Conversely, two Syk ligands were approximately twofold enriched with the S297A mutant, i.e. Igβ and ubiquitin. Hence, our “reverse proteome approach” directly confirmed the critical role of the major Syk phosphorylation site for 14-3-3 binding and indicated that this complex inhibits BCR recruitment and ubiquitinylation of Syk. Reduced BCR recruitment is likely to attenuate Syk function while ubiquitinylation of Syk

has been associated with its increased degradation 8, Opaganib research buy 9. We tested the functional impact of 14-3-3γ for Syk-mediated activation of the Ca2+ mobilization pathway. Importantly, all subsequently described studies were conducted with batches selleckchem of retrovirally transduced B cells expressing identical amounts of WT or mutant Syk (Fig.

4A, right panel). Hence, we could exclude that conclusions are based on individual responses of single cell clones produced and selected by conventional transfection methods. We immunoprecipitated the proximal Syk substrate SLP65 from resting and BCR-activated B cells expressing either WT Syk or its S297A variant, and subjected the obtained proteins to anti-phosphotyrosine immunoblot analysis (Fig. 4A, upper left panel). SLP65 purified from S297A-expressing cells showed strongly enhanced and prolonged phosphorylation compared to SLP65 obtained from cells expressing WT Syk. Similarly, PLC-γ2 that was co-immunoprecipitated with SLP65 and also acts as important Syk substrate exhibited increased and sustained tyrosine phosphorylation in the absence Thymidylate synthase of the Syk/14-3-3γ complex (Fig. 4B, upper left panel). The latter finding was directly demonstrated by anti-phosphotyrosine immunoblotting of anti-PLC-γ2 precipitates (Fig. 4B). Equal loading of purified proteins was confirmed by reprobing the blots with antibodies to SLP65 or PLC-γ2, respectively (Fig. 4A and B, lower panels). Hence, loss of 14-3-3γ binding promotes phosphorylation of Syk substrates. Flow cytometric recording

of BCR-induced Ca2+ responses demonstrated that this effect translated into dramatically prolonged Ca2+ fluxing (Fig. 4C). Interestingly, the maximal Ca2+ peaks of WT and mutant B cells were almost identical. We conclude that 14-3-3γ binding to phospho-S297 of Syk serves as negative feedback regulation that limits the activation of BCR-proximal signaling events. Next, we assessed how 14-3-3γ inhibits Syk function. Two main mechanisms control Syk activation and interaction of Syk with downstream targets. Doubly phosphorylated ITAMs in Igα and Igβ recruit Syk to the plasma membrane and concomitantly provide an allosteric trigger for its catalytic activity. The latter is further amplified by auto- and trans-phosphorylation on activatory tyrosine residues 6.

Notch signaling was found to be important for in vitro development of adult [[58]] and fetal CLPs [[20]] into RORγt+ ILCs. Interestingly,

www.selleckchem.com/products/VX-770.html the latter study suggested a stage-specific requirement of Notch signaling in the development of RORγt+ ILCs as Notch signaling was required in an early stage of development of these cells but inhibited a subsequent step [[20]]. The relevant Notch for this role could be Notch2 [[58]] but this has yet to be confirmed in in vivo experiments. Rorγt+ cells in Ahr−/− mice express lower levels of the anti-apoptotic protein Bcl-2 and accordingly are more apoptotic [[54]]. Bcl-2 might be induced by the major cytokine receptors expressed on Rorγt+ ILCs, namely IL-7Rα and ckit; Tipifarnib manufacturer however, there are conflicting data with regard to the link of AhR and IL-7Rα. In one study, expression of IL-7Rα was decreased by AhR ablation [[54]], whereas another group did not observe any change in IL-7Rα expression on Ahr−/– ILCs

[[55]]. cKit, which is the receptor for stem cell growth factor, may be a direct downstream target of AhR since expression of this receptor is strongly decreased in Ahr−/− ILCs [[55]]. It is possible that the Rorγt+ ILC numbers are regulated by AhR in a cKit dependent manner. This suggestion comes from observations made in KitWv/Wv mice, which express a ckit variant with impaired kinase

