Individual analysis of NKG2A on CD8+ T cells showed no difference among groups (Fig. 2b). However, by combinational analysis, the percentage of NKG2A+NKG2D−CD8+ T cells was higher in the AIDS group than in the HIV-negative group (P < 0.01, Fig. 2c). The frequencies of CD8+ T cell expression of NKG2D was not significantly different among the groups (Fig. 2d). However, the percentage of NKG2D+NKG2A−CD8+ T cells was lower in the AIDS group than in the HIV-negative normal control group (P < 0.001, Fig. 2e). Interestingly, our data also indicated that the frequency of NKG2D+NKG2A+CD8+ T cells tended to be higher selleck in the AIDS group than in the HIV-negative normal control group (P > 0.05,Fig. 2f). Individual

analysis of KIR3DL1+CD8+ T cells revealed no significant differences among any of SAHA HDAC the groups (P > 0.05, Fig. 2g). However, KIR3DL1+NKG2D−CD8+ T cells tended to be more prevalent in the AIDS group than in the HIV group or the normal control group (P > 0.05, Fig. 2h). As for CD8+ T cells, individual analysis of NKG2A expression on CD3+CD8− cells revealed no significant differences among the HIV-negative normal control group, the HIV group and the AIDS group (Fig.

3a). However, by combinational analysis, the percentage of NKG2A+NKG2D−CD3+CD8− cells in the AIDS group was higher than that in the HIV-negative normal control group (P < 0.05) (Fig. 3b). By individual analysis, there was no significant difference in percentage of NKG2D Carbachol expression on CD3+CD8− cells among the HIV-negative normal control group, the HIV group and the AIDS group (Fig. 3c). However, by combinational analysis, the percentage of NKG2D+NKG2A−

on CD3+CD8− cells was higher in the AIDS group and the HIV group than in the HIV-negative normal control group (P < 0.01, P < 0.05, respectively, Fig. 3d). Additionally, the percentage of NKG2D+KIR3DL1− on CD3+CD8− cells in the AIDS group was higher than that of the normal control group (P < 0.05, Fig. 3e). The results for NKG2D on CD3+CD8− cells were quite opposite to that on CD8+ T cells. While analysis of CD3+CD8− cell expression of KIR3DL1 revealed no significant differences between any of the groups (Fig. 3f). The individuals in the HAART group began receiving treatment after developing AIDS. Once the antiviral therapy had suppressed their viral loads to undetectable levels for more than one year, these patients were asked to participate in our study. Expression of the NKRs NKG2A, NKG2D and KIR3DL1 on CD8+ and CD3+CD8− cells were then analyzed. HAART treatment reversed changes in NKR expression on CD8+ T cells compared with AIDS group. The percentage of NKG2A+NKG2D−CD8+ T cells in the HAART group was not significantly different from normal controls (Fig. 2c). Treatment increased the percentage of NKG2D on CD8+ T cells, there is no difference for the percentage of NKG2D+NKG2A−CD8+ T cells in the HAART group compared to normal controls (Fig. 2e).

Secondary immune responses to A. ceylanicum in immune hamsters are known to be directed primarily

at the invasive larvae and possibly developing L4 stages (19), reducing worm burdens of these developmental stages rapidly within 2–3 days of re-infection, although usually some worms manage to complete development and then survive for many weeks. Despite giving a low-level challenge in the current experiment, there was a significant reduction in worm burdens in the immunized-challenged animals (Group 5, primary + secondary infections), compared with the challenge controls (Group 4), that was already apparent on day 10 p.c. as reported previously (19), but no evidence of any further significant loss over the following 3 weeks of the worms that had managed to establish successfully and survived the critical early H 89 nmr phase of development. And this despite continuing erosion of villus height, hypertrophy of crypt depth, increased mucosal mitotic activity, greatly enhanced goblet cell and eosinophil density AZD2014 mw and increased Paneth cell counts. Surprisingly, compared with primary infections, mast cell counts remained unimpressive during secondary infections in immune animals (Figure 3), although they were raised marginally relative to naïve

animals in the third week after challenge. This was unexpected and it contrasts with earlier published data (19) in which an increase in mast cells CYTH4 was detected in immune-challenged animals during the first 3 weeks post-challenge. However, in that experiment heavier challenge doses were used, and it is possible that with lower doses of larvae, as used here, too few worms established to generate and sustain a more intense mast cell response, such as that seen in animals harbouring

