The level of serum FGF23 increases with developing chronic kidney disease. However, it is still unclear the effect of hemodialysis (HD) and type of P-binder on regulation of FGF23. We determined the change of serum FGF23 after initiation of HD and compared between calcium bicarbonate (C) and lanthanum carbonate (La) group in FGF23 regulation. Methods: Eighteen patients, introducing hemodialysis from April to September

in 2012, were participated under the informed consent. The participants were randomly divided into two groups, i.e. C and La group. Serum level of FGF23, whole parathyroid hormone (PTH), calcium and phosphate were measured at the initiation of HD and subsequent 3 months. Results: The levels check details of FGF23 increased after introducing HD, although the serum phosphate was managed completely. The level of whole PTH was decreased after the starting HD. There was no significant difference in the serum FGF23 level between C and La group. Urinary P excretion was also different between them. Conclusion: Maintaining

removal of uremic substances by HD and type of P-binder did not influence the FGF23 buy Tofacitinib regulation. Longer observation might be needed to determine the trend of serum FGF23 in patients. HONG YU AH1, KO GANG JEE1, JUNG MI YEON1, CHO YOO SUN1, OH SOO YOUNG1, SEO JAE HEE1, PYO HEUI JUNG1, SUH SANGIL2, KWON YOUNG JOO1 1Department of Internal Medicine, Korea University College of Medicine; 2Department of Radiology, Korea University College of Medicine Introduction: Cinacalcet has been played a role in treatment of secondary hyperparathyroidism (SHPT) refractory to previous medical treatment. However, the method predicting

treatment response of cinacalcet was not established yet. We aimed to investigate whether radiologic Pazopanib manufacturer examinations would be helpful to determine the response of cinacalcet treatment. Methods: The research was done with two study populations. First, 26 patients who received dialysis more than 3 months in single center were evaluated the size of parathyroid glands with three different radiologic examinations, which were sonographic measurement for diameter and volume of each gland by 3 dimentional reconstruction by one expert, and computed tomography (CT). After 20 weeks of cinacalcet treatment, predicting value of each radiological examination for the responder group who were defined as patients with PTH Results: Among 26 patients, 17 patients were responders (65.3%). Baseline serum calcium and PTH, and post-treatment ALP and PTH were lower in responder group. The means of diameter in sonography and CT, and gland volume measured by sonography were not significantly different between responder and nonresponder.

A number of parallel pathophysiological pathways have been implicated in the pathogenesis of BPH and PCa, including age-related prostate tissue remodelling, hormonal and metabolic alterations, and the previously neglected inflammatory disorder. Recently, PCa and BPH have been considered in the context of local immune reactions and inflammatory response of the prostate, which may also be reflected systemically [2]. The normal, healthy prostate is infiltrated by small numbers of T cells, B lymphocytes, and macrophages, all of which provide physiological

protection to the tissue [3]. BPH, which is stromal hyperproliferation and epithelial overgrowth of the prostrate tissue, is associated with increased leucocyte infiltration [4] relative to the intensity of the inflammation [3]. Several lines of evidence have shown that Peptide 17 the prostate tissue in patients with BPH contains diffuse infiltrates of T lymphocytes, predominantly CD4+ cells, in the stroma [5]. Similarly, in PCa, tissue-infiltrating lymphocytes (TILs) have been observed in

and around the cancer tissue [6]. Although GSK126 manufacturer previous studies on various cancers have shown that tumour infiltration with TILs is associated with increased survival [7–9], there does not appear to be a correlation between the presence of TILs and survival of patients with PCa. This may be because of the infiltration of regulatory T cells, which negatively correlates with the immune response against cancer [10]. However, Kasic and Viola [11] performed phenotype analysis and showed that TILs of PCa samples were predominantly CD8+ cells. Another possible reason for ineffective surveillance in patients with PCa could be the inadequate expression of cytotoxic molecules, such as perforin (P), in and around the tumour [12]. However, in BPH tissue, P-expressing cells were rare, although the survival of these patients was not affected [12]. Moreover, little is known about the role of NK cells, which are potent effectors of innate immunity

in the first line of tumour defence. C-X-C chemokine receptor type 7 (CXCR-7) P is the primary mediator of short-term cytotoxicity and forms pores in the membranes of target cells (pore-forming molecule). It is accumulated in response to pro-inflammatory cytokines (IL-12, IL-15 and IL-18), stored in the cytoplasmic granules of cells with a cytotoxic phenotype (T lymphocytes, NK cells and NKT cells as a unique subpopulation of T lymphocytes which share common characteristics of T and NK cells), and released upon activation [13–18]. At the ‘cellular synapse’, the released P monomer begins to polymerize in the presence of Ca+ ions and imbeds in the membrane of target cells, forming pores that allow ion exchange. This leads to osmotic imbalance and ultimately, necrosis of the target cell [19].

