[12] In contrast, a randomised phase III study evaluating granulocyte transfusions in neutropaenic cancer patients with febrile neutropaenia

and pulmonary or soft-tissue infiltrates after conventional or high-dose chemotherapy demonstrated no impact on the course and outcome of infection.[13] Unfortunately, no sub-analyses are available for patients suffering from mucormycosis, which is most likely due to the low number of patients included with these infections. Beside neutrophils, lymphocytes, in particular CD4+ T cells, may also provide critical defence mechanisms against mucormycosis (Fig. 2). This hypothesis is supported by the clinical PF-02341066 in vitro observation that mucormycoses often occur several months after allogeneic HSCT, at a time, when neutropaenia and mucositis have already resolved, but adaptive immune responses are still hampered. A recent study reported that the median time of diagnosis of mucormycosis was 173 days (range, 7–2254) after transplantation; this time frame is comparable to the findings in invasive aspergillosis, which occurs at a median of 82 days (3–6542) after allogeneic HSCT.[14]

Notably, allogeneic HSCT transplant recipients have a low number of anti-Aspergillus TH1 cells for months after transplantation,[15] and it has been demonstrated that TH1-biased immunity correlates with protection and a better outcome in invasive aspergillosis.[16] These observations formed the rationale of transferring functionally active Aspergillus-specific EX 527 manufacturer TH1 cells to allogeneic HSCT recipients at high-risk for or suffering from invasive

aspergillosis. In fact, a proof of principle study in 10 patients after haploidentical HSCT with evidence of invasive aspergillosis demonstrated that transfusion of anti-Aspergillus TH1 cells resulted in a clinical benefit.[17] In patients receiving adoptive immunotherapy, galactomannan as a surrogate marker for the invasive fungal disease new decreased significantly earlier as compared to patients not receiving immunotherapy, and only one of 10 patients receiving immunotherapy died as compared to six of the 13 controls. This observation might be transferred to invasive mucormycosis and suggests that the reconstitution of the cellular immunity by the administration of donor-derived antifungal-TH1 cells against mucormycetes could improve the prognosis of allogeneic HSCT recipients suffering from mucormycosis. Our in vitro studies showed that in all healthy individuals tested, a cellular immune response against Rhizopus oryzae could be detected.[18] These interferon (IFN)-γ producing T cells could be enriched and cultivated, and according to the phenotype and cytokine secretion upon restimulation with R.

None of the authors has any conflicts of interest associated with this study. “
“Bone morphogenetic proteins (BMPs) are multifunctional growth factors regulating differentiation and proliferation in numerous systems including the immune system. Previously, we described that the BMP signaling pathway is functional in human monocyte-derived dendritic cells (MoDCs), which were found to express both the specific receptors and the Smad proteins required for signal transduction. In this study, see more we provide evidence that human MoDCs

produce BMP-4 and that this production is increased over the maturation process as is BMP signal transduction. When DCs are matured in the presence of an inhibitor of the BMP pathway, the expression of the maturation BAY 73-4506 concentration markers PD-L1 and PD-L2 is reduced, while cytokine production is not affected. As a result, these mature DCs present an augmented ability to stimulate both T cells and NK cells. Eventually, the inhibition of BMP signaling during maturation causes a reduced expression

of IRF-1, a transcription factor that positively regulates the expression of PD-L1 and PD-L2. The present study indicates that the BMP signaling pathway regulates PD-L1 and PD-L2 expression in human MoDCs during the maturation process, probably through the IRF-1 transcription factor, and also points out that the manipulation of BMP signaling might considerably improve the immunogenicity of MoDCs used in immunotherapy. “
“Recent years have witnessed an explosion in the amount of genomic information available for Toxoplasma gondii and other closely related pathogens. These data, many of which have been made publicly available prior to publication, have facilitated a wide variety of functional genomics studies. In this review, we provide a brief overview of existing

database tools for querying the Toxoplasma genome and associated genome-wide data and review recent publications that have been facilitated by these data. Topics covered include strain 4��8C comparisons and quantitative trait loci mapping, gene expression analyses during the cell cycle as well as during parasite differentiation, and proteomics. The primary repository for functional genomics data for Toxoplasma can be found at EupathDB.org (1,2). This site provides access to data from 22 species of apicomplexans and kinetoplastids and provides a variety of search tools to mine data, as well as genome browsers for each species. The site has complex query building software built in to allow users to customize searches and filter the results based on a number of relevant criteria. These include polymorphism and orthology profiles, gene expression across strains and developmental stages, and genomic location. From a comparative genomics perspective, the current version of EupathDB allows for searches to be conducted both within and between species. This is an incredibly powerful tool for comparative genomics.

