In the reports by Gallina et al., graft overgrowth was observed in all transplanted patients and as early as 4 months after surgery. The latter tissue growth had virtually ceased 9–10 months after transplantation. find more However, the grafts had enlarged aberrantly and were not confined to the surgical target sites. In fact, they encompassed regions of the white matter within the overlying cortex and ventral striatum. Hypermetabolic activity was demonstrated by FDG-PET 6–9 months after surgery but had decreased by 12 months after transplantation. Changes in D1 receptor binding varied between patients,

which correlated with limited improvement, if any [21,52]. One additional MRI report showed large cysts and well-delimited masses in one patient 10 years after transplantation [45]. The very first post-mortem study of a transplanted HD-affected brain was conducted in a patient who died 18 months after transplantation of causes unrelated to the procedure.

This study provided the initial proof of concept that solid foetal striatal grafts could survive in a human HD brain [42,53] (Table 3). In this learn more patient, most grafts survived (six out of 10), with three localized in the right putamen, two in the left putamen as well as one in the anterior limb of the internal capsule. The majority of transplants could be identified macroscopically. Using immunohistochemical staining, the grafts exhibited a compartmentalized organization with the formation of striatal patchy areas known as p-zones, as well as areas lacking a striatal phenotype (non p-zones) [54]. Large and medium-sized neurones were predominantly seen in the p-zones of the grafts using typical striatal

markers such as dopamine receptor-related phosphoprotein 32 kDa (DARPP-32), calretinin, acetylcholinesterase (AChE), calbindin, enkephalin and substance P. Interneurones positively stained for choline acetyltransferase (ChAT), NADPH-diaphorase (NADPH-d) and parvalbumin were also detected within p-zones. Non p-zones were largely devoid of these markers but were richer in glial fibrillary acidic protein (GFAP)-positive astrocytes. Human leucocyte antigen-DR (HLA-DR), a marker for Ibrutinib macrophages and microglia, was rarely found in the transplant but was abundantly expressed in the host brain. There was no perivascular cuffing or T-cell infiltration, as visualized with CD4 and CD8. mHtt inclusions within the grafted tissue were not detected [42]. One additional case from the Freiburg University cohort provided a description of graft status at early time interval following transplantation [22] (Table 3). In that report, the authors confirmed the presence of three putaminal and two caudate grafts per hemisphere. DARPP-32-positive neurones, as visualized by immunohistochemistry, were found within the grafted tissue and were interspersed with calretinin- and somatostatin-positive interneurones.

, 2002), and studies using a B. burgdorferi CptA (carboxyl-terminal protease A) deletion mutant indicated that the C-terminal cleavage was likely a result of CptA proteolysis (Ostberg et al., 2004). P13 porin activity was detected using planar lipid bilayer assays, from which it was determined that P13 possesses cation-selective pores with a single channel conductance of 3.5 nS in 1 M KCl (Ostberg et al., 2002). This channel-forming activity was eliminated in a P13-deficient B. burgdorferi mutant (Ostberg et al., 2002). Unlike P66, however, P13 is not known to be associated ACP-196 supplier with virulence-related functions, and its expression has not been reported to be regulated by temperature or mammalian host-specific

signals. Interestingly, P13 is a member of a B. burgdorferi paralogous gene family, which contains eight additional plasmid-encoded P13 paralogs (Fraser et al., 1997; Noppa et al., 2001; Pinne et al., 2004). One of these paralogs, selleckchem BBA01, displays channel-forming properties

similar to the chromosomally encoded P13 protein (Pinne et al., 2004, 2006). Furthermore, loss of the 3.5 nS membrane conductance from a p13 null mutant was restored by complementation with BBA01, suggesting that these proteins are possibly redundant at the functional level (Pinne et al., 2006). Although P13 and P66 have been verified to possess channel-forming activity characteristic of known bacterial porins, neither protein is structurally well characterized, and both P13 and P66 have been suggested to form atypical porin structures (Bunikis et al., 1995; Noppa et al., 2001; Pinne et al., 2004). P13 is predicted to span the OM by transmembrane α-helices, which is contrary to the amphipathic β-sheet-containing beta-barrel secondary structure typical of enteric Gram-negative proteobacterial porins (Koebnik et al., 2000; Schulz, 2002). Initially, P66 was also thought to span the membrane by two http://www.selleck.co.jp/products/CHIR-99021.html α-helical transmembrane domains (Bunikis

et al., 1995), although recent sequence analyses suggest that P66 may in fact form a 20-22-stranded β-barrel structure (Barcena-Uribarri et al., 2010). Future crystallography studies will be needed to fully delineate the P13 and P66 protein structures. Another B. burgdorferi protein termed Oms28, which is encoded by ORF bba74, was originally reported to be OM localized and to exhibit channel-forming activity (Skare et al., 1995, 1996). Additionally, Cluss and co-workers demonstrated that this protein was secreted from borrelial cells (Cluss et al., 2004). However, more recent biophysical and cellular localization data have suggested that BBA74 is a membrane-associated periplasmic protein that contains no integral membrane domains (Mulay et al., 2007). Surface-located membrane protein 1 (Lmp1), encoded by ORF bb0210, is a chromosomally encoded B. burgdorferi protein whose function, although still under investigation, may involve protection from host-adaptive immunity.

In addition, whether polyclonal Tregs or antigen-specific Tregs are used will influence the dose. Of note, studies using antigen-specific Tregs showed that lower numbers were able to achieve the Vemurafenib manufacturer same functional efficacy as larger numbers of polyclonal Tregs [86, 87]. Finally, whether a single injection or multiple injections are required

is a matter of debate and may be determined in a Phase II efficacy study, where patient outcomes should also be measured and an in-depth patient monitoring planned. The use of molecular diagnostic tools can help to assess the increased expression of biomarkers of operational tolerance in patients receiving cellular therapy and whether these can be used as surrogate end-points of efficacy [101-103]. The same approach can be used Palbociclib research buy to define whether or not the patients have decreased expression of biomarkers of acute rejection [104, 105].

Furthermore, phenotypic analysis of patient PBMCs, using flow cytometric analysis, can determine whether or not the number of Tregs has increased or the composition of the T cell compartment has changed as a result of the intervention [106]. Using the same analysis, the cytokine profile of the cells that have been phenotyped can