers of exTregs. We induced Th2-type allergic airway inflammation in Bcl6Foxp3-/- mice, and found that while exTreg cytokine expression was normal, Bcl6-deficient Tregs expressed higher levels of the Th2-specific regulator Gata3 than Bcl6+ Tregs. Copanlisib purchase Bcl6Foxp3-/- mice had increased numbers of Th2 cells after induction of airway inflammation and increased T cells in the broncho-alveolar lavage (BAL) fluid. These data show both Treg-intrinsic and Treg-extrinsic roles for Bcl6 in controlling Treg stability and Th2 inflammation,

and support the idea that Bcl6 expression 4��8C in Tregs is critical for controlling Th2 responses. This article is protected by copyright. All rights reserved. “
“To determine whether down-regulation of TIMP3 expression promotes TACE expression and increases in TNFα production by placental trophoblast cells. Placental expression of TIMP3 and TACE was examined by immunostaining and Western blot. Effects of TIMP3 on TACE expression and TNFα production were assessed by transfection of TIMP3 siRNA into trophoblasts isolated from normal placentas. Effects of oxidative stress on trophoblast TIMP3 expression and TNFα production were also determined. Trophoblast production of TIMP3, TACE and TNFα were measured by ELISA. TIMP3 expression was markedly reduced in preeclamptic placentas compared with normal placentas; oxidative stress down-regulated trophoblast TIMP3 expression and production, P < 0.01. Down-regulation of TIMP3 expression by TIMP3 siRNA resulted in significant increases in TACE expression and TNFα production, P < 0.01.

The recent emergence of Extensively Drug Resistant (XDR) strains

The recent emergence of Extensively Drug Resistant (XDR) strains of M. tuberculosis, along with HIV-associated TB, has further compounded the problem. M. bovis Bacille Calmette–Guerin (BCG) is still the most widely used vaccine, but exhibits variable efficacy 1. In order to improve upon the current efficacy of BCG vaccination, it is critical to understand the requirements for effective vaccine-induced immune responses following BCG vaccination. The interleukin (IL)-12 type 1 T helper (Th1) pathway

is critical for host immunity against M. tuberculosis in humans 2, and in experimental models 3. Consistent with these findings, BCG vaccine-induced protection against TB is also dependent on the accumulation of Th1-cell memory cells that produce the cytokine IFN-γ that activates selleck screening library macrophages for mycobacterial control 4. However, factors required for effective generation of Th1-cell responses following BCG vaccination are not completely understood. The identification of factors required for BCG vaccine-induced

Th1-cell responses will result in a major improvement in our ability to vaccinate effectively against TB and contribute to better control of global TB burdens. The cytokine IL-12, made up of IL-12p35 and IL-12p40 subunits, is critical for the induction of IFN-γ from T and NK T cells 5. IL-23, composed of the p40 and p19 subunit 6, is selleck products required for maintenance of Th type 17 (Th17) cells 7, 8. Th17 cells produce the cytokines IL-17A (IL-17), IL-17F, IL-21, and IL-22 9 and are involved in the induction of inflammation associated with models of autoimmune diseases 10. In contrast, IL-23-dependent IL-17 responses are important for protective immunity against extracellular bacterial infections via induction of chemokines required for neutrophilic recruitment and bacterial killing 11. However, more recently we and others have shown that IL-17

is also required for protective immunity against some intracellular pathogens such as Francisella tularensis LVS 12 and Chlamydia muriduram 13. IL-17-induced protective immunity against these intracellular pathogens occurs via IL-17-dependent induction of IL-12 in DCs 12, 13 and the resulting generation of Th1-cell responses 12. Accordingly, the absence of the IL-23/IL-17 pathways results in decreased induction of Th1-cell immune responses Adenylyl cyclase and increased susceptibility to infection 12, 13. Interestingly, pulmonary acute infection with M. bovis BCG also requires IL-17 to drive Th1-cell immune responses, without playing a role in protection 14. These studies project the important question why some intracellular bacteria such as F. tularensis, C. muridarum, and M. bovis BCG 12–14 require IL-17 to induce Th1-cell immunity. In light of these recent findings and since the BCG is the most widely used vaccine worldwide, the goal of this study was to determine if the generation of BCG vaccine-induced Th1-cell immune responses and subsequent protection against M.