However, the inhibitory effect was found in the SN of R-DC-induced Treg (Fig. 2A). Both purified CD4+ and CD8+ peripheral blood T cells were cocultured with R-DC and each of their SNs contained this suppressive factor (Fig. 2B and C), because the SN again showed a strong T-cell inhibitory capacity. This factor was not released by naïve T cells, isolated from human CB, as the SN of naïve T cells cocultured with R-DC was not inhibitory (Fig. 2D). Additionally, naïve T cells cocultured with Ibrutinib R-DC did not show a reduced proliferation (Supporting Information Fig. 1A and B). This contrasts strongly to the finding that in

the coculture of peripheral blood T cells and R-DC, T-cell proliferation is impaired 12. Thus, R-DC-mediated inhibition is specific for CD4+ and CD8+ effector T cells, but not for naïve T cells. Inducible Treg can develop from mature T-cell populations under certain conditions, e.g. upon stimulation with tolerogenic DC. They act via release of soluble factors such as IL-10, a well established inhibitory molecule. In order to NVP-BKM120 elucidate if the inhibitory effect was mediated through IL-10 or other factors, we added the SN of our R-DC-induced Treg to an MLR and investigated whether the inhibitory effect was reversible with neutralizing Ab to IL-10, TGF-β, or IFN-α 11, 19.

The levels of the respective factors in the T-cell/R-DC SN were determined previously 12. The inhibitory quality of the SN of R-DC-induced Org 27569 Treg was not reversible with mAb against IL-10, IFN-α, and TGF-β (Fig. 3A). The inhibitory effect of IL-10, TGF-β or IFN-α on a T-cell/DC coculture and the reversibility of this effect with neutralizing Ab is depicted in Supporting Information Fig. 2. Furthermore, size fractionation of the T-cell/R-DC SN revealed that the inhibitory factor is found in the >50 kDa fraction and not in the <50 kDa molecular weight range (Fig. 3B). The observation that the inhibitory factor is expected to be >50 kDa leads us to investigate IL-35, a heterodimeric cytokine consisting of EBI3 and the p35 subunit of IL-12 with inhibitory

function and a molecular size of 78 kDa 5. We found that T cells cultured with R-DC showed elevated levels of EBI3 and p35 mRNA, but no changes in the p28 levels, which forms IL-27 together with EBI3 (Fig. 4A). Furthermore, intracellular stainings showed that EBI3 was also upregulated at the protein level in peripheral blood T cells, stimulated with R-DC in comparison to T cells cocultured with DC (Fig. 4B, left column). In naïve T cells stimulated with R-DC we did not observe an upregulation of EBI3 (Fig. 4B, right column). P35 is constitutively expressed in DC or R-DC stimulated peripheral blood T cells or naïve T cells (Fig. 4B). This is in accordance to previous findings, which show that p35 is constitutively expressed in various types of human T cells 6.

Cells were then washed in PBS and re-fixed in 4% formaldehyde. Some samples were thereafter

stained with 5 μg/mL FM4-64× (Molecular probes) in PBS for 30 s on ice and then fixed again with 4% formaldehyde without prior wash, in order to visualize the membrane of the cells during microscopy. Primary antibodies were from BD Biosciences. After staining, coverslips were mounted on a microscope slide, sealed with nail polish and stored dark at 4°C before imaging by confocal microscopy within 24 h. The slides were examined with an LSM 510 Meta confocal microscope (Carl Zeiss, Jena, Germany) equipped with a 63× objective, and using Osimertinib research buy the LSM software v. 3.2 (Carl Zeiss). Several representative images from each sample were acquired with similar scanning parameters (63× plan-apochromat/1.4 oil, confocal slide of 1–2 μm). Image analysis and quantification of co-localization was performed using the LSM software v. 3.2, and co-localization between vaccines with each other or with Lamp-1 was defined as overlapping fluorescence, and is shown with arrows on the representative images. Statistical differences between selected means were analyzed with a Student’s t-test. Whenever more than one comparison was made in the same experiment, the approximate Bonferroni correction was used, where samples are considered significant at the overall level of α if α (sample)<α (overall)/n, where n is the number