Intrahepatic mononuclear cells were isolated from six unimmunized individual mice and the expression of various TCR Vβ on CD8+ T cell subsets was determined by flow cytometry using a commercially available screening kit. The pattern of TCR Vβ usage by liver CD8+ T cells was conserved between individual mice (Figure 2a). As has been reported previously, the most commonly used TCR Vβ families in C57BL/6 mice were Vβ5.1,5.2 and Vβ8.1,8.2 (28,29). As livers from unimmunized mice do not typically contain TEM cells, we only analysed the repertoires expressed by CD8+ TN and TCM cells. The frequency of TCR Vβ usage was similar for TN and TCM CD8+ T cells; however, there was more variability

Selleck ABT 737 in TCR Vβ usage by CD8+ TCM cells, perhaps reflecting differences in generation of different epitope specificities in individual mice. As immunization with Pbγ-spz promotes the appearance of CD8+ TEM cells in the liver [Figure 1a; (8)], we sought to determine whether

CD8+ TEM cells induced by γ-spz maintain a diverse TCR Vβ repertoire or whether the repertoire becomes focused. One week after the final immunization, we analysed the TCR Vβ expression on liver CD8+ T cell selleck chemical subsets. Figure 2(b) shows combined results from the analyses of 10 individual mice. The frequencies of CD8+ TN and TCM cells expressing a particular TCR Vβ were similar to that observed in CD8+ T cells from the livers of unimmunized mice. In contrast, the expression of TCR Vβ by CD8+ TEM cells was much more SPTLC1 variable. Many mice had an increase in the expression of one or more TCR Vβ on CD8+ TEM cells compared to TN/TCM cells. We performed the analyses on 10 mice, three mice showed an expansion of the Vβ7 and the expression of Vβ11 on CD8+ TEM cells was elevated in most mice. However, the frequencies of the majority of TCR Vβ expressed by CD8+ TEM cells either remained the same or appeared lower than that of TN/TCM. To determine whether challenge altered the TCR Vβ repertoire of CD8+ TEM cells, a cohort of mice was challenged with 10 K infectious spz 7 days

after the last boost immunization with Pbγ-spz, and 1–2 weeks after the challenge, we analysed the TCR Vβ expression on the CD8+ T cell subsets. For example, the mouse depicted in Figure 1b has an expansion of Vβ7 and Vβ8.3 CD8+ TEM cells. Vβ7 was expressed on 4·6% of TN, 6·7% of TCM and 21·5% of TEM, while Vβ8.3 was expressed on 6·7% of TN, 8·4% TCM and 21·1% of TEM CD8+ cells. Calculation of the absolute number of CD8+ T cells demonstrated that there were 2·4 × 104 Vβ7+CD8+TN, 3·2 × 104 Vβ7+CD8+TCM, 15 × 104 Vβ7+CD8+TEM, 2·5 × 104 Vβ8.3+CD8+TN, 1·2 × 104 Vβ8.3+CD8+TCM and 12·9 × 104 Vβ8.3+CD8+TEM per liver. Data in Figure 3 show the combined analyses performed on liver CD8+ T cells from 18 individual mice.

30 Moreover, LPS was shown to induce the up-regulation of COX2/PGE2 in RAW macrophages.31 The effects of a brief (10 min) treatment with PGE2 on CGRP release from dorsal root ganglion cultures have been reported before.32,33 We observed here that longer PGE2 treatment (24 hr) induced or enhanced LPS-stimulated CGRP release from RAW macrophages. As PGE2-induced CGRP release was blocked by the co-treatment with actinomycin-D or cycloheximide, de novo mRNA transcription and protein synthesis are most

likely involved. These findings suggest that long-term PGE2 treatment may not only increase the release of CGRP, but R788 manufacturer also its transcription and synthesis in RAW macrophages. However, the PGE2 EP receptor subtype(s) involved here, as well as downstream signal transduction pathways, requires further studies. In parallel with previous reports showing that NF-κB is involved in LPS-induced production of inflammatory mediators in monocytes/macrophages,12,34 co-treatment of LPS with an inhibitor of IκB phosphorylation suppressed LPS-induced CGRP release. This finding suggests that the NFκB signalling pathway is involved in LPS-induced CGRP synthesis in RAW macrophages. Our data are comparable