Also, the focal/multifocal distribution pattern of the lympho-pla

Also, the focal/multifocal distribution pattern of the lympho-plasmacytic reaction, which frequently made it the predominant cell infiltrate in certain fields, may have biased our scoring over the whole slide in the previous study. We could also not demonstrate the difference

in the inflammation score and composition of the cell infiltrate between neoplastic and non-neoplastic cases that we previously observed (5). Myeloid cells and especially neutrophils play a major role in the innate local inflammatory response in the spirocercosis-induced nodule. Myeloid cells can have an important role in cancer induction by generating proteases, free radical and nitrogen species that can cause oxidative damage to the DNA (6). They can also play a crucial role in establishing cytokine-induced tumour rejection (20), and they also play a major part in endothelium-mediated lymphocyte trafficking and antigen presentation.

Polymorphonuclear cells have shown both pro- and anti-inflammatory activities. They may participate in the switch to immune suppression by Th2 and Tregs through up-regulation of IL-10 (20). More recently, neutrophils have been shown to play a pivotal role in the regulation AZD1152-HQPA solubility dmso of the inflammatory response against cancer (21). For instance, neutrophils can be induced by serum amyloid A (SAA)1 to secrete IL-10 that induces suppression of immune surveillance Calpain (22). In the present study, T cells outnumbered B cells. To further differentiate between the different T-cell types, especially into CD4+ or CD8+ cells, frozen sections (which were not available in this study) would be necessary. Based on the current knowledge of helminth-associated chronic inflammation, these cells are likely to be Th2 CD4+ cells (8). Th2 responses are generally correlated with suppressed cell-mediated immune response and with enhanced tumour promotion and progression. B-cell response is often associated with Th2 cell response and also with increased risk for neoplastic progression

(23–25). Additionally, immunoglobulins and more specifically immune complexes are regarded as tumour-promoting (23). The humoral response in spirocercosis warrants further investigation for its role in the carcinogenesis in spirocercosis and also for the potential use of serology as a diagnostic tool in this disease. This study reports for the first time an approach to the identification of FoxP3+ cells in excised diseased canine tissue. We hypothesized that Tregs will be present in high numbers in the spirocercosis-induced nodules and that their numbers will increase as the nodule progressed towards sarcoma, but although FoxP3+ cells were found in large numbers within CD3+ regions of lymph nodes, they were rarely observed in S. lupi-associated oesophageal nodules and when present, they were usually in very small numbers.

Spontaneous diabetes in NOD/IL-1β KO mice is indistinguishable to

Spontaneous diabetes in NOD/IL-1β KO mice is indistinguishable to that of WT and heterozygous littermates Antiinfection Compound Library solubility dmso (p>0.6, log-rank test) (Fig. 4). Additionally, IL-1β deficient NOD/SCID recipient mice are equally susceptible to autoimmune diabetes as IL-1β sufficient NOD/SCID recipient mice when adoptively transferred with either total NOD spleen cells

(p>0.4, log-rank test) (Fig. 5) or purified CD4+ T cells (p>0.5, log-rank test ) (Fig. 6). We conclude from these results that, contrary to our expectations, IL-1β is essential for neither spontaneous nor transferred diabetes. Here we show that Fas expression is required for the adoptive transfer of diabetes by CD4+ T cells. CD4+ T cells are essential effectors in the induction of islet infiltration and β-cell death 19, but so far no clear link has been delineated between CD4+ T cells and the molecular pathway triggered to cause the destruction of β cells. We have observed BVD-523 that primed CD4+ T cells require the presence of Fas on NOD/SCID recipients to cause T1D. The expression of Fas within islets has mostly been associated with intra-islet macrophages, dendritic cells and to a lesser extent to infiltrating lymphocytes 31. Fas expression is, however, upregulated on islet

