Complete remission was seen in 32% at a mean time of 6.4 months, partial remission in 23% at a mean time of 5.7 months and 45% had no remission. Relapse rate was 14% at a mean time of 2.8 years during follow up. FSGS- NOS was the commonest subtype of FSGS (present in 56%), followed by tip variant in 24%, perihilar type in 10%, cellular in 9% and collapsing in 1%. PS-341 cell line Persistent nephrotic proteinuria at 3rd and 6th month and presence of interstitial fibrosis and tubular atrophy >30% in renal biopsy were independent predictors of poor response

to treatment. Male gender, nephrotic proteinuria at onset, persistent nephrotic proteinuria at 3 and 6 months, renal failure at onset, persistent renal failure at 3 and 6 months, presence of hypertension, anemia, interstitial fibrosis

and tubular atrophy of >30% in renal biopsy and no remission after treatment predict the progression to CKD. Renal survival at 5 years for complete remission was 69%, partial remission was RGFP966 manufacturer 49% and no remission was 42%. Conclusion: FSGS-NOS was the commonest subtype(56%) in our study. Persistent nephrotic proteinuria at 6 months, interstitial fibrosis and tubular atrophy >30% and no remission after treatment were found to be independent risk factors and presence of interstitial fibrosis and tubular atrophy >30% in renal biopsy was the strong predictor for development of ESRD in our study. Renal survival at 5 years for complete remission was 69%, partial remission was 49% and no remission was 42%. ZHANG CHANGMING1, ZHANG WANFEN1, CHEN HUIMEI1, LIU CHUNBEI1, WU JUNNAN1, LI LIMIN2, SHI SHAOLIN1, ZEN KE1,2, LIU ZHIHONG1 1Research institute of nephrology, Jinling hospital, Nanjing University

School of Medicine, Nanjing, China; 2JERC-MBB, State Key Laboratory of Pharmaceutical Biotechnology, School of Life Sciences, Nanjing University, Nanjing, selleck compound China Introduction: MicroRNAs (miRNAs) are stable in circulation, and their unique expression profiles can serve as fingerprints for various diseases. In this study, we determined whether human plasma miRNAs could be used as biomarkers to diagnose active focal segmental glomerulosclerosis (FSGS). Methods: Pooled plasma samples from 9 FSGS patients with nephrotic range proteinuria (active FSGS, FSGS-A) and 9 normal controls (NC), respectively, were analyzed by miRNA TaqMan Low Density Array (TLDA), and the two miRNA profiles were compared. The differentially expressed miRNAs were confirmed by real-time reverse transcription-PCR (qRT-PCR) using 32 patients of FSGS-A versus 30 NCs and 37 patients of FSGS-A versus 35 FSGS in remission (FSGS-CR), respectively. Receiver operation characteristics (ROC) curves were utilized to evaluate the specificity and sensitivity of the miRNAs in predicting FSGS. Results: TaqMan Low Density Array analysis of plasma samples identified 45 miRNAs that were elevated or detectable only in FSGS-A group.

These results suggest that a primary function of the activating NK receptors in immune regulation is to control NK-cell production of immunomodulatory factors [76]. The human KIRs, which recognize HLA class I molecules as ligands, are functional homologs to the Ly49 receptors in mice [75]. KIR2DL4 is the human homolog of Ly49D in mice, therefore the genetic changes observed in KIR-activated human NK cells and Ly49D-activated mouse NK cells are mostly the same [75]. KIR2DL4 (CD158d) resides in endosomes within NK cells and binds to its soluble ligand, HLA-G, which is produced by fetal trophoblast cells during early pregnancy [66]. KIR2DL4 is an unusual member

of the polymorphic KIR family because Selleckchem Ku 0059436 it possesses an NK-cell-activating function despite harboring an inhibitory