heavier adult worm burdens, as in Group 2, the continuous primary infection group. Nevertheless, we feel that this is unlikely given the vigorous goblet cell and eosinophil responses. It may simply be that in this particular experimental setting, the mast cell response was eclipsed by the vigour of the other cellular responses, which were amongst the most intense that we have ever observed in this host–parasite system. Equally it is possible that the mast cells in the immune-challenged animals were highly reactive and degranulating rapidly in the mucosa, before they could be fixed and quantified, as the method employed here was based on the specific staining of mast cell inclusions. This idea can be tested by assessing plasma and tissue levels of mast cell proteases, but unlike in mice and rats, no comparable antibody capture-based assays are available yet for hamster mucosal mast cell proteases.

However, the other clinical and histological findings, electron microscopic findings and renal survivals did not differ among the four groups. Proteinuria was independently associated with an increase in risk of doubling of creatinine (P = 0.005), however, IgG and IgM depositions

I-BET-762 cell line were not by multivariate Cox regression. Conclusion:  The presence of other Ig classes, besides IgA deposits, was found to be associated with glomerular obsolescence and tuft adhesions, however, without any effect on renal survival in IgAN. “
“Diabetic Kidney Disease (DKD) incidence is rising in Singapore. While measures to prevent onset and early detection of diabetes as well as optimal diabetes and blood pressure control are important, early detection and treatment of DKD at primary care are crucial to ameliorate its course. This study aimed to evaluate the prevalence of DKD in a primary care cluster in Singapore and identify its risk factors in a multi ethnic Asian population. 57,594 patients with Type 2 Diabetes Mellitus (T2DM) followed-up at the National Healthcare Group Polyclinics with eGFR and at least two urine Albumin/Creatinine Ratio (UACR) were stratified into DKD stages: Normoalbuminuria

(NA, UACR <30mg/g), Microalbuminuria (MI, UACR 30-299mg/g), Macroalbuminuria (MA, >300mg/g) and Renal Impairment (RI, eGFR <60mL/min/1·73m2). Factors associated with DKD stages were evaluated. Overall Pirfenidone research buy DKD prevalence (T2DM with MI, MA or RI) was high at 52·5%; 32·1% had MI, 5·3% had MA and 15·1% had RI. DKD prevalence within ethnic subpopulations was different: 52·2% of Chinese, Nitroxoline 60·4% of Malays and 45·3% of Indians had DKD respectively. Malays had a 1·42-fold higher while Indians had a 0·86-fold lower of DKD prevalence. Other independent risk factors were age, female gender, duration of diabetes and hypertension, HbA1c and BMI. The high prevalence of DKD and its interethnic differences suggest need

for additional measures to optimise the care of T2DM at primary care to mitigate its progression. “
“YAMAMOTO RYOHEI1, MARUYAMA SHOICHI2, YOKOYAMA HITOSHI3, MATSUO SEIICHI2, IMAI ENYU4 1Department of Geriatric Medicine and Nephrology, Osaka Univeristy; 2Department of Nephrology, Nagoya University Graduate School of Medicine; 3Department of Nephrology, Kanazawa Medical University Graduate School of Medicine; 4Nakayamadera Imai Clinic Introduction: Previous studies have reported persistent nephrotic-range proteinuria resistant to immunosuppressive therapy as a significant predictor of renal prognosis in primary nephrotic syndrome. However, optimal time period to diagnose resistance to immunosuppressive therapy remains unknown.

At day 2, the well plates were centrifuged at 488 g for 10 min. Supernatants were collected for cytokine analysis (see below). For all cultures, the whole medium was then replaced. After 5 days of co-culture, supernatants

were again collected as described above and analysed for cytokines Tamoxifen (see below). The cells were then resuspended in phosphate-buffered saline (PBS; Invitrogen) with 0·5% FCS (Biochrom) and 2 mM ethylenediamine tetraacetic acid (EDTA) (Sigma-Aldrich). The lymphocytes were thus separated from the MSCs, washed and prepared for flow cytometry (see below). MSCs were detached with trypsin as described above, washed in whole medium and resuspended in PBS with 0·5% FCS and 2 mM EDTA. MSCs were then prepared for flow cytometry (see below). CD4+ Selleck Alvelestat T cells enriched in Tregs were generated as described above by magnetic bead separation. The cells were resuspended in 48-well plates, each well containing 1 ml of medium (see above) and 50 000 T cells. In one group, the medium was supplemented with 5 ng/ml IL-6 (Miltenyi Biotec); in another, 10 ng/ml IL-6 was added to the medium. A third group was supplemented with supernatants from passage 2 bone marrow-derived MSCs cultured in DMEM-LG with 10% FCS and 1% penicillin/streptomycin. Cell cultures