activity. These mice not only show diminished numbers of Rorγt+ ILCs, but also reduced numbers and sizes of CPs and ILFs. These findings strongly suggest that AhR regulates maintenance of RORγt-dependent ILCs by controlling ckit expression. As in Th17 cells, AhR also appears to be required for optimal IL-22 production Parvulin by the ILC22 population. The reduction of Rorγt+ ILC numbers in the gut, and the decreased capacity of these cells to produce IL-22, has functional consequences because AhR-deficient mice succumb to infection with C. rodentium and hydrodynamic injection of an IL-22-expressing plasmid into the tail vein reestablishes protection against C. rodentium [[54]]. In this setting, IL-23, produced by activated macrophages and DCs, controls IL-22 production by ILCs. Interestingly, AhR-deficient mice display reduced IL-23 receptor expression and IL-23 responsiveness [[52]]. It is likely that AhR directly controls IL-22 expression, as the Il22 locus contains multiple AhR-responsive elements [[54]]. Interestingly these elements are clustered with Ror-responsive elements and, in the Il22 locus, both Rorγt and AhR bind directly to their response elements. Whereas AhR recruitment to the well-known AhR target Cyp1a1 is unaffected by Rorγt, AhR binding to the Il22 locus is strongly enhanced by Rorγt [[54]].

The age-specific prevalence of patients with ESKD was estimated using a logistic regression model with generalized estimating

equation based on the data of high-income countries. The ratio between number BIBW2992 nmr of RRT and estimated number of ESKD (RRT/ESKD ratio) \ were computed for all countries on the basis of gross national income levels for each country. Results: The number of patients with ESKD was estimated to be 7.8 million, of which 2.3 million (30%) had access to RRT, leading to 5.5 million preventable deaths. The proportion of patients who did not received RRT among patients with ESKD was greater in lower income countries. The largest differences in the number of patients with ESKD and those receiving RRT were observed in Asia, Africa and Latin America. Global use of RRT is estimated to increase up to 5.2 million over next two decades, with most growth in Asia. Conclusion: Globally, ESKD continues to cause many premature deaths, mainly in developing regions. The prevalence

of ESKD as well as RRT is projected to increase over next two decades, mainly in Asia, but a similar number of people will continue to die due to lack of access to treatment. Effective prevention and management of CKD, coupled with the development of affordable dialysis and kidney transplant services for ESKD should be priorities for the renal community. PERIYASAMY MUTHUKUMAR, THANIGACHALAM DINESHKUMAR, NATARAJAN GOPALAKRISHNAN, JEYACHANDRAN DHANAPRIYA, RAMANATHAN SAKTHIRAJAN, T BALASUBRAMANIAM Madras Medical College Introduction: Rheumatoid arthritis (RA), a chronic crippling disease can affect all selleck chemicals components of the kidney. Renal involvement may be due to disease or drugs used to treat the condition. We intend to study the renal lesions in RA and its clinic o pathologic correlations. Methods: Prospective observational study Arachidonate 15-lipoxygenase was conducted at department of nephrology, Rajivgandhi Government general Hospital, Chennai, India between 2010 to 2013. RA patients with abnormal urine sediments (>3 RBC, s or RBC cast), proteinuria (>0.3 gms/day) or eGFR (<80 ml/min) were included in the study. Those with normal renal parameters were

excluded. Results: Three hundred patients with RA were screened. Mean follow up was 23 months. 52 patients found to have renal disease. Mean age was 45 years (range 18–67). 60 % patients were female. (Male: female ratio 1.5:1). Mean duration of illness was 8.5 years. 30% had odema, 4% had macrohaematuria, 52% were asymptomatic. The common renal syndromes observed in our study were chronic kidney disease (CKD-44%) Hypertension (20%), nephrotic syndrome(13%), acute kidney injury(4%). 29 patients (56%) underwent renal biopsy. The common histological pattern of renal biopsy observed were mesangial proliferation (10), focal endocapillary proliferation(5), IgA nephropathy(3), minimal change disease(2), membranous (2) and Amyloidosis(2).