to those in a previous report showing that NF-κB plays a role in IL-1β-induced CGRP secretion from human alveolar epithelial cells.16 However, how NF-κB mediates selleck LPS-induced synthesis of CGRP has yet to be fully established. Unexpectedly, we found that CGRP receptor accessory protein RAMP1 and NGF/trkA receptor signalling were negatively involved in LPS-induced CGRP synthesis. The CGRP receptor is a rather unique G protein-coupled receptor, because it shares a seven trans-membrane domain protein, CLR, with adrenomedullin (AM, a peptide member in the CGRP superfamily) and

also requires accessory protein RAMP1 to be functional. The RAMPs are essential accessory Adenylyl cyclase proteins to chaperone CLR to the cell surface, which determines the receptor specificity.35 RAMP1 enables CLR to form CGRP receptor while RAMP2 and RAMP3 enable CLR to form AM1 and AM2 receptors,36 respectively. To our surprise, neutralizing antisera against either CGRP/RAMP1 or NGF/trkA receptor dramatically enhanced LPS-induced CGRP release, suggesting that RAMP1 and trkA exert negative feedback effects on the synthesis of CGRP. Neutralizing trkA or RAMP1 antiserum on their own had no effects on basal CGRP release from RAW macrophages, suggesting that the negative feedback action of trkA or RAMP1 occurs only when NGF or CGRP is up-regulated by inflammatory stimuli. Accordingly, when NGF or CGRP is increased, activation of RAMP1 or trkA receptor signalling can exert an inhibitory action on CGRP synthesis in RAW macrophages. This hypothesis is supported by a recent report showing that levels of serum CGRP in homozygous RAMP1-deficient mice were dramatically and transiently increased following peritoneal LPS challenge.

“
“Aim:  To investigate the possible association of gene polymorphisms of tumour necrosis factor (TNF)-α MLN2238 chemical structure (-238 and -308), interleukin (IL)-10 (-592 and -819) and 3′ untranslated region (3′UTR) of the IL12B (-1188) and hepatitis B in Chinese Han haemodialysis (HD) patients. Methods:  The genotyping of TNF-α -238 and -308, IL-10 -592 and -819 and 3′UTR of the IL12B were performed by polymerase chain reaction (PCR) restriction fragment length polymorphism (RFLP) method. Results:  The TNF-α-238 A allele, the

IL12B 3′UTR C/C, C/A genotypes were associated with decreased susceptibility to hepatitis B viral infection (P = 0.047, P= 0.003 and P = 0.001 respectively). The frequencies of IL-10–592 A/A genotype, IL-10–819 T/T genotype check details were lower in the HBV persistence group (P = 0.029 and P = 0.019) than those in the virus clearance group. Conclusions:  TNF-α and IL12B 3′UTR gene polymorphisms may be associated

with HBV susceptibility and IL-10 gene polymorphisms may be related to the HBV persistence infection in Chinese Han HD patients. “
“Aim:  Activation of β1-adrenergic receptor (β1AR) enhances contractility and heart rate. The polymorphism Arg389Gly in the β1AR gene was found to be functionally important in determining receptor activity. The relationship between this polymorphism and the risk of cardiovascular disease was investigated in Chinese subjects with overt diabetic nephropathy. Methods:  A total of 219 type 2 diabetic subjects with nephropathy were recruited. Genotyping of the β1AR Arg389Gly polymorphism was determined. Patients were followed up to 96 months for the development of cardiovascular events. Results:  There were 122, 86 and 11 patients with Arg/Arg, Arg/Gly and Gly/Gly genotype, respectively. At 96 months, the event-free survival of primary

composite cardiovascular end-point was 33.0% and 44.3% for Gly+ and Gly- groups, respectively (log–rank test, P = 0.105), while the event-free survival for first ischaemic heart disease was 62.4% and 75.9%, respectively (log–rank test, P = 0.038). However, with multivariate analysis by the Cox proportional hazard model to adjust for confounders, only low-density lipoprotein and baseline glomerular filtration rate were independent predictors of first ischaemic heart event. Conclusion:  The β1AR Arg389Gly Meloxicam polymorphism is not an independent predictor of cardiovascular events in subjects with overt diabetic nephropathy. “
“Aim:  Peroxisome proliferator-activated receptor gamma (PPARγ) is generally accepted as renoprotective factor in type 2 diabetes mellitus, and PPARγ agonists have been reported to reduce albuminuria. However, little is known about renal PPARγ expression in chronic kidney disease, and especially human data are scarce. We hypothesized that renal PPARγ expression is associated with extent of proteinuria, kidney function, histological diagnosis and inflammatory mediators.