ITIM [77]. Microarray analysis of human NK cells undergoing sustained activation after treatment with a soluble anti-KIR2DL4 agonist mAb revealed upregulated genes typical of a senescent signature (such as Il6, Il8, IL1B, and p21), and the supernatants from KIR2DL4-activated NK cells could increase vascular permeability and promote angiogenesis [66]. click here Thus, sustained activation of NK cells induces senescence in response to soluble HLA-G in the microenvironment, and may contribute to remodeling the maternal vasculature in early pregnancy [66]. An independent study using a human cytokine array to evaluate mRNA expression of 114 common human Ureohydrolase cytokine genes also showed that activation of human dNK cells by anti-KIR2DL4 mAb or HLA-G homodimer upregulates proinflammatory cytokines including IFN-γ, IL-6, IL-8, and TNF-α as well as proangiogenic protein vascular endothelial growth factor, which are essential for a successful pregnancy [77]. Malaria infection has been shown to trigger early activation and expansion of NK cells [78]. Microarray analysis of early blood responses in mice infected with erythrocytic-stage Plasmodium chabaudi revealed

that NK-cell-associated transcripts (such as lectin-like killer cell receptors, Prf1 and GzmA) in the blood increase dramatically, which was confirmed by the observations of increased NK-cell numbers and frequency in both the blood and spleen 72 h after infection [79]. At the molecular level within these P. chabaudi infection induced pNK cells, subsequent microarray analysis revealed a cell proliferation signature consistent with the above findings [79]. NK cells are essential for controlling certain viral infections in the host. Murine cytomegalovirus (MCMV) infection induces NK-cell activation and expansion, and thus serves as an ideal model for physiological NK-cell activation [41, 80, 81]. Bezman et al.

The DiabCare Indonesia 2008, this was a non-interventional, cross-sectional study. It was recruited 1785 patients from secondary and tertiary medical centers across Indonesia that it was eligible for analysis. The mean age of the patients was 58.9 ± 9.6 years. The mean duration of diabetes was 8.5 ± 7.0 years. Majority (97.5%) of the patients had type 2 diabetes. 67.9% had poor control of diabetes (A1c:8.1 ± 2.0%).

47.2% had click here FPG>130 mg/dL (161.6 ± 14.6 mg/dL). Dyslipidemia was reported in 60% (834/1390) and 74% (617/834) of those received lipid lowering treatment. Neuropathy was most common complication (63.5%); other complications were: Diabetic retinopathy 42%, nephropathy 7.3%, severe late complications 16.9%, macrovascular complications 16%, microvascular complications 27.6%. About 81.3% of patients were on OADs (± insulin), 37.7% were on insulin (±OADs). Majority used biguanides followed by sulfonylureas. Majority of the WHO-5 well being index responses fell in positive territory (Pradana et al, 2010). The DiabCare Malaysia 2008, analysis from 1549

patients showed deteriorating glycemic control with mean HbA1c of 8.66 +/- 2.09% with only 22% of the patients achieving ADA target of <7%. 80.3% of patients were hypertensive and 75% were on anti-hypertensive medication. 46% of patients had LDL levels > 2.6 mmol/L; 19.8% had triglycerides > 2.2 mmol/L; GSI-IX mw 27.4% had HDL < 1 mmol/L despite 85% of the patients being on lipid lowering agents. Microvascular, macrovascular and severe late complications were reported in 75%, 28.9% and 25.4% patients respectively. The rates of diabetic complications were cataract 27.2%, microalbuminuria 7%, neuropathy symptoms 45.9%, leg amputation 3.8% and history of angina pectoris was 18.4%. Quality of life evaluation showed that about one third of patients have poor quality of life (Mafauzy et al, 2012). The DiabCare Philippines, a total of 770 diabetics were recruited from general hospitals, diabetes clinics and referral clinics, Mannose-binding protein-associated serine protease out of which 724 were type 2 diabetic patients. Results: The mean HbA1c was 8.03 ± 1.96 % and only 15.0% of the patients achieved ADA target of <7%.