This problem stems from several issues: first, selleck compound many of the markers used to identify Tfh cells, such as PD-1, ICOS and CXCR5, are also commonly expressed by activated CD4+ T cells.3,6,7 As a result, Tfh cells are often identified as the cells expressing the highest levels of these molecules; thus, it is easy to see how this can quickly become a problematic definition. Secondly, the term ‘Tfh cell’ is used by individual researchers to describe different populations of cells. Hence, while the original reports used the term to describe CD4+ CXCR5+ T cells located in the follicle, in more recent times ‘Tfh cell’ has come to be used by many to describe only those cells that

are found within CX-5461 mouse the germinal centre (GC), while CD4+ CXCR5+ T cells found elsewhere in the follicle are termed ‘pre-Tfh cells’. In contrast, others have maintained the usage of ‘Tfh cell’ to describe all CD4+ CXCR5+ T cells in the follicle and refer instead to those cells located specifically in the GC as ‘GC-Tfh cells’. Even given a consensus on the terminology for these cell populations, it remains to be determined whether follicular and GC-Tfh cells can be distinguished phenotypically or whether they can only be identified by imaging which reveals their location. Although some reports have suggested that molecules such as GL720 are able to identify specifically cells found

in the GC, other reports have suggested that at different times during the response, cells outside the GC can also express why these molecules.21 Once again, this probably reflects the problem that many markers of Tfh cells are also found on activated cells. The story is complicated further by recent reports that demonstrate that even Bcl-6, considered one of the gold standard markers of Tfh cells, cannot be used on its own to identify Tfh cells. These studies revealed that CD4+ T cells express Bcl-6 very quickly following

activation, long before they migrate deep into the follicle, let alone into the GC.21–23 Moreover, they identified cells with a Tfh-like phenotype (e.g. CXCR5 and PD-1 expression and GC localization) that did not express Bcl-6 as well as cells that expressed Bcl-6, but not other Tfh cell markers such as PD-1.21,22 This suggests that the role of Bcl-6 in regulating Tfh cell differentiation may be more complex than first anticipated. However, for the purposes of this review we will consider Tfh cells to be CXCR5+ PD-1+ Bcl-6+ cells that express IL-21 and are found in the follicle. A further problem has arisen in studies of human TFH cells, particularly in the investigation of patients suffering from immunodeficient or autoimmune conditions. In these patients it would be helpful to be able to identify Tfh cells to determine whether the generation or function of these cells is dysregulated.

1a). Moreover, no

correlation was found between PD-1 expression on HIV-specific CD8+ T cells and the remaining non-activated, non-HIV-specific CD8+ cells; this suggested that PD-1 levels on cytotoxic Alpelisib ic50 T cells for a given individual were not set at a generalized level, but were rather dependent upon the nature of the antigen and infection activity. Due to technical limitations in the flow cytometry analyses, PD-1 estimates were not available for the naive, memory and effector CD4+ and CD8+ T cell subsets, thus some of the antigen-specific differences in PD-1 expression might have been attributed partly to different distributions of resting and effector CD8+ T cells [35,36]. Day et al. [30] found that PD-1-blocking monoclonal antibodies (mAbs) enhanced CD4+ T cell responses to HIV antigens, which suggests indirectly that PD-1 is

up-regulated even on HIV-specific CD4+ T cells. Here, we confirmed this concept because PD-1 was up-regulated particularly on Gag- and Nef-responsive CD4+CD154+ T cells compared to the majority of non-activated cells (Fig. 1a). In contrast to PD-1 on CD8+ T cell subsets, PD-1 on CMV-specific CD4+ cells was both similar to (Fig. 1a) and correlated with PD-1 on both Gag- (r = 0·57, P = 0·02) and Nef-specific (r = 0·72, P < 0·01) CD4+ T cells. Subsequently, we examined how HIV-specific immune Erlotinib clinical trial responses to Gag, Nef and Env related to progression and other predictors including CD38, current CD4 count and viral load in asymptomatic untreated patients. In the lack of clinical events, progression was measured as current and prospective CD4+ T cell change rates. CD38 density was measured on CD8+ T cells and on the CD8+PD-1+ subset. These measures for CD38 correlated (r = 0·80, P < 0·01), but in accordance with our previous results [14], CD38 on the PD-1+ subset was, in general, statistically stronger. CD38 density will henceforth therefore be reported only for the CD8+PD-1+ T cell subset (Table 1). Gag-specific CD8+ T cell responses relate to the CD4 change rate and markers of chronic immune activation.  Only Gag-specific CD8+ T cell responses correlated with both the current and the prospective

CD4 count change rates, particularly the total concentrations of CD8+ dipyridamole Gag-specific T cells in the circulation (Table 3). Moreover, patients who had the highest frequency of Gag-specific CD8+ cells (upper tertile) demonstrated substantially slower current CD4 loss rates than those having few (lower tertile) [−62·9 versus−195·1 CD4 cells/µl/year (medians), respectively, P = 0·04] (Fig. 2a). Furthermore, these observations were confirmed in those patients whose prospective CD4 change rate could be calculated (r = 0·85, P < 0·01) (Table 3). In agreement with these results, CD38 correlated only with Gag-specific responses (Table 3), but not with Env- and Nef-responses, current CD4+ T cell count, viral load, D-dimer, nor to time infected or age.