A load dose of antibodies injected in homologous species are expected to remain in circulation at fair titers for a period of 4–6 weeks based on the decay rate of biological half-life of antibodies of 3 weeks. Furthermore, the amount required for interception of implantation would be modest at this stage as only a limited number of embryonic cells make hCG. Thus, only a small volume buy Talazoparib of high titer recombinant antibodies would be needed to ward off pregnancy. Repeated intercourses often occur during holidays. Two- to four-week vacations are given officially to all in France and in many other countries of Europe. Labor hailing from rural areas working

in cities go back home for about a month each year. A single injection can take care of worries following planned or unplanned intercourses. The dependence of early pregnancy on corpus luteum support is reported to be for 7–9 weeks.36 This seemingly banal use of antibodies RGFP966 order for a process easily performed in clinics can be useful in societies (and countries) where medical termination of pregnancy (MTP) is not legal. It can be practiced in remote villages where no hospitals exist. Also it offers privacy to affected women, who

do not wish to continue with an accidental or unwanted pregnancy. Scientific evidence for termination of early pregnancy by anti-hCG antibodies is available from studies in baboons.37 Interestingly, hCG made by trophoblasts of implanted embryo stimulates the production of progesterone by the ovarian corpus luteum, which is vital for sustenance of gestation. Interruption of this process by anti-hCG antibodies would result in termination of pregnancy. The remarkable work of Köhler and Milstein38 ushered in the era of monoclonal antibodies, which are homogeneous, and of consistent affinity for binding a given epitope. Cloned hybridoma cells secrete very high titers of pure antibody in culture. Mouse monoclonals are at present precious agents for immunoassays and diagnostic kits. Although approved by regulatory

agencies for use in humans for therapeutic purposes in earlier years, such as Orthoclone (anti-CD3), LymphoCide (anti-CD22), and Panorex 17-1A (anti-EpCAM), their repeated Thymidylate synthase use is contra-indicated owing to the formation of anti-mouse antibodies in humans (HAMA). Humanization of mouse monoclonals has been achieved in more than one laboratories. Replacement of mouse constant regions in antibody chains by human IgG and kappa/lambda and its fusion with mouse variable fragments (Fab) preserves the antigen binding region of the mouse monoclonal, giving rise to chimeric (human–mouse) antibodies, which are approved by USFDA and many other Drugs Regulatory Authorities for therapeutic use in humans. We reported several years ago the development of a monoclonal antibody PiPP, against hCG,39 which had high affinity for binding hCG (Ka = 3 × 1010m−1). It was devoid of reactivity with human FSH and TSH and had <5% cross-reaction with hLH.

Empty vectors were used as controls. The plasmids were transfected into WT and Stat1−/− cells using Lipofectamine LTX (Invitrogen). In some cases, luciferase plasmids were co-transfected with various Stat1 constructs,

into Stat1−/− cells. pRL-SV40 (Promega) encoding Renilla luciferase, was co-transfected at a luciferase : firefly ratio of 1:10. Nivolumab research buy Whole-cell lysates were prepared 48 hr post-transfection, and the assay was carried out using the dual-reporter luciferase assay kit (Promega). Samples were read on a Berthold luminometer. Luciferase values were normalized to Renilla expression for each sample. Typically, STAT1 regulates gene expression upon stimulation with IFN, but STAT1 has been also implicated in regulating the constitutive expression of several genes.22–25 Thus, we tested whether STAT1 would have an effect on the constitutive expression of GILT. We hypothesized that the lack of STAT1 regulation in Stat1−/− MEFs

would either not affect the constitutive expression of GILT or would decrease it when compared with WT MEFs.22,24Stat1−/− MEFs19,26 and WT MEFs were tested for the expression of GILT by Western blotting. Surprisingly, semiquantitative Western blot analysis of Stat1−/− MEFs showed an increased expression of GILT protein that was not dependent on IFN-γ treatment (Fig. 1a). Tyrosine Kinase Inhibitor Library When WT MEFs were treated with IFN-γ, GILT expression was increased (Fig. 1b), whereas the levels of GILT in IFN-γ-treated Stat1−/− MEFs remained unchanged. These MEFs were derived from C57BL/6 mice. The same result was achieved using MEFs derived from CD1 mice (data not shown), therefore excluding the Celecoxib possibility that this phenotype is specific to this particular fibroblast cell line. Increased expression of GILT protein in Stat1−/− MEFs led to the hypothesis that STAT1 may actually play a negative role in regulating the GILT promoter activity under basal conditions.