2.5% of patients had LDL levels >2.6 mmol/L; 14.3% had triglycerides >2.2 mmol/L; 19.2% had HDL < 1 mmol/L and 53.9% of the patients were on lipid lowering agents. 68.4% patients were hypertensive and 64.4% were receiving anti-hypertensive medication. Microvascular, macrovascular and severe late complications were reported in 68.1%, 14.8% and 9.4% patients respectively. The rates of diabetic complications were cataract 32.7%, neuropathy symptoms 45.2%, microalbuminuria 15.8%, history of angina pectoris 10.7% and cerebral stroke 4.7% (Jimeno et al, 2012). The DiabCare Bangladesh 2008, results from 1860 diabetics showed deteriorating glycaemic control with mean HbA1c of 8.6±2.0% with only 23.1% of the patients achieving American Diabetes Association (ADA) target of <7%. 896 (47.0%) patients were hypertensive and 850 (94.

p.m. and (2) stationary. Biofilms were quantified using the standardized crystal violet method (O’Toole Ipilimumab et al., 1999; Dusane et al., 2008a). Adhesion of bacteria to 96-well polycarbonate microtiter plate surfaces was carried out by inoculating 20 μL of overnight grown culture in 0.5 × LB containing 180 μL of the growth medium. The plates were incubated at 37 °C for 72 h and biofilm formation was estimated by a routine crystal

violet staining method (Dusane et al., 2008b). The experiments were carried out in triplicates. Biofilm formation was also analyzed in glass test tubes (Tomaras et al., 2003). The biofilms were formed by adding 0.1 mL of the culture to 10 mL LB (0.5 ×) dispensed AZD1208 nmr in glass test tubes. The experiment was performed in duplicates and

the cultures were incubated at 37 °C for 72 h under two sets of different conditions: (1) shaking at 200 r.p.m. and (2) stationary. After incubation, the medium was removed, the tubes were washed with distilled water, air dried and biofilms were assayed using the crystal violet method. Strains of Escherichia coli HB101 and Pseudomonas aeruginosa PA01 were used as controls for the biofilm experiments (Kazemi-Pour et al., 2007). In vitro assay of bacterial adhesion to the catheter surface was assessed as described earlier with some modifications (Sheth et al., 1983). The selected isolates used for this study were cultivated for 24 h at 30 °C in 0.5 × LB containing 0.25 × minimum

inhibitory concentration (MIC) (0.5 μg mL−1) and 0.5 × MIC (1 μg mL−1) concentrations ID-8 of colistin (Sigma, India). After the incubation period, antibiotic was removed from the culture by rinsing twice with sterile saline followed by centrifugation (6000 g for 10 min). The bacterial cells were resuspended in sterile saline and the OD of each suspension was measured colorimetrically at 540 nm to achieve the cell density equivalent to 1–5 × 107 CFU mL−1 (confirmed by plate count). Cultures without antibiotics were used as the controls. Urinary catheters (Rusch GmbH, Kemen, Germany), 7 mm in diameter were cut into 1.5-cm-long segments. The segments were then immersed in 13 × 100 mm tubes containing suspensions of the previously standardized strains and kept at room temperature for 30 min. After this contact, each fragment was placed in a tube (18 × 160 mm) containing 15 mL of sterile saline solution, and the tubes were manually inverted 40 times. This procedure was repeated 15 times, transferring the fragment to 15 tubes successively, with the objective of removing the nonadherent bacteria. After the 15 rinses, the catheter fragments were removed from the tube and rolled over the surface of 10 Petri dishes (90 × 15 mm) containing LB agar. After an incubation period of 24 h at 30 °C, the bacterial colonies were counted.

Activation of endothelia by VEGF in normal tissues led to VVOs fusing to form trans-endothelial channels, which enlarged into the well-known openings associated with increased vascular permeability of acute inflammation. More recently, the Dvoraks’ group [4] has investigated caveolae and VVOs in caveolin knock-out mice (cav −1−). They confirmed