of comparisons. click here For multiple comparisons of more than three means, one-way ANOVA was used with Turkey’s post test for multiple comparisons, and statistical are differences marked by asterisks in figures and explained in figure legends. Statistics were performed

with comparisons of means from the one experiment shown in the figures only, and never between repeated experiments, since these were not completely matched regarding sample size and day of analysis. This work was supported by The Bill and Melinda Gates Foundation, the Tuberculosis Vaccine Cluster-European Commission Resveratrol (TBWA-EC) Grant contract no. CT2003–503367 and the Option Foundation. The authors thank Timothy Mark Doherty for critical reading and comments on the manuscript. The excellent technical assistance provided by Charlotte Fjordager, Kristine Persson, Benjamin Anderschou Holbech Jensen, Lene Rasmussen, Merethe Henriksen, Katja Bøgebjerg Carlsen and Janne Frandsen as well as the animal technicians at the Statens Serum Institut is gratefully acknowledged. Conflict of interest: P.A, C.A., J.D. and C.V. are co-inventors of patents relating to tuberculosis fusion protein vaccine Ag85B-TB10.4. All rights have been assigned to the Statens Serum Institut. The authors have no other relevant affiliations or financial involvement with any organization or entity with a financial interest in or financial conflict with the subject matter or materials discussed in the article apart from those disclosed. “
“Citation Lee HJ, Kim H, Ku S-Y, Kim SH, Kim JG.

3a; data shown only for the CD4+ CD25− CD127−/+ effector population from HNSCC patients). At the 1 : 1 ratio, the CD25inter Selleckchem OTX015 Treg cell population consistently induced a greater percentage of suppression compared with CD25high Treg cells regardless of the effector T-cell population being suppressed. This trend was also observed at the different Treg : effector T-cell ratios; however, with increased proportions of effector T cells the level of suppression induced by the two Treg cell populations became less pronounced (Fig. 3a). As all samples were tested at a 1 : 1 ratio of Treg : effector

T cells these data were used for statistical analysis of differences between various cell populations and clinicopathological parameters. Both Treg cell populations (CD25inter and CD25high) from HNSCC patients suppressed the proliferation of CD4+ CD25− CD127−/+ effector T cells to a greater extent than those from healthy controls, but this only reached significance for the CD25high Treg cells (Fig. 3b). The significance Apoptosis Compound Library datasheet observed arose primarily from the oropharyngeal cohort, in particular those with early stage tumours, as both these patient groups induced a significantly greater level of suppression compared with healthy

controls (Table 2). In addition, patients with advanced stage cancer of the larynx and patients with nodal involvement also had CD25high Treg cells with significantly greater suppressive activity than the healthy controls (Table 2). No differences were observed in the suppressive activity between patients with laryngeal and oropharyngeal cancer, early and advanced stage tumours and tumours with and without nodal involvement for both CD25inter and CD25high Treg cells (data not shown). When using the CD4+ CD25+ CD127+ effector T-cell population the only significant difference found was that CD25high Treg cells Obeticholic Acid solubility dmso from patients with tumours that had metastasized to the lymph nodes had a greater suppressive activity than those isolated from patients without

nodal involvement (22·80 ± 2·92% versus 11·21 ± 4·50%; P = 0·04). Both the CD25inter and CD25high Treg cells exerted a greater level of suppression on the proliferation of the CD4+ CD25− CD127−/+ effector T cells compared with the CD4+ CD25+ CD127+ effector T-cell population for all HNSCC patient cohorts; however, this only reached significance for the CD25high Treg cells isolated from patients with cancer of the oropharynx (25·41 ± 4·65% versus 19·33 ± 3·36%; P = 0·03). The percentage of suppression induced by CD25inter Treg cells on the proliferation of CD4+ CD25− CD127−/+ effector T cells at a 1 : 1 ratio was consistently higher compared with CD25high Treg cells, regardless of tumour stage, subsite and nodal status and including healthy controls.