without supplementation to the media were used as controls. At day 2, the 48-well plates were centrifuged at 488 g for 10 min. Supernatants were

collected and analysed for cytokines (see below). For all cultures, the whole medium was then replaced. After 5 days of culture, supernatants were collected as described above and analysed for cytokines (see below). The cells were then resuspended in PBS (Invitrogen) Baricitinib with 0·5% FCS and 2 mM EDTA (Sigma-Aldrich) and prepared for flow cytometry. One-colour cytometry (MSCs) and three- and four-colour cytometry (T cells) was performed using a MACS QuantTM analyser and MACS Quantify version 2.1 software (Miltenyi Biotec). Positive fluorescence was defined as any event above the background fluorescence, which was defined by a line where 99·5% of the events in isotype antibody-labelled cells were considered negative. The following anti-human antibodies were used in the experiments: for T cell analysis, CD4 fluorescein isothiocyanate (FITC) mouse immunoglobulin (Ig)G1, CD25 phycoerythin (PE) or allophycocyanin (APC) mouse IgG2b (Miltenyi Biotec), CD127 APC or PE-Cy5 mouse IgG2a (BD Biosciences, Heidelberg, Germany). FoxP3 intracellular staining was performed with the FoxP3 staining buffer set and FoxP3-PE mouse IgG1 antibodies (BD Biosciences), according to the manufacturer’s protocol.

The two-sided two-sample t-test was used to compare the mean change in TGF-β between the treatment group and the control group. The significance level was 0·05. For secondary outcomes, the change from baseline (day 0) to values at days 3, 14, 28 and 63 was compared by group. Secondary measurements included expression of CD26 on lymphocyte subsets in PBMCs, percentages of lymphocyte subsets within PBMCs, cytokine and chemokine concentrations in plasma, cytokine

and chemokine Sotrastaurin in vivo concentrations in LPS-stimulated PBMCs, clinical complete blood count (CBC) values, gene expression in whole blood, proliferation and production of cytokines and chemokines (including TGF-β) in supernatants from anti-CD3-stimulated PBMCs. Comparison of the two groups at specific time-points was performed with t-test or Mann–Whitney

U-test for quantitative variables and χ2 or Fisher’s exact test for categorical variables. The primary analysis of these secondary variables included day 28 only, and did not adjust for baseline. Subsequent analyses used generalized linear models to investigate changes over time and a Bonferroni’s correction was applied to account for the multiple time-points. A P-value of 0·0125 was used. These analyses included an adjustment for baseline and log transformation GSK2118436 as needed. The analysis of correlations between the change in activity level of DPP-4 and changes

in immune parameters was performed using Pearson’s correlations using GraphPad Prism. Each individual’s percentage change in DPP-4 activity level Niclosamide was calculated from their individual day 0 value and each subsequent on-drug time-point (days 3, 14, 28); Pearson’s correlations were then calculated between this percentage baseline DPP4 activity and immune parameters (calculated as change from baseline at each time-point, as indicated above). A significant increase in active GLP-1 levels was observed in the sitagliptin group but not the placebo group, indicating that this group was taking active drug (Fig. 2a). As expected, because participants were fasting at the time of the blood draws, GLP-1 levels were low, with an average of 4·9 pg/ml at baseline (day 0). In addition, DPP-4 enzyme activity levels were measured, and a significant drop (P < 0·0001) in the percentage activity compared to day 0 was observed in the sitagliptin group, but not the placebo group (Fig. 2b). On average, while taking sitagliptin, this group showed 50–60% inhibition of activity. The primary outcome for this study was the change in total plasma TGF-β levels from baseline (day 0) to day 28, comparing the group that received sitagliptin and the placebo group.