To address this possibility, we used the luciferase assay to determine the specific activation of the GILT promoter in WT and Stat1−/− MEFs. The GILT promoter, 772 bp in length, was cloned into the pGL3 basic vector encoding the firefly luciferase reporter gene. The activity of the firefly luciferase reporter gene under control of the GILT promoter in WT cells and in Stat1−/− cells is shown in Fig. 1c. The decreased expression of GILT in unstimulated WT MEFs implies that phosphorylation of STAT1 is not required for the negative regulatory function of STAT1. Therefore, we transfected Stat1−/− cells with alternatively spliced forms of Stat1 (Stat1α and Stat1β), as well as with the phosphorylation-deficient mutants Stat1α-Y701F, Stat1α-S727A and Stat1β -Y701F, and the double mutant Stat1α-YF/SA, along with firefly luciferase plasmids expressing the GILT promoter.

We showed IRAK-1 downregulation and decreased MyD88-dependent signaling activity in response to early LPS activation in MoDC development in the absence of any detectable change in the survival rate. Some activation stimuli, including zymosan, HKSA or CL075, inhibited the upregulation of CD1a and the downregulation of CD14 on a subset of the developing MoDCs by day 2. Other factors, like PAM3Cys, TNF or

CD40L had, on the other hand, no effect on phenotypic MoDC differentiation although these molecules were able to induce a functional MoDC exhaustion. Although both mechanisms might operate, downmodulation of TLR pathway intensity during early MoDC activation might induce tolerance to further activation irrespective of the differentiation stage of the cells. SOCS1 upregulation, however, represents a potent negative feedback mechanism FK506 order that can decrease DC activation, as demonstrated by our results showing higher IL-12 production in LPS-activated DCs following SOCS1 downregulation and also by the increased Th1-type T-cell responses induced by DCs of SOCS1−/− mice 31. SOCS1 might directly interfere with NF-κB

activation 32 or it can contribute to the degradation of the adapter protein Mal, associated to TLR4 and TLR2 33. The several PCI-32765 research buy inhibitory mechanisms suggest that SOCS1 could most probably influence DC activation not only through Epothilone B (EPO906, Patupilone) blocking DC differentiation. Indeed, Mal modulation might explain why SOCS1 downregulation increased TLR4-mediated activation but did not affect the IL-12 production triggered by a ligand for TLR7 and TLR8, receptors that do not utilize Mal. Nevertheless, our results showed no effect of

SOCS1 downregulation on the permanent inactivation of MoDCs that developed in the presence of continuous TLR ligation, indicating that the LPS-induced SOCS1 molecules act as short-term inhibitory factors. Most studies on macrophage or DC inactivation by persistent TLR stimulation have been limited to in vitro conditions. Endotoxin tolerance of monocytes has been described in septic patients 14, 34; however, a broader significance of macrophage and DC exhaustion in response to persistent activation signals is still unknown. MoDCs might be affected by the inhibitory signals originated from constant activation when differentiating in inflamed tissues. A recent study showed a very rapid DC differentiation of peripheral blood monocytes followed by their lymph node homing in mice that received LPS injections 6. Circulating monocytes might thus differentiate into migratory DCs within a time frame short enough to preserve their full functionality. Such rapid differentiation was not observed when ligands for other TLRs were injected, suggesting that the migratory DC differentiation from blood monocytes might be a mechanism specifically triggered by Gram-negative bacteria.

Effective antimuscarinic treatment of OAB might act mainly on the muscarinic receptors in sensory pathways and alter urinary NGF production, which in turn reduces

the urgency sensation during bladder filling. If urinary NGF can be demonstrated to reduce in OAB patients with symptomatic improvement after antimuscarinic treatment, urinary NGF level could therefore DNA/RNA Synthesis inhibitor be used as an objective tool to assess the therapeutic outcome of antimuscarinic treatment. Urinary NGF levels were measured in 38 normal controls and 70 patients with OAB. Patients were treated with tolterodine 4 mg once daily (QD). Urinary NGF/Cr levels and urgency severity scale (USS) were compared at baseline, 1, 2 and 3 months after antimuscarinics and 1 month after discontinuing treatment.42 This study demonstrated that urinary NGF levels decreased in association with the reduction of urgency severity and increased when OAB symptoms recurred. However, after antimuscarinic treatment for 3 months,