Even cross-presentation capacity, which has been attributed solely to CD8+ cDCs and CD103+ mDDCs in many models, has also been observed in mLCs, CD11b+ mDDCs and/or CD11b+ cDCs [18-26]. In this review we will discuss how underlying limitations of murine experimental models may have led to these apparently contradictory findings. CD11b CD103+ CD11b+ CD103 CD11b CD103 DC subset function

is often inferred from ex-vivo assays that measure the response of antigen-specific T cells co-cultured with DC subsets purified from the draining LNs and/or spleens of immunized or infected mice. Additionally, lymphatic cannulation of larger mammals such as in rats, pigs, sheep and cattle has been used to recover migrating dendritic cells for ex-vivo phenotypical and functional studies https://www.selleckchem.com/products/epz015666.html (reviewed in [27]). T cell proliferation and effector function in these ex-vivo assays generally reflect the extent of antigen presentation at the time of DC harvest, and thus provide an indirect measure of the efficiency of in-vivo antigen uptake and processing by a given DC subset. However, ex-vivo assays

can also be affected by changes in DC immunogenic properties resulting from the physical manipulation involved in DC isolation [28, 29]. In addition, co-culture overrides microanatomical factors that may constrain the probability of in-vivo contact between DCs and T cells within the T cell zones of lymphoid organs. For example, the majority of splenic CD11b+ cDCs are located outside the T cell zone in the steady state and would contact IWR1 T cells only after Toll-like receptor (TLR)-dependent signals

drive their relocation into the T cell zone, yet they may still present antigen oxyclozanide to activate T cells in vitro [30]. In skin-draining LN, the peak arrival of mLCs after immunization is on day 4, compared with days 1–2 for mDDCs [6], so that assays performed on day 2 would not detect the capacity of mLCs migrating from the immunization site to present antigen [31]. Another major limitation of ex-vivo assays is that in-vitro T cell responses do not always mimic their in-vivo counterparts [3, 32, 33]. Effective concentrations of cytokines such as IL-2 are higher in vitro yet T cell division times are longer, and are accompanied by much higher rates of spontaneous cell death [33]. T cell cytokine production tends to be polarized more strongly in vitro than in vivo (reviewed in [34]). Long-term regulation of T cell effector and memory differentiation in vitro is also highly dependent on addition or withdrawal of exogenous cytokines. Most importantly, the conditions that induce T cell deletion in vivo are not replicated effectively in vitro. In-vivo tolerogenic responses to soluble peptide begin with a proliferative burst that is followed rapidly by deletion in the absence of effector cytokine production [33, 35].

This may delay the development of protective immunity and consequently lead to reinfection with low number of parasites. This study

was supported by grants from Fundação de Amparo à Pesquisa do Estado de PD0325901 supplier Minas Gerais (FAPEMIG) and CNPq. Acknowledgement is also due to Juliana Froeseler, Remo de Castro Russo, Cristiana Couto Garcia, Rodrigo Guabiraba Brito, Florence Mara Rosa, José Carlos dos Reis and Selma Fernandes for the technical support rendered during the experiments. “
“Investigation was made of changes in immune system parameters during the course of neonatal infection. The study population consisted of 95 full-term neonates matched for chronological age and sex, divided into three groups: suspected infection (n = 20), sepsis (n = 25), infection-free control subjects (n = 50). Serial measurements were made of the cytokines interleukin-6 (IL-6), interleukin-1b (IL-1b) and tumour necrosis factor-α (TNF-α), lymphocyte subsets [CD3+, CD4+, CD8+, natural killer (NK) cells and B cells], the immunoglobulins (Ig) (IgG, IgM and IgA), C-reactive protein

(CRP), and the total blood count, before, 2 days after initiation of treatment and after stopping treatment (time periods first, second and third, respectively). IL6, TNF-α, IL1-b and CRP were higher at the first time period in the sepsis group, and IL6 and TNF-α continued to be higher in this group at the second period. IL-6 and TNF-α were precise sepsis predictors with sensitivity and specificity of 0.92, 0.98 and 0.91, 0.92, respectively. NK cells, B cells, CD3+, CD4+, CD8+ CHIR 99021 were higher in the sepsis and suspected infection groups, but the ratios CD3+/CD4+, CD3+/CD8+, CD4+/CD8+ showed no difference from the controls. IgG was lower and IgM higher in the sepsis group. In the control subjects CD3+, CD4+, CD8+ lymphocytes increased with increasing age. It is concluded that IL-6 and TNF are good diagnostic markers of sepsis in full-term neonates. Lymphocyte subsets were affected by both the clinical condition and the chronological age. NK and B cells may be

elevated in suspected and documented sepsis, and further studies are needed to determine their clinical significance. Neonates are vulnerable GNE-0877 to bacterial infections, and sepsis is one of the major causes of neonatal morbidity and mortality. It is important to identify neonatal infection as early as possible, but clinical signs are usually unreliable in neonates, while the routine diagnostic tests lack precision [1]. The immune system of the neonate, although immature, reacts to infection in several ways. It produces acute phase reactants, such as C-reactive protein (CRP), cytokines, such as interleukin-6 (IL-6) and tumour necrosis factor-α (TNF-α), and reacts with changes in the white blood cell (WBC) populations.