cells upon exposure to cytokines 6–8. Fas has been detected by cytometric analysis of β cells in in vivo models of accelerated, but not spontaneous, diabetes 32. Two recent reports have revealed that Fas is actually necessary to induce β-cell apoptosis in NOD mice 16, 17. Although in pancreatic islets from Fas-deficient NOD/SCID lpr/lpr mice there are other cell types in addition to pancreatic β cells, which are also deprived of Fas expression,

mostly dendritic cells and macrophages 31. sublethally irradiated NOD mice, when adoptively transferred with spleen cells from either pre-diabetic or diabetic NOD donor do not develop diabetes 2. In this experimental Carbohydrate approach, donor splenocytes included Fas-sufficient macrophages, dendritic cells and other hematopoietic subpopulations that could replace the Fas-deficient recipient cell types. Nonetheless, total spleen cells from a Fas-sufficient donor are not able to transfer diabetes to Fas-deficient sub lethal irradiate NOD recipients, which clearly suggests that Fas deficiency on β cells is responsible for the absence of diabetes onset. Moreover, in our experimental setting, the adoptively transferred CD4+ T cells are already primed, and therefore only require proper antigen presentation by local antigen presenting cells (dendritic cells and macrophages) to activate their effector functions. Our results are consistent with a scenario in which Fas-deficiency on target pancreatic β cells, and not on other cell types (macrophages and dendritic cells), is responsible for the impaired diabetes induction. Our results are supported by those from Nakayama et al.

, 2007) Altogether, these results suggest

, 2007). Altogether, these results suggest that the outer membrane composition is disturbed in the clumping strain and that OMVs could be overproduced in this strain. Because exopolysaccharide and extracellular matrices are responsible for the adhesive properties of bacteria (Quintero & Weiner, 1995), we compared the adherence abilities

of the MG210 clumping and wild-type strains in a classical adherence assay. We tested the ability of the wild type, the wild type carrying the vector control (planktonic strains) and the exopolysaccharide-producing strains to attach to a 96-well polystyrene microtiter plate. In this assay, bacteria were inoculated in 2YT and grown at 37 °C overnight in this 96-well plate. Then, cells were removed, wells were rinsed and adherent bacteria were detected by crystal violet staining (see Materials and methods). As shown in Fig. 8, the MG210 LY2157299 concentration strain showed an adherence on polystyrene wells twofold stronger than both control strains. None of the strains showed significant differences in the growth rate that could potentially account for differences in adherent bacteria accumulation (data not shown). This result shows that the clumping strain possesses an increased ability to adhere to polystyrene surfaces. The direct involvement

of the exopolysaccharide in surface adherence is still to be demonstrated. Finally, we compared the adhesion of the B. melitensis wild-type strain and B. melitensis MG210 strain to cells, why a biotic surface that

Brucella spp. encounter during their infectious cycle. HeLa cells were infected with an equal quantity of bacteria of the wild type or the MG210 clumping strain. After 1, 24 and 48 h of infection, cells were observed by scanning electron microscopy (SEM) and the number of intracellular bacteria was evaluated. Here again, while no difference in either internalization or intracellular replication could be found between both strains (Fig. 9), we observed that as early as 1 h postinfection, the AHL-acylase overexpressing strain is strongly adherent to HeLa cells compared with the parental one: several clumps from different sizes are observable both on coverslips and on the surface of the cells in the MG210-aggregating strain (Fig. 10). This work provides the first insights into the composition and the preliminary structure of the exopolysaccharide overproduced in B. melitensis strains affected in the AHL communication system. These strains exhibit a clumping phenotype not only because exopolysaccharide is overproduced but also because the aggregates contain extracellular DNA (eDNA). In addition to exopolysaccharide and eDNA, the clumping strain was shown to overproduce OMVs. The aggregative strain was also demonstrated to possess increased adherence properties both to polystyrene and to HeLa cells compared with the wild-type strain.