an increase in plasma protein flux into skeletal muscle, but failed to see enhanced transport of macromolecules into skin. While they confirmed find more that caveolae and small vesicles were much reduced in of cav −1− mice, 10% were still present in capillary endothelia and 20% in venular endothelia. Furthermore, the numbers of VVOs in endothelial cells of venules remained unchanged in cav −1− mice, although their response to stimuli such as VEGF was diminished. So how do the new findings of Wagner et al. [25] contribute to this long standing check details controversy? First, they provide a three-dimensional picture of the clusters of vesicles in endothelial cells with far better resolution than has been achieved previously. Secondly, by showing that both labeled and unlabeled vesicles can be present in mammalian endothelial cells, they quash assertions that free vesicles do not occur. Thirdly, they confirm the earlier findings of Wagner and Chen [24] that the vesicle system can act as

a transport pathway, whether or not this is its primary function. Fourthly, by demonstrating the presence of fused chains of vesicles forming a pathway through the endothelial Urease cells between the plasma and interstitial fluid, they raise the question once more of whether these

channels could be the “large pores” proposed over half a century ago to account for the trans-capillary exchange of macromolecules. Before any positive claims can be made on their behalf, it will be necessary to show that they are present in numbers consistent with microvascular permeability to macromolecules in the particular type of endothelia investigated and that they are present in the endothelia of cav −1− mice. “
“Microcirculation (2010) 17, 39–46. doi: 10.1111/j.1549-8719.2010.001.x Objective:  Lysophosphatidic acid (LPA) increases permeability of cerebral endothelium in culture, but it has been suggested that histamine release is required in vivo. Methods:  Cerebral venular permeability was measured by using the single-vessel micro-occlusion technique, and fura-2 ratios were used to track changes in endothelial [Ca2+]. Results:  Topical acute LPA application dose-dependently increased permeability (log EC50−9.4; similar to the Kd of the LPA1 receptor). The calcium response to LPA was similar to histamine, but the permeability response was unaffected by H2-histamine receptor antagonism, and was blocked by Ki16425, a LPA1 receptor antagonist. The permeability response was blocked by nitric oxide synthase and free radical scavenging, which were carried out together, but not separately. Intravascular LPA bolus injection increased permeability.

The Congress was attended by over 600 participants representing 31 countries with the bulk coming from the various states of India. A special effort was made to encourage the participation of young immunologists and post doctoral scientists

by providing them bursary support and a platform for competitive presentation. The Congress was held in Hotel Le Meridien which provided an excellent scientific ambience. Situated in the heart of Delhi, very close to the historical monuments, and with the weather turning out to be brilliant, the week-long activity was a perfect blend of high science Doramapimod cell line and social interaction. The Congress format was organized into 10 master lectures delivered by experienced

researchers, nine theme-based symposia with 54 invited speakers and six parallel workshop sessions featuring 65 oral presentations selected from over 400 submitted abstracts. In addition, there were two dedicated poster review sessions. The program covered a wide range of important topics that included the immunological basis of autoimmune and infectious diseases including HIV and type LY2157299 1 diabetes, cross talk between innate and adaptive immunity, immunodeficiencies, issues related to organ and bone marrow transplantation, immunological tolerance, tumor immunology, stem cells and regenerative medicine and new developments towards vaccine, immune diagnostics and cell therapy. The organizing committee introduced e-poster presentation at this Congress as an effective means of promoting Montelukast Sodium peer networking and healthy discussion. Twelve

computer stations were provided and these displayed the submitted posters in 3–4 screen pages each. The participants had the opportunity to view, at their convenience, the allotted posters of each day on big screens by clicking the poster number of interest; this also facilitated the discussion of the data with others and with the poster judges. Six best posters (2 for each day of the Congress) were awarded a cash prize and certificate during the valedictory ceremony. The awards were made available through a small grant from International Immunology (facilitated by the Editor-in-chief, Tadamitsu Kishimoto), which is published by Oxford University Press, on behalf of the Japanese Society for Immunology. An important highlight of the Congress was the session ‘Ten best oral presentations’, the participants of which were selected by a panel of international experts. Several awards were instituted to recognize the hard work put in by young researchers, with the ultimate goal being to promote excellence in research. Another important feature of the Congress was the ‘Round Table discussion’ session highlighting the issues related to ‘Gender equality and career development’.

Because both activated

CD4+ T cells and DCs express Tim-1, we first tested the effect of Tim-1 crosslinking on CD4+ T cells in an APC-free system. In an APC-free culture, activation with anti-CD3/anti-CD28 in the presence of 3B3 anti-Tim-1 increased the frequency of IL-4- and IL-10-producing CD4+ T cells, while the treatment did not significantly change IFN-γ+ or IL-17+ T cells (Fig. 3A). However, when naïve CD4+ T cells were cultured with syngeneic DCs plus antigen together with 3B3, the responding T cells produced more IFN-γ and IL-17, in addition to IL-4 and IL-10 (Fig. 3A). Interestingly, in the absence or presence of DCs, RMT1-10 increased only Th2 responses (IL-4 and IL-10 production) but had no obvious modification

on Th1 (IFN-γ) or Th17 (IL-17) responses, suggesting that the low-avidity anti-Tim-1 RMT1-10 does not modulate DC function MK-2206 ic50 (Fig. 2). These data suggest that Tim-1 crosslinking with both high-avidity and low-avidity anti-Tim-1 promotes Th2 responses regardless of the presence or absence of DCs. However, only the high-avidity anti-Tim-1 enhances Th1 and Th17 responses when DCs are present in the cultures. To demonstrate that Tim-1 signaling in DCs is responsible for promoting Th1 and Th17 responses in vivo, PLP139–151-loaded/anti-Tim-1-treated DCs were subcutaneously transferred into syngeneic SJL mice. Draining LN cells were then isolated and antigen-specific T-cell responses were examined ex vivo. We found that immunization with 3B3-treated DCs enhanced the production

of IFN-γ and IL-17 as well as IL-4 and IL-10 in PLP139–151-responding T cells, whereas immunization with RMT1-10-treated DCs seemed not to significantly PLX 4720 modulate any of these cytokines (Fig. 3B). LPS-treated DCs enhanced the production of IFN-γ and IL-17 but strongly inhibited IL-4 and IL-10 from T cells (Fig. 3B). There was no detectable 4��8C production of these cytokines in the absence of antigen in any case (data not shown). These data further confirm that only the high-avidity anti-Tim-1 induces DCs activation, and Tim-1 signaling-activated DCs promote Th1 and Th17 as well as Th2 responses. TGF-β acts on naïve T cells to induce Foxp3 expression and these cells attain most of Treg properties. Addition of 3B3 anti-Tim-1 in the presence of either CD11b+ or CD11b− DCs to cultures where TGF-β was used to induce Foxp3+ Tregs led to the inhibition of Foxp3+ Treg generation. The frequency of Foxp3+ Tregs upon 3B3 treatment of CD11b− DCs was only about 4% compared with about 40% induction under control conditions (Fig. 3C). However, addition of 3B3 in APC-free cultures did not significantly change Foxp3+ Treg generation, with about 70% of Foxp3+ cells regardless of whether anti-Tim-1 was used. However, 3B3 treatment increased CD103 expression on both Foxp3+ and Foxp3− T cells (Fig. 3C). Furthermore, treatment with 3B3 increased the production of IL-17 from T cells in the presence of DCs (Fig. 3D).

33 μM. After 3 min of incubation, cells were vortexed at room temperature and incubation continued for 2 additional minutes. One tenth of the volume of FCS Rucaparib molecular weight was added and the cells were vortexed and incubated for 1 min. Samples were washed three times in complete media and used in experiments. Percent divided, division, and proliferation indices were determined by FlowJo software. Purified B cells (5 × 105) were used ex vivo or after 24–48 h of stimulation with media or 10 μg/mL anti-IgM in the presence of vehicle or dimedone.