This study was supported by National Nature Science Foundation of China grant 81070766 to Ze Zhang Tao, and a Young Foundation of Hubei University of Science and Technology grant (KY10058) to Shui Bin Wang. Shui Bin Wang is

the main writer. Ze Cheng and Bo Kui Xiao performed the main animal experiment and gained the preliminary data. Yu Qin Deng performed English interpretation and correction of the manuscript and performed click here the statistical analysis. Jie Ren performed the production of image. Ze Zhang Tao designed the whole study and is responsible for the study. There is no conflict of interest related to this study. “
“The molecular definition of major histocompatibility complex (MHC) class I-presented CD8+ T-cell epitopes from clinically relevant Mycobacterium tuberculosis (Mtb) target proteins will aid in the rational design of T-cell-based diagnostics of tuberculosis (TB) and the measurement of TB vaccine-take. We used an epitope find more discovery system, based on recombinant MHC class I molecules that cover the most frequent Caucasian alleles [human leucocyte antigen (HLA)-A*0101,

A*0201, A*0301, A*1101, A*2402, B*0702, B*0801 and B*1501], to identify MHC class I-binding peptides from overlapping 9-mer peptides representing the Mtb protein TB10.4. A total of 33 MHC class I-binding epitopes were identified, spread across the entire amino acid sequence, with some clustering at the N- and C-termini of the protein. Binding of individual peptides or closely related peptide species to different MHC class I alleles was frequently observed. For instance, the common motif of xIMYNYPAMx bound to six of eight alleles. Affinity (50% effective dose) and Selleck Rapamycin off-rate (half life) analysis of candidate Mtb peptides will help to define the conditions for CD8+ T-cell interaction with their nominal MHC class I-peptide ligands. Subsequent construction of tetramers allowed us to confirm the recognition of some of the epitopes by CD8+ T cells from patients with

active pulmonary TB. HLA-B alleles served as the dominant MHC class I restricting molecules for anti-Mtb TB10.4-specific CD8+ T-cell responses measured in CD8+ T cells from patients with pulmonary TB. Tuberculosis (TB) is a major health problem world-wide; increasing resistance and coinfection with the human immunodeficiency virus (HIV) lead to an increased disease burden in many countries. Although anti-mycobacterial drugs and a vaccine, Bacillus Calmette–Guérin (BCG), are available, neither has proved to be the solution in controlling the disease. The immune mechanisms controlling Mycobacterium tuberculosis (Mtb) are not fully understood, but it is known that both the innate and adaptive parts of the immune system are involved in Mtb control,1 and cell-mediated immunity, involving both CD4+ and CD8+ T cells, has been shown to be important for effective Mtb containment.

IgG4-RD can affect almost all organs in the body, and each affected organ has common histopathological features of lymphoplasmacytic infiltration with characteristic fibrosis called storiform fibrosis. In particular, dense IgG4-positive plasma cell infiltration is a hallmark of this disease. Clinical features include a male and middle- or old-age predominance, Pexidartinib ic50 hypergammaglobulinemia and elevated serum IgG4 levels. In our experience of 74 cases, frequently affected organs were salivary glands (55%), lacrimal glands and other ophthalmic components (54%), lungs (31%), kidneys (26%), aorta/periaorta (24%), and pancreas (20%). Lymphadenopathy was

also noted (27%). IgG4-RD is sometimes asymptomatic or tends to cause relatively mild clinical symptoms. Coexistent autoimmune disease is rare, and rather it has a close association with allergic disorders such as allergic rhinitis and bronchial asthma. Although IgG4-RD is

a steroid responsive condition, delayed diagnosis and treatment result in irreversible fibrosis. In this overview, I will outline this systemic disease including some up-to-date topics of particular interest. NAGATA MICHIO1,2 HARA SATOSHI1,3 MIZUSHIMA ICHIRO3 KAWANO MITSUHIRO2,3 SAEKI TAKAKO2 UBARA YOSHIFUMI2 OHARA NOBUYA2 SATO YASUHARU2 YAMADA KAZUNORI3 NAKASHIMA HITOSHI2 NISHI SHINICHI2 YAMAGUCHI YUTAKA2 HISANO SATOSHI2 YAMANAKA NOBUAKI2 SAITO TAKAO2 1Department of Kidney and Vascular Pathology, University GSK-3 cancer of Tsukuba, Japan; 2′IgG4-related Kidney Disease’ working group, Japan; 3Department of Rheumatology, Kanazawa Graduate School of Medicine, Japan Patients with IgG4 related systemic disease often complicate renal dysfunction. Among several characteristic features in IgG4-related kidney disease, tubulointerstitial nephritis is the most responsible for renal dysfunction. We have summarized distinctive features of tubulointerstitial lesions