Using SCID-Hu mouse models, Dick and colleagues showed that only 1/250 000 AML CD34+CD38– cells were capable of establishing leukaemic haematopoiesis in the recipient [21,22]. These cells could be targeted by alloreactive T cells recognizing minor antigens on the leukaemia stem FDA-approved Drug Library cells [7,8]. These models should be interpreted with caution, as the

xenogeneic milieu of the recipient mouse underestimates the number of cells capable of self-renewal and do not provide clear evidence that long-lived AML progenitors are subject to the same degree of immune attack. Furthermore, they do not identify whether all subtypes of AML have comparable hierarchies of long-lived progenitors. Indeed, an alternative model of leukaemia cure is that a sustained T cell response to the progeny of the AML stem cell but not the small stem cell pool itself could contain the leukaemia at a minimal disease level, resulting in a functional cure [3]. Although the concept of immune surveillance is well accepted, evidence for IS specifically in AML is largely indirect, revealed through relationships between treatment outcome and JQ1 solubility dmso immune parameters and adaptive changes made by the leukaemia favouring immune evasion, unlike viral-induced malignancies. Perhaps the most compelling evidence for a significant role of immune control of AML comes from several observations indicating that

lymphocyte recovery following induction chemotherapy is strongly predictive for outcome. T cells are reduced after chemotherapy Palmatine but have a rapid clonogenic potential which allows a swift T cell recovery [23]. Patients achieving the highest lymphocyte counts within 6 weeks of chemotherapy have the lowest relapse rates [24–26]. Long-term survival in AML is also favoured by normalized lymphocyte counts [27]. These data all suggest that an intact immune system can protect against relapse of disease, but do not define whether the effect is mediated through T cells or NK cells. There are diverse abnormalities in AML at presentation and relapse that suggest how the leukaemia may develop despite immunosurveillance and how an established leukaemia may acquire new characteristics to defeat immune control. Figure 1 depicts the interactions between AML cells and the immune environment. Genetic features are emerging that may favour the development of AML in the presence of an intact immune system. There is an increased frequency in AML of a particular genotype of the co-stimulatory molecule cytotoxic lymphocyte antigen -4 (CTLA-4) [28]. The inhibitory KIR molecule KIR 2DL2 is expressed more frequently in AML, again suggesting a predisposition for AML through some form of immune escape [29]. There is also strong evidence that an established AML can mutate to escape immune control.

1 µg/mL) but not low (<2.1 µg/mL) CETP group. In the patients with hypertriglyceridemia, the high CETP group had a significantly smaller LDL size than the low CETP group. Among the patients with above-median TG selleck chemicals levels, the CC genotype and CETP were independent negative determinants of LDL size. In the whole group and the high CETP group, the patients with CAD had a significantly smaller LDL size than those without CAD. Finally, DM and smaller LDL size were identified as independent

risk factors for CAD prevalence. Conclusion:  These suggest that a smaller LDL size, which is associated with higher levels of TG and CETP and the HL/CC genotype, may serve as a risk factor for CAD in HD patients. “
“Aim:  A possible link between the renin–angiotensin–aldosterone system (RAAS) and fibrinolysis has recently been suggested. Systemic infusion of angiotensin II results click here in an increase in plasminogen activator inhibitor type 1 (PAI-1) levels and angiotensin-converting enzyme inhibitors

(ACEI) have been shown to decrease PAI-1 levels. Moreover, recent data indicated that plasma aldosterone levels were positively correlated with plasma PAI-1 levels. This study was designed to compare the effects of an ACEI with an ACEI in combination with an aldosterone antagonist on PAI-1 levels in chronic hypertensive patients. Methods:  Patients were randomized into two groups and were treated with either low salt diet plus fosinopril (group 1, n = 43) or low salt diet plus fosinopril plus spironolactone (group 2, n = 42). Plasma PAI-1, tissue plasminogen activator (tPA) and plasma renin activity (PRA) levels were measured before and after 24 week treatment in both groups. Results:  The mean basal PRA levels were similar in both groups. After antihypertensive therapy, the mean PRA increased significantly in both groups (P < 0.005). The mean plasma PAI-1 levels were reduced in both treatment groups (P < 0.005). However, the reduction in group 2 was