2 mm) was significantly higher in non-responder group (p = 0 038)

2 mm) was significantly higher in non-responder group (p = 0.038). Among 70 patients in 2nd study population, 45 patients were responder (64.2%), and the proportion of patients who had larger parathyroid glands than cutoff value was significantly higher in nonresponder group (responsder vs nonresponder 60.5 vs 87.0%, p = 0.028). Conclusions: Measurement of parathyroid gland diameters with CT scan was useful to predict the response of cinacalcet therapy. KURASHIGE MAHIRO1,2, HANAOKA KAZUSHIGE1, IMAMURA MINAKO2, UDAGAWA TAKASHI1, KAWAGUCHI YOSHINDO1,3, HASEGAWA TOSHIO1,3, HOSOYA TATSUO1, YOKOO TAKASHI1, MAEDA

SHIRO2 1Division of Kidney and Hypertension, Department of Internal Medicine, The Jikei University, School of Medicine, Minato, Tokyo, Japan; 2Laboratory for Endocrinology, Metabolism and selleck Kidney Diseases, RIKEN Center for Integrative Medical Sciences, Yokohama, Kanagawa, Japan; 3Department of Medicine, Kanagawa Prefectural Shiomidai Hospital, Yokohama, Kanagawa, Japan Introduction: Autosomal

Dominant Polycystic Kidney Disease (ADPKD) is a common hereditary kidney disorder, and most of its heritability could be explained by mutations in two genes, PKD1 and PKD2 in populations of European descent. However little is known about Asian ADPKD including Japanese. To elucidate the genotypic and phenotypic characteristics of ADPKD in Japanese populations, we performed a comprehensive search for mutations in PKD1 and PKD2 in 180 Japanese ADPKD patients from 161 unrelated tuclazepam families. Methods: We screened the entire coding regions and their flanking regions of the PKD1/PKD2 by direct sequencing, and evaluated candidates for causal variants by subsequent in-silico and/or bio-analyses. We also searched for large genomic rearrangements within PKD1/PKD2 loci by using quantitative PCR. Results: We identified 111 mutations within 134 families (detection rate = 83.2%), including 88 PKD1 mutations (48 truncating, 6 atypical splice, 29 missense and 5 in-frame mutations) in 96 families, and 23 PKD2 mutations (18 truncating, 1

atypical splice and 3 missense mutations and 1 large deletion) in 38 families. Patients with PKD2 mutations account for 23.6% of all Japanese ADPKD families in this study. Seventy-four out of the 111 mutations have not been reported previously. The estimated glomerular filtration rate (eGFR) decline was significantly faster in patients with PKD1 mutations than in those with PKD2 mutations (−3.25 and −2.08 ml·min−1·year−1 for PKD1 and PKD2, respectively, p < 0.01). Conclusion: Mutations within PKD1 and PKD2 can be linked to most of the cases of Japanese ADPKD, and the renal function decline was faster in patients with PKD1 mutations than in those with PKD2 mutations also in the Japanese ADPKD. We also found that PKD2 mutations were more frequent in Japanese ADPKD than that in European or American ADPKD.

This case adds to our current knowledge of spontaneous reversion

This case adds to our current knowledge of spontaneous reversion of mutations in ADA deficiency and shows that the effects of the ERT may vary among these patients, suggesting that it could depend on the cell and type in which the somatic mosaicism is established upon reversion. Autosomal recessive severe combined immunodeficiency caused by adenosine deaminase deficiency (ADA-SCID, OMIM #102700) is characterized by severe and recurrent

early-onset infections, profound lymphopenia, absent cellular and humoral immunity and failure to thrive [1]. Its incidence is estimated between 1: 200,000 and 1: 1,000,000 live births and is the second most prevalent form of SCID, accounting for up to 20% of all cases. ADA is involved LY2157299 nmr in the metabolism of purine nucleosides,