Cells were harvested and surface stained with B220-allophycocyanin as described above. After surface staining, cells were resuspended in 7-amino-actinomycin D (7-AAD) and Annexin-V FITC (BD Pharmingen) for 15 min at room temperature according to the manufacturer’s protocol. Cells were acquired immediately on a FACSCalibur Instrument. All samples were analyzed using FlowJo Software. Purified (5 × 105) B cells were stimulated with 10 μg/mL anti-IgM in the presence of vehicle or dimedone. At 45 h, samples were pulsed with 10 μM BrdU (Sigma-Aldrich) for 3 h and labeling was performed as described previously [14]. Briefly, cells were harvested and resuspended in 1%

paraformaldehyde with 0.05% Igepal (Sigma-Aldrich), vortexed, and incubated at 4°C overnight. Samples were washed at room temperature two times with PBS at 1200 rpm for 6 min, resuspended in 1 mL PBS, and 4.2 mM MgCl2 containing 50 Kunitz U/mL DNase I (Sigma-Aldrich), and incubated at 37°C for 30 min. Following

two washes in wash buffer (PBS supplemented Talazoparib with 5% FCS and 0.5% Igepal) at 1200 rpm for 6 min at 4°C, samples were resuspended in the same buffer containing 2% mouse serum and a 1/5 dilution of anti-BrdU FITC (BD Pharmingen). Samples were incubated on ice for 45 min. After two washes, cells were resuspended in 10 μL 7-AAD (BD Pharmingen) plus FACS buffer for 15 min on ice. Cells were acquired immediately on an FACSCalibur Instrument. Purified B cells (2 × 106) were stimulated in the presence or absence Etofibrate of dimedone with 10 μg/mL anti-IgM. After stimulation, cells were pelleted, washed with PBS, and lysed in buffer described previously [14]. Samples were boiled in the presence of reducing sample buffer, ran on a 7.5% precast SDS-PAGE gel (Bio-Rad), transferred to a PVDF membrane, and probed for phospho-Syk (Y525/526) (C87C1), Syk, phospho-p44/p42 MAPK (T202/Y204), or p44/p42 (Cell Signaling) according to the manufacturer’s protocol. For phospho-tyrosine detection, 2.5 × 106 purified B cells were stimulated in the presence or absence of dimedone with 10 μg/mL anti-IgM. Samples were lysed, ran on a SDS-PAGE, transferred to a membrane, and probed for tyrosine phosphorylated proteins (4G10-HRP, Millipore) as previously described by Fujimoto et al. [48]. After the blot was developed and imaged, it was stripped and probed with anti-actin as previously described [14].

3D), whereas in CRIg-Fc-treated EAU mouse retina, only mild foci of infiltration were seen, and retinal structure was largely preserved click here (Fig. 3E). On average, there was a 54% reduction in the inflammatory cell infiltration score and a 58% reduction in the structural damage score in CRIg-Fc-treated mice as compared with PBS-treated EAU mice (p<0.05) (Fig. 3A–F). When CRIg-Fc was injected after T-cell priming and the initiation of EAU (i.e. from day 18 to day 24 p.i.), retinal inflammation was also significantly reduced (Fig. 3G). However, when CRIg-Fc was injected only at the T-cell priming stage, i.e.

from day 1 to day 10 p.i. no significant reduction in EAU severity was observed (Fig. 3H). In addition to reduced retinal inflammation (Fig. 3G), complement C3d deposition in the photoreceptor/RPE layer (Fig. 4A and B), the ganglion cell layer (Fig.

4C and D), and the ciliary body (Fig. Ku-0059436 mw 4E and F) was also markedly reduced by CRIg-Fc treatment, indicating decreased AP-mediated complement activation. Furthermore, quantitative real-time PCR (qRT-PCR) analysis revealed that the 59-fold increase in CFB expression in isotype-IgG1 EAU mice was restored to the essentially normal values by treatment with CRIg-Fc (Fig. 4H). There was also a 50% reduction in CFB gene expression in RPE/choroid/sclera tissue of CRIg-Fc-treated mice as compared with that of isotype IgG1-treated EAU mice, although the reduction did not reach statistical significance (Fig. 4H). To further understand the mechanism of CRIg-Fc-mediated inhibition of retinal inflammation, the proliferation of T cells from EAU mice treated with or without CRIg-Fc was evaluated. Without in vitro IRBP stimulation, splenocytes from PBS-treated EAU mice showed low levels of spontaneous Acetophenone proliferation (500 CPM on 3H incorporation, Fig. 5A). Cells from CRIg-Fc treated (days 1–22 p.i.) EAU mice had the same levels of 3H incorporation as the cells of nonimmunized

normal mice (around 200 CPM, Fig. 5A), indicating the lack of proliferation. After IRBP peptide (25 μg/mL) stimulation, splenocytes from PBS-treated EAU mice proliferated massively as compared with cells from nonimmunized normal mice (Fig. 5A). However, the level of cell proliferation in CRIg-Fc-treated EAU mice was significantly lower than that of PBS-treated EAU mice (Fig. 5A). Splenocytes from day 18 to day 24 p.i. CRIg-Fc-treated EAU mice showed similar results (data not shown). When splenocytes from PBS-treated EAU (day 25 p.i.) mice were activated in vitro with retinal antigen (i.e. human interphotoreceptor retinoid-binding protein peptide (pIRBP), 25 μg/mL) or nonspecifically with Con A (2.5 μg/mL) in the presence of different concentrations of CRIg-Fc, CRIg-Fc dose-dependently suppressed cell proliferation (Fig. 5B). Splenocytes from day 25 p.i.

The proportion of steroid sensitive ACRs was similar Deforolimus molecular weight in both study groups (SD–83.3%, RD–65.4%; p = 0.2). The number of patients with deranged graft function at the end of the study was higher in the RD group (2.3% vs 12.3%; p = 0.001). Patient survival and infection rates were similar in the two study groups. Conclusion: We conclude that short term outcomes of SD transplants are not inferior to RD transplants. Lesser use of induction therapy in the RD group may explain the poorer outcomes as compared

to the SD group. MATSUKUMA YUTA1,3, MASUTANI KOSUKE1, TSUCHIMOTO AKIHIRO1, OKABE YASUHIRO2, KITADA HIDEHISA2, TSURUYA KAZUHIKO1,3, KITAZONO TAKANARI1 1Department of Medicine and clinical science, Kyushu University; 2Department of Surgery and Oncology, Kyushu University; 3Department of Integrated Therapy of Chronic Kidney Disease, Kyushu University Introduction: Polyomavirus BK nephropathy (BKVN) is an important infectious complication in kidney transplant patients. Regular screening using polymerase chain reaction (PCR) for BKV DNA in

plasma and urinary cytology are effective for early diagnosis of BKVN. However, methods of follow-up and therapeutic targets are not well described. Methods: Ten patients with BKVN who received biweekly urinary cytology and re-biopsies after diagnosis were retrospectively studied. Histological remission Target Selective Inhibitor Library of BKVN was determined when biopsy revealed negative SV40 large T-antigen (TAg) staining. Results of urinary cytology and re-biopsy findings were compared. Results: Urinary

decoy cells disappeared in 8 of 10 patients 55 ± 25 (range 13–79) days after index biopsies. In those cases, allograft function was preserved and the final serum creatinine level was 2.14 ± 1.19 (0.80–4.55) mg/dl after 962 ± 393 (325–1563) days of follow-up. Two cases with persistent urinary decoy cell shedding lost their graft 195 and 362 days later. Amongst 29 re-biopsies, there were 13 TAg positive and 16 negative biopsies. In 12 of 13 Tag-positive biopsies (92%), urinary decoy cells were still positive, whereas at the same time in 15 Tag-negative biopsies, decoy cells had already disappeared (94%). Conclusion: Cytology testing is advantageous because of its cost effectiveness. Clearance of decoy cells from urine was closely related to histological Gemcitabine chemical structure remission of BKVN, and may possibly be a therapeutic target in BKVN. RUNGTA ROHIT, RAY DEEPAK SHANKAR, DAS PRATIK Rtiics, Kolkata Introduction: Although primary graft dysfunction is not very common in live donor renal transplantation (incidence: 13.2%) But a good number of recepients do not pass urine in the operation theatere. In such cases an early diagnostic clue is extremely helpful in planning subsequent management. Biopsy from a surgically perfect graft is safe & can provide significant help towards predicting the diagnosis and future events.