more pronounced (P < 0.05). Although after the treatment mean plasma levels of PAI-1 significantly reduced in both groups, the reduction of PAI-1 levels was more pronounced in group 2. Conclusion:  Although learn more the plasma levels of PAI-1 significantly reduced after treatment in both groups, the reduction of PAI-1 levels was more pronounced in group 2. These data indicated that administration of aldosterone antagonists in combination with ACEI had additional benefit on fibrinolysis in chronic hypertensive patients. “
“Aims:  Diabetic nephropathy (DN) is the major cause for end-stage renal disease (ESRD) and the pathogenesis for DN developing into ESRD is not clear at present. Results from published studies on the relationship between angiotensin-converting enzyme (ACE) insertion/deletion (I/D) gene polymorphism and ESRD risk in DN patients are still conflicting.

18,19 The PK/PD studies complete dose titration studies aimed to select rational dosage regimens. Drug levels are measured on undiluted samples, diluted samples, in tissue and on individual cells. For the measurement of intracellular levels good quality standardized cell samples are required. Finally, cervical and rectal biopsies are used to determine anti-HIV activity of microbicides in explant models.20 As Selumetinib purchase yet, samples from clinical trials have not been used for this. Quantification of soluble mucosal immune factors and HIV specific

responses is possible in undiluted samples and samples diluted in a standard volume. In contrast, the dilution effect of a CVL interferes with the exact quantification and values are usually expressed as percentages. For example, a CVL performed with 10 mL saline results in a diluted sample volume ranging from 9.7 to 10.1 mL. Therefore it is important to be able to quantify the volume of cervicovaginal secretions collected and accurately approximate the dilution CHIR-99021 chemical structure factor of a soluble component introduced by the washing. Lithium chloride, an inert substance, can be used to measure

the dilution factor when added to CVL21; however, the analysis can be cumbersome and requires the use of flame atomic absorption spectrophotometer.11 Alternatively, one could measure total protein or IgA.11 Furthermore, the collection of the same type of samples at multiple time points in clinical trials allows for comparisons of soluble markers within the same individual. The mean volumes collected with undiluted sampling methods are often small; Weck-Cell 50 μL, swab 200 μL, vaginal cup 500 μL, aspirator 500 μL. This disadvantage has to be taken into account when designing the objectives of a trial and the trials laboratory assays to measure the endpoints. From the start of protocol discussions, a team of clinicians, epidemiologists

and laboratory scientists should agree on sampling methodology linked to Dimethyl sulfoxide laboratory assays and study the volumes needed for each assay. If the recovered volumes are thought to be insufficient, alternatives will need to be explored. For example, one could take multiple samples and pool them, dilute the sample or suspend the sample device in a standard volume, or perform a CVL. The multiplex cytokine assays were not originally validated for genital tract secretions; nevertheless, performance and experience with the multiplex is mounting and standardization efforts are ongoing.22 The multiplex kits can be custom made to fit the panel of cytokines selected for any study design.

, 2000). Chemotherapy with praziquantel is the cornerstone of schistosomiasis control. Assessment of the impact of mass treatment with praziquantel is usually by determining the prevalence of the infection and presence of PPF (Mohamed-Ali et al., 1991). In Sudan, Mohamed-Ali et al. (1991) and Doehring-Schwerdtfeger et al. (1990) reported a reduction of egg excretion and reversibility of PPF 7 and 23 months, respectively, after praziquantel RAD001 price treatment, while the same finding was reported by Homeida

et al. (1996) after both annual and biennial treatment. Reports by the Homeida group, in their studies in Sudan, have shown that the factors that control fibrosis regression are age, gender and the grade of fibrosis. Young patients with lower PPF grades tend to respond more to antischistosomal chemotherapy (Homeida et al., 1991, 1996; Kheir et al., 2000).