and its deficiency causes excessive accumulation Vismodegib datasheet of Ado and dAdo and preferential conversion of the latter to the toxic compound dATP, leading to its accumulation in plasma, red blood cells (RBC) and lymphoid tissues, where it impairs lymphocyte development and function throughout different mechanisms (reviewed in [2]). More than 65 different mutations have been described in the ADA gene in humans, from which nearly 70% are missense and the rest non-sense and splicing mutations [3, 4]. Interestingly, these mutations usually correlate with the residual enzymatic activity as well as the extent of substrate accumulation and are reflected in a spectrum of clinical Glutamate dehydrogenase phenotypes [1, 3], being the most frequent the early onset or fatal infantile onset (ADA-SCID), characterized by the absence of enzyme activity and total dAXP increased by 300- to 2000-fold in RBC. Other less frequent variants include delayed or late onset and late or adult onset in some patients, as well as a partial ADA deficiency in a few healthy relatives of ADA-deficient patients [3–5]. ADA-SCID is commonly fatal within the first year of life, unless the immune system is reconstituted by haematopoietic stem cell transplantation (HSCT)

or gene therapy (GT) [6]. Yet another option of treatment for patients who lack an immediate HLA-matched stem cell donor is enzyme replacement therapy (ERT) with pegylated bovine ADA (PEG-ADA) [6]. Continued administration of PEG-ADA eliminates dAXP and protects lymphocytes, restoring the immune function within 2 to 4 months in most patients [1]; however, in some patients, long-term treatment leads to lower lymphocyte counts as well as abnormalities in lymphocyte function [7,8]. In recent years, a small number of ADA-deficient patients have shown spontaneous and partial clinical remission with increasing numbers of peripheral blood (PB) lymphocytes, as a result of reversion of inherited mutations to wild type (ADA deficiency with somatic mosaicism) [9–13]. This phenomenon is being recognized in other primary immunodeficiencies (PID) as well, and it might provide a model for the process of development of cell and gene therapy in these diseases [14].

035), Fig  4A IFNγ, CXCL9, CXCL10 and CCL2 titres in MTBs-stimul

035), Fig. 4A. IFNγ, CXCL9, CXCL10 and CCL2 titres in MTBs-stimulated whole blood

cell supernatants from patients with L-ETB and D-ETB were found to be similar (data not shown). We further investigated MTBs-induced cytokine responses in L-ETB patients with disease at different sites. When responses of patients with unilateral pleurisy or LNTB were compared, it was found that MTB-induced IFNγ titres in patients with LNTB were higher (P = 0.002), Fig. 4B. The MTBs-stimulated CXCL9, CXCL10, CCL2 and IL10 levels between the two groups were found EPZ-6438 supplier to be similar (data not shown). The D-ETB group was too small to separately study site-specific immune responses, and therefore, no intragroup differences observations could be made. This study compares the utility of whole M. tuberculosis sonicate and recombinant

antigens ESAT6 and CFP10 in dissecting host immunity in TB. It illustrates that MTBs-induced IFNγ, IL10, CXCL10 and CCL2 levels differ according to the extent of disease in the host. Of the three antigens tested, only ESAT6-induced IFNγ responses differed between TB and EC groups. Increased ESAT6-induced IFNγ in patients with TB corresponds with previous data and can be attributed to the M. tuberculosis specific–IFNγ from CD4 memory T cells in infected individuals [28, 29]. We observed that CFP10-induced IFNγ levels in patients with TB were of a higher magnitude than those induced by ESAT6; however, the CFP10-induced IFNγ response did not discriminate between TB and EC groups. This corresponds Bay 11-7085 with previous selleck compound reports that have shown that CFP10 does not discriminate between active TB and uninfected controls [30–32]. In addition, as antigens related to ESAT6 and CFP10 are present in some NTMs that are likely to be present in this high TB endemic region, it is possible that because of cross-reactivity to these, the discriminatory power of ESAT6 and CFP10