in IgG4-related CYTH4 TIN, i.e., (1) well-demarcated borders between involved and uninvolved areas; (2) involvement of the cortex and medulla, often extending beyond the renal capsule and with occasional extension to retroperitoneal fibrosis; (3) interstitial inflammatory cells comprising predominantly plasma cells and lymphocytes, with a high prevalence of IgG4-positive cells often admixed with fibrosis; (4) peculiar features of interstitial fibrosis resembling a “bird’s-eye” pattern comprising fibrosis among inter-plasma cell spaces; and (5) deposits visible by light and immunofluorescent microscopy in the tubular basement membrane, Bowman capsule, and interstitium that are restricted to the involved portion, sparing normal parts. Ultrastructural analysis revealed the presence of myofibroblasts with intracellular/pericellular collagen accompanied by plasma cell accumulation from an early stage. As such lesion is depending on the stage and extension, renal biopsy samples contains limited information to assess background pathophysiology.

TRP2/HepB human IgG1 DNA stimulated similar frequency but higher avidity responses to peptide-pulsed DC. Other studies have failed to show protection from established tumors in TRP2 peptide immunized mice but peptide-pulsed DC induced tumor rejection 30. If the technology Protein Tyrosine Kinase inhibitor described here can be transferred into a clinical setting, it would allow a vaccine to be manufactured that is superior to DC vaccination. It would

also overcome the variability, expense and patient specificity problems associated with conventional DC-based therapies. Previous studies have shown xenogeneic DNA immunization breaks tolerance to self epitopes but using syngeneic DNA is only successful if Ag is linked to a foreign immunogenic protein

31, if it is encoded within a viral vector 32 or if various adjuvants are used 33, 34. The generation of therapeutic find more anti-tumor immunity has also been demonstrated in the absence of regulatory T cells 35. Enhanced responses of TRP2/HepB human IgG1 DNA immunization compared to syngeneic Ag DNA suggests that epitope removal out of the whole Ag context overcomes the inhibition by any regulatory elements within that whole Ag sequence. How does immunization with TRP2/HepB human IgG1 DNA enhance avidity? In vitro stimulation of splenocytes, from B16 GM-CSF-immunized mice with low doses of TRP-2 180–188 peptide generates high-avidity responses. These results indicate that a repertoire of T cells specific for the TRP2 180–188 epitope exists and that they can be modulated to high functional avidity 27. It is therefore possible that TRP2/HepB human IgG1 DNA to may be working by providing a low dose of Ag to stimulate high-avidity responses. The difference in responses generated from TRP2 human IgG1 DNA compared to the protein equivalent suggests that the direct transfection of skin APC plays a role in the generation of these immune responses. The gene gun was initially believed to stimulate CTL by direct transfection

of skin APC but has more recently been shown to also induce CTL via cross presentation 36, 37. We have also shown that the FcγR is important in generating high-avidity but not high-frequency responses from the DNA vaccination. It is of interest that there is often low and high-frequency groups within the immunized mice (see Fig. 3A). This probably reflects the degree of direct versus cross presentation. If immunization fails to transfect a significant number of APC they will have a lower response than mice with efficient APC transfection. This is a parameter which is hard to control with either gene gun or electroporation and is not enhanced with the use of cytokines such as GM-CSF or adjuvants such as imiquimod (result not shown). Reports in the literature have previously demonstrated that vaccine induced T-cell responses can be enhanced by Ab 38–40. A recent elegant study by Saenger et al.

MBP Ac1–9[4K] and rhIL-2 at a final concentration of 10 μg/mL and 20 U/mL, respectively,

were added to the cell suspension, and cultures were incubated in 6-well plates at 37°C and 5% CO2 humidified atmosphere. After at least 5 days, the cultured splenocytes were washed and CD4+ T cells were isolated by positive selection. Temsirolimus 5×104in vitro expanded CD4+ T cells from peptide-treated Tg4 mice were co-cultured with an equal number of untreated CD4+ T cells, or at ratios from 1:1 to 1:32 of peptide-treated to untreated CD4+ T cells, at 100 μg/mL of MBP Ac1–9[4K] in the presence of 1×105 APC/mL. After 72 h, wells were pulsed with 0.5 μCi [3H] thymidine overnight and the incorporated radioactivity was