Based on the above findings, and because the SM2 locus was reported to control the progression of the disease (Henri et al., 2002), it was suggested that the regression of PPF (reversibility) could also be under genetic control. Thus, the aim of this study is to evaluate the factors controlling the regression of liver fibrosis in S. mansoni-infected subjects after praziquantel therapy. This study was carried out between 1999 and 2002 in Um-Zukra village, Gezira state, Managil province, Central Sudan. The village is about 350 km south of Khartoum (the capital)

and 110 km west of Wad Medani town, in the Managil extension Pifithrin-�� order agricultural scheme. The Gezira and Managil irrigated scheme involves about two million acres, cultivated by cotton and other crops, and populated by about 1.5 2-hydroxyphytanoyl-CoA lyase million individuals. The study area was selected according to the prevalence of S. mansoni infection. Random stool samples were obtained from different villages in the Gezira state, and examined for S. mansoni eggs. The highest prevalence (50%) was found in Um-Zukra village. The population of Um-Zukra is about 4000individuals (according to a census performed in 1999), belonging to three tribes, mainly the Kawahla (80%), in addition to Rawashda and Galeen (20%). The village is surrounded by cultivated area and the canal is only 450 m from the center of the village. There are two water pumps (wells) that are used for drinking water. The other water source for domestic use (washing and bathing) is the canal. Each house was given a number from 1 to 629. The numbers were written on metallic plates and fixed on all houses, and pedigrees for the study subjects were drawn. Plastic containers for stool samples were distributed to the villagers according to the house and individual numbers. The Schistosoma mansoni egg count g−1 stool was conducted in November 1999 using Kato’s method (Katz et al., 1972) on three stool samples collected on different days before treatment.

Conclusion: Erythrosin B method is superior to PR-Mo method and comparable to TIA in the sensitivity to albumin. This method will be useful for the diagnosis of microalbuminuria with 80% cost saving compared with TIA. Further study is needed Doxorubicin to elucidate why HPLC assay showed less relation to other methods. RAHMAN ASADUR1, HITOMI HIROFUMI1,2, OSAFUNE KENJI2, NISHIYAMA AKIRA1 1Department of Pharmacology, Faculty of Medicine, Kagawa University,

Kagawa, Japan; 2Center for iPS Cell Research and Application, Kyoto University, Kyoto, Japan Introduction: Anemia is a common consequence of chronic kidney disease (CKD) and recombinant human erythropoietin improves anemia in patients with CKD. We examined the effects this website of erythropoietin originated by erythropoietin producing cells, which were derived from human induced pluripotent stem (hiPS) cells, in adenine-induced renal anemic mice. Methods: Adenine (50 mg/kg/day, p.o.) was administered for 28 days in C57BL/6 mice. Then, purified newly derived erythropoietin (0.1 IU/mice) or commercially available recombinant human erythropoietin (rhEPO; 5 IU and 0.1 IU/mice) were administered subcutaneously at every alternate day for 12 times. Results: Adenine administration resulted in a severe tubulointerstitial fibrosis and anemia in C57BL/6

mice. Administration of newly derived erythropoietin (0.1 IU) and rhEPO at a dose of 5 IU, but not 0.1 IU, significantly increased the hematocrit in anemic mice. Both hemoglobin and total red blood cell count were also increased by treatment with newly derived erythropoietin and rhEPO at 5 IU, but not rhEPO at 0.1 IU.

None of the treatment affected white blood cell and platelet counts. Interestingly, human erythropoietin concentrations in plasma were significantly higher in the newly derived erythropoietin-treated mice, as compare to the high dose of rhEPO (5 IU)-treated mice. Conclusion: These data suggest that erythropoietin originated by hiPS cell-derived erythropoietin-producing cells improves renal anemia. De novo erythropoietin may provide a novel cost effective physiological therapeutic approach for renal anemia in patients with CKD. VIJAYAN MADHUSUDAN1, ABRAHAM GEORGI1, ALEX MERINA ELIZABETH1, N VIJAYSHREE1, FERNANDO EDWIN2, YUVARAJ ANAND1, NAIR SANJEEV1, MATHEW MILLY1 1Madras Thalidomide Medical Mission; 2Stanley Medical College Introduction: This aim of this multi-centric cross sectional study was to assess the nutritional status in Indian CKD patients and to compare the nutritional indicators between Stage 5 dialyzed(CKD-D) patients below the poverty line(BPL), and Stage 3–4 non-dialyzed(CKD-ND) patients above(APL) and below the poverty line. Methods: Patients were selected from a government medical college hospital, a charity-based outpatient dialysis unit and a non-profit tertiary care center. The study groups included BPL CKD-ND (n = 100), BPL CKD-D (n = 98) and APL CKD-ND (n = 92) patients, based on a cut-off of per capita income US $1.25 a day.