for identification of M. tuberculosis–infected individuals may be reduced. Mycobacterium tuberculosis whole sonicate induced the greatest magnitude of IFNγ secretion in both healthy controls and patients, but these levels were comparable between groups. Higher levels of IFNγ in healthy or latently infected individuals have been associated with a protective response to M. tuberculosis [33]. In endemic regions, IFNγ can also be regulated by the natural exposure to M. tuberculosis or NTMs as well as BCG vaccination [34, 35]. Similar MTBs-stimulated IFNγ responses in EC and TB could also be attributed to cross-reactivity with MTBs in BCG-vaccinated study subjects [29–32]. We found that MTBs induced lower levels of IFNγ and CXCL10 in patients with Adv-PTB as compared with Mod-PTB. Reduced IFNγ levels in advanced PTB are in line with previous results [36]. Previous studies have identified a decrease in M. tuberculosis–specific CD4 T cell responses in PTB with cavitary sites as compared with non-cavitary sites [37].


PARK JI HYEON, PARK KYUNG SUN, JANG HYE RYOUN, LEE JUNG EUN, HUH WOOSEONG, KIM YOON-GOO, OH HA YOUNG, KIM DAE JOONG Division of Nephrology, Department of Internal Medicine, Samsung Medical center, Sungkyunkwan University School of Medicine, Seoul, Republic of Korea Introduction: Living-unrelated donors (LURD) have been widely Dinaciclib order used for kidney transplantation (KT). We compared clinical outcomes of

KT from LURD and from concurrent living-related donors (LRD), and identified risk factors associated with acute rejection, graft and patient survival in living KT. Methods: We retrospectively reviewed 779 patients who underwent living donor KT (264 from LURD, 515 from LRD) at Samsung Medical Center from January 2000 to December 2012. Results: Median follow-up was 67 months. Mean age (43.2 vs. find more 38.4 years, P < 0.001), mean number of total HLA mismatches (4.1 vs. 2.5, P < 0.001) and HLA-DR mismatches (1.2 vs. 0.8, P < 0.001) were higher, and mean estimated glomerular filtration rate (eGFR) was lower (87.6 vs. 90.9 ml/min, P = 0.007) in LURD. Acute rejection-free survival (64.9% vs. 72.7% at 5 years, P = 0.018) and graft survival (92.9% vs. 96.5% at 5 years, P = 0.025) were lower for LURD than LRD whereas patient survival rate was comparable (97.9% vs. 98.7% at 5 years, P = 0.957). Cox-regression analysis showed that HLA-DR mismatches (OR 1.77, 95% CI 1.20–2.62, P = 0.004

for 1 mismatches; OR 2.63, 95% CI 1.64–4.20, P. Conclusion: Our data suggest that HLA-DR mismatches and donor eGFR are independent risk

factors for clinical outcomes of living KT. In living KT, these factors should be considered to prevent acute rejection and improve graft survival. ADACHI HIROKI, MUKAI KIYOTAKA, OKUSHI YUKI, OKINO KAZUAKI, SHOJIMA KIYO, MATSUI YUKI, FUJIMOTO KEIJI, ATSUMI HIROKATSU, OKUYAMA HIROSHI, YAMAYA HIDEKI, YOKOYAMA HITOSHI Division of Nephrology, Kanazawa Medical University Endonuclease School of Medicine Introduction: Although the risk for morbidity and mortality is studied in subjects with renal transplantation, there are very limited data to access the reno-protective effects of lipid and adiponectin. Methods: We studied 105 adult subjects (age 19- to 72-year old; 66 males, 21 cadaveric donors) between January 2004 and December 2012, with at least three years of allograft survival in our hospital. We examined clinical backgrounds, donor types (living or cadaver), treated drugs, blood pressure (BP, mmHg), body mass index (BMI), blood chemistry including cholesterol (total, LDL-C, HDL-C), glucose, glycated hemoglobin (HbA1c), and total, high- and low-molecular adiponectin (ADPN) levels. Results: The initial 4 years alteration of eGFR was at −2.2(−14.3∼7.0) ml/min/1.73 m2/year in 105 subjects. In single analyses, both LDL-C/HDL-C ratio below 2.0 and statin treatment also decreased the reduction rate of eGFR at −1.4 and −1.0 ml/min/1.73 m2/year (p = 0.01, p = 0.02), respectively, but not by total ADPN levels.