measured on a liquid scintillation β-counter (1450 Microbeta; Wallac). click here Staining for intracellular cytokine expression was performed using BD CytoFix/CytoPerm Plus Kit (BD Biosciences). Splenocytes from peptide-treated mice were collected 2 h after the last treatment and restimulated with PMA and ionomycin (Sigma-Aldrich) at a final concentration of 5 ng/mL and 500 ng/mL of culture, respectively, for 4 h in the presence of GolgiStop (BD Biosciences). After the incubation, cells were stained with anti-Vβ8 FITC (BD Biosciences), fixed, permeabilized and stained intracellularly with anti-IL-2 APC, anti-IL-4 PE, anti-IL-10 APC, anti-IL-17 PE and anti-IFN-γ PE antibodies, or Ig isotype controls (BD Biosciences). Fluorescence intensity was measured on a FACSCalibur or BD™ LSR II flow cytometer (BD Biosciences) and analyzed using FlowJo software (Tree Star). Conventional sandwich ELISA was carried out according to instructions from the manufacturer using paired antibodies to assay the quantity of IL-2, IL-10 and IFN-γ (BD Biosciences) in cell culture supernatants. Optical densities

were measured at 450/595 nm on a SpectraMax 190 microplate reader and the amount of cytokine present quantified with standard curves using SoftMax Pro software (both from Molecular many Devices). Statistical analyses were performed where stated using GraphPad Prism (GraphPad Software) software. The statistical significance of differences between data groups was determined by an unpaired t-test. A p value of ≤0.05 was considered to be significant. We thank Drs. C.A. Sabatos-Peyton and J. Verhagen for critical reading of this manuscript. We also thank Miss L.E.L. Falk and ASU staff for assistance with the breeding of mice. This work was supported by the Wellcome Trust and the MS Society of Great Britain and Northern Ireland. Conflict of interest: The authors declare no financial or commercial conflict of interest. Detailed facts of importance to specialist readers are published as ”Supporting Information”. Such documents are peer-reviewed, but not copy-edited or typeset. They are made available as submitted by the authors.

ALHOMRANY MOHAMMED, A1, ALGHAMDI https://www.selleckchem.com/products/ulixertinib-bvd-523-vrt752271.html SAEED, M2, MOUSA DUJANAH3, ALHOWEISH ABDULLA4, ALHARBI ALI5, KARI JAMEELA6, ALSAAD KHALED7, ALWAKEEL JAMAL8 1King Khalid University; 2King Faisal specialist hospital, Jeddah; 3Ryadh Military Hospital; 4Dammam University; 5Security Forces Hospital, Ryadh; 6King Abdulaziz University; 7King Abdulaziz Medical City, Ryadh; 8King Saud University Introduction: Renal disease is a common medical problem

in Saudi Arabia. Varieties of renal lesions if not treated properly or not discovered early will lead to chronic kidney disease. Identifying the types of renal lesions can help in identifying high risk patients and appropriate treatment can be provided. Glomerulonephritis is considered

one of the leading cause of ESRD in the country. The prevalence of different renal lesions were identified by different reports, however, these reports showed inconsistency. One important reason for such differences is related to the lack of unified methods in diagnosing and processing renal tissues and to the fact that different reports were reported by different pathologists. In addition, the differences in the reported results may reflect patients click here selection’s bias for renal biopsy or to the different policies and protocols adopted by different nephrologists. Methods: This is a prospective multi centers study involved different patients from different institutes and from different regions

of Saudi Arabia in order to delineate the pattern of renal diseases based on renal biopsies and to be a nucleus for establishing renal biopsy registry in Saudi Arabia. Results: 405 cases were collected and studied during the period from August 2008 to June 2009. This preliminary report shows that the commonest primary renal lesion in Saudi Arabia is focal segmental sclerosis (FSGS) in 24.1% followed up by IgA nephropathy PFKL (15.2%), mesangioproliferative non IgA, (13.2%) and membranoproliferative GN (12.4%). lupus nephritis was the commonest cause of secondary GN in 66% of the secondary causes. Conclusion: Establishment of renal biopsy registry should help to overcome these differences and data collected by the register will not only help in identifying the common renal lesions but also will add several important advantages. Combined data obtained from renal replacement therapy (RRT) registration and renal biopsy registry can be used to organize an epidemiologic study which gives additional information on the long term outcome of patients with renal diseases in Saudi Arabia.