the mean USS had not decreased to zero and urinary NGF levels also remained significantly higher than those of controls. Elevated urinary NGF level might imply the existence of a residual inflammation in the bladder or central nervous system. In a recent study of urinary NGF levels in patients with cerebrovascular accident (CVA), NGF/Cr levels were found significantly higher in CVA patients than in normal subjects.43 Urinary NGF/Cr levels correlated well with the severity

of neurological impairment. Patients with mild/moderate impairment and severe impairment MG-132 in vitro had significantly greater urinary NGF levels than that of none/minimal impairment, suggesting that urinary NGF might be a result of neurologic lesion rather than a cause of bladder dysfunction in CVA. However, previous studies in patients with OAB and DO found that about 30% of patients with OAB symptoms do not have an elevated urinary NGF level.37 It is difficult to explain why some OAB patients do not have elevated urinary NGF levels. Stress-related events may result in increased plasma NGF levels and involvement of neuroendocrine functions.44 Patients with OAB may have Nintedanib (BIBF 1120) symptoms which wax and wane without definite treatment. It is possible that the sources of NGF production in OAB might be either local (bladder) or systemic (central nervous system). Thus urinary NGF levels can fluctuate due to the effects of different general conditions and stress-related environments. Several urological diseases, including bacterial cystitis, lower ureteral stone, and urothelial cell carcinoma, may develop storage symptoms mimicking OAB or interstitial cystitis/painful bladder syndrome (IC/PBS). It is essential to understand whether these disorders can also produce a high amount of urinary NGF and whether increased urinary NGF production isrelatedto the associated storage symptoms in these diseases45.

03 times Transmembrane Transporters inhibitor in DM/N, 2.02 times in DN/DM respectively). Conclusion: The differentially expression of serum miR-1179, miR-148b and miR-150 may be responsible for the pathogenesis of diabetic nephropathy and are potential biomarkers for DN. YOSHIDA TOSHIKO Yodogawa Christian Hospital Introduction: Immunotactoid Glomerulopathy is a rare disease entity diagnosed only by kidney biopsy. Patients typically

present with nephrotic syndrome and kidney function deteriorate within several years. Specific therapeutic approaches have not been established. We report a rare case of immunotactoid glomerulopathy presented with acute kidney injury and thrombocytopenia, which recovered completely with plasmapheresis. Case: Sixty-nine-year-old male was admitted to our hospital because of oliguria and thrombocytopenea. Hemolytic uremic syndrome was suspected and he was treated with plasmaphereis and hemodialysis. His serum creatinin rose up to 13 mg/dl on the seventh hospital day and declined gradually in accordance with the recovery of platelet count. He became free from dialysis on the 50th hospital day and

kidney function has remained stable thereafter. The first kidney biopsy performed on 20th hospital day showed endocapillary glomerulonephritis by light microscopy and randomly arranged fibrillary deposits (28 to 35 nm in diameter) in mesangium and subendothelial area by electron microscope. Second biopsy performed 6 month later, when urinalysis and laboratory data returned normal, showed mild mesangeal proliferation by light microscopy and remaining fibrillary deposits in mesangium by electron microscope. After 10 years of follow up, kidney function remains stable with trace selleck compound proteinuria. Conclusion: This was a rare case of immunotactoid glomerulopathy with acute kidney injury. Kidney function recovered completely without immunosuppressive therapy and has remained stable for more than 10 years of follow up. Fibrillary deposits

were repeatedly observed by second biopsy when proteinuria disappeared and kindey function recovered. THANIGACHALAM DINESHKUMAR, NATARAJAN GOPALAKRISHNAN, JEYACHANDRAN DHANAPRIYA, RAMANATHAN SAKTHIRAJAN, T BALASUBRAMANIAM, PERIYASAMY MUTHUKUMAR Madras Medical College Introduction: Studies on geriatric nephrology in India are limited, that too in glomerular diseases were scarce. Tau-protein kinase We analyzed the spectrum of glomerular diseases in the elderly and its clinico pathological correlation. Methods: It is a cross sectional descriptive study, done on elderly patients of age 60 or more years with clinical diagnosis of glomerular diseases who underwent renal biopsy in the department of Nephrology, Madras Medical College, Chennai, from August 2010 through December 2012. The patients were classified into five renal syndromes according the clinical presentations namely nephrotic syndrome, acute nephritic syndrome, rapidly progressive glomerulonephritis (RPGN), acute kidney injury and chronic kidney disease.