1). A landmark study of 32 065 haemodialysis patients, mean follow-up of 2.2 years, reported that deaths from cardiac arrests were most common after the long 2

day inter-dialytic break (after long inter-dialytic break, 1.3 vs 1.0 deaths per 100 person-years on other days, P = 0.004).[42] The DOPPS investigators reported similar findings in haemodialysis patients from the United States, Europe and Japan.[43] Possible explanations are manifold, including hypervolaemia, circulatory collapse, or electrolyte and metabolite build-up between dialysis sessions. Potassium is important for regulation of trans-membrane potential of cardiac myocytes, and there is evidence to support the hypothesis that potassium shifts, relative hypokalaemia post-dialysis[44] and pre-dialytic RG-7388 hypokalaemia predispose to arrhythmia. In one multivariate

Cox regression analysis of the risk factors for SCD in 476 chronic haemodialysis patients, GSK1120212 cost pre-dialytic hyperkalaemia conferred 2.7-fold increase (95% CI = 1.3–5.9).[45] In an observational study of 81 013 haemodialysis patients, the optimum pre-dialysis serum potassium in respect of long-term survival was between 4.6 and 5.3 mmol/L.[46] In a review of 400 dialysis unit cardiac arrests, patients who were dialysed against a low potassium dialysate (0 or 1.0 mmol/L) were twice as likely to have had a cardiac arrest.[47] It has also been reported that a dialysate potassium of <2 mmol/L (or <3 mmol/L, if pre-dialysis potassium is <5 mmol/L) confers increased risk of SCD.[3, 6] Electrical conduction is also dependent on intra-cardiac calcium handling; a low calcium dialysate (1.25 mmol/L) is associated Carnitine palmitoyltransferase II with aberrations in cardiac conduction

as assessed by electrocardiography, such as increased QTc dispersion or prolonged QT interval.[48] In view of these findings, there is a need for future studies to concentrate on the composition of dialysate in the hope of reducing arrhythmia burden. High rates of fluid removal may result in intra-dialytic hypotension, myocardial stunning and injury. In turn, this may predispose to arrhythmia or circulatory collapse. In DOPPS, a large ultrafiltration volume (>5.7% of post-dialysis weight) conferred an HR of 1.15 for sudden death (defined as deaths due to arrhythmia, cardiac arrest and/or hyperkalaemia).[6] Similarly, in a case-control study of 502 haemodialysis patients who had a sudden cardiac arrest with 1632 age- and dialysis-vintage-matched controls who did not, increased ultrafiltration volumes conferred an adjusted OR of 1.11 (95% CI = 1.02–1.033, P = 0.02). A recent observational study reported that depressed heart rate variability is associated with fluid overload in chronic haemodialysis patients.[49] This may be one of the pathophysiological mechanisms by which fluid overload predisposes to arrhythmias.

Likewise IPPS QoL improved significantly

at 6 weeks in all three treatment groups (P < 0.001) and again improvement was more marked with combination GSK-3 inhibition therapy than alfuzosin (P = 0.04) and tadalafil (P < 0.001). Post-void residual urine significantly improved in all the treatment groups (P < 0.01) but improvement in combination group was significantly better than alfuzosin (P = 0.04) and tadalafil group (P < 0.01). Likewise, Qmax also significantly improved in all the treatment groups (P < 0.001), with combination therapy having similar improvement with alfuzosin alone and significantly greater improvement than tadalafil (P < 0.01). The improvement in all the parameters studied was more at 12 weeks in all three groups than at 6 weeks. There was significant improvement in IPPS total, IPSS-S and IPSS-V in all the three groups

(P < 0.001), again improvement was more in combination therapy than alfuzosin (P = 0.004) or tadalafil (P < 0.001). Likewise, there was significant improvement in IPPS QoL in all three groups, but combination therapy was better than alfuzosin (P = 0.015) or tadalafil (P < 0.001). Combination therapy showed significantly more reduction in PVR than alfuzosin (P = 0.003) or tadalafil alone (P < 0.001). www.selleckchem.com/products/MLN-2238.html The improvement in Qmax in combination therapy was similar to alfuzosin (P = 0.22) and better than tadalafil (P < 0.0001). At 6 weeks EDS improved in all three groups(P < 0.0001) but there was only a modest improvement with alfuzosin (0.8 ± 1.3) on comparison with tadalafil (2.3 ± 2.1, P = 0.027) or combination therapy (2.5 ± 2.2, P = 0.002). The improvement in EDS with combination therapy at 6 weeks was similar to that in tadalafil (P = 0.07) and better than alfuzosin (P = 0.003). At 12 weeks EDS improved significantly in combination therapy (4.3 ± 3.4) and tadalafil

group (3.2 ± 2.6), whereas modest improvement was seen in the alfuzosin group (1.8 ± 1.7). The improvement was significantly greater with combination therapy (P = 0.002) and tadalafil (P = 0.027) when compared to alfuzosin. There was no significant difference between the improvement seen with combination therapy and tadalafil (P = 0.22). The efficacy on IPPS, IPSS-S, IPSS-V, IPSS QoL, Qmax, PVR and EDS are summarized in Tables 2 and 3. Lower urinary tract symptoms/BPH is one of the most common Etofibrate ailments of aging males. The pathophysiology of LUTS is complex and multifactorial. Alpha-blockers are considered to be a first line monotherapy for the treatment of LUTS suggestive of BPH. The favorable effect of alpha-blockers on sexual function is either indirect through an improvement of LUTS[3] or via a direct effect on corpus cavernosum.[4] Alpha-blockers may contribute to improvement in ED by impacting the balance between contraction (detumescence) and relaxation (erection) of corpus cavernosum smooth muscle.4 The improvement in sexual function by alpha-blockers has been proven in a meta-analysis.[5] Among the alpha-blockers, tamulosin is the most widely used drug.

After treatment with the BTK inhibitor probiotic, inflammatory biomarker levels significantly decreased. Uraemic rats demonstrated superficial mucosal

erosion and inflammatory cell infiltration in the small intestine, and administration of the probiotic alleviated these lesions. The probiotic B. animalis subsp. lactis Bi-07 alleviate bacterial translocation and ameliorate microinflammation through the recovery of intestinal mucosal integrity. “
“Background:  Accurate estimation of glomerular filtration rate (GFR) allows early detection of renal disease and maximizes opportunity for intervention. Aim:  To assess the accuracy of estimated GFR (eGFR) in an Australian and New Zealand cohort with chronic kidney disease using the 4-variable Modification of Diet in Renal Disease equation (MDRD4V), the Chronic Kidney Disease Rucaparib molecular weight Epidemiology Collaboration (CKD-EPI) equations, and the Cockcroft and Gault equation

with actual and ideal body weight. Methods:  Retrospective review of patients who had measured GFR (mGFR) by 51Cr-EDTA clearance and simultaneous measurements of serum biochemistry and anthropometrics. eGFR was compared with mGFR using the concordance correlation coefficient (CCC) and Bland–Altman measures of agreement. Results:  178 patients had 441 radioisotope measurements of GFR. Mean mGFR of was 22.6 mL/min per 1.73 m2. The MDRD4V equation using the ‘black’ correction factor was most accurate with a mean eGFR of 19.74 (CCC 0.733, bias −2.86). The CKD-EPI equations also using the ‘black’ correction factors were almost as good at 19.11 (CCC 0.719, bias −3.49). The Cockcroft–Gault creatinine clearance values had the poorest agreement with mGFR. In the 18 nonwhite non-Asian patients, the MDRD4V and CKD-EPI equations were generally less accurate although the

use of the ‘black’ correction factor resulted in greater accuracy for both Tideglusib equations. Conclusion:  The MDRD4V equation was the most accurate. However, its accuracy might be less for nonwhite non-Asian patients if the ‘black’ correction factor is omitted. Further study of the estimation of GFR in Australian and New Zealand ethnic subgroups would be helpful. “
“Early intervention in patients with chronic kidney disease (CKD) significantly improves the prognosis. The present widely used markers of renal function, such as serum creatinine (sCr), fail to reflect early renal damage and predict the progression of disease. The authors aimed to evaluate whether neutrophil gelatinase-associated lipocalin (NGAL), a novel specific biomarker of acute kidney injury, could predict the progression of CKD. We identified 92 patients with stage 2–4 CKD caused by primary chronic glomerulonephritis. The patients were followed for 2 years, the changes in NGAL levels in the progressive and non-progressive groups were compared. First, the serum NGAL levels of patients with stage 2–4 CKD were significantly increased compared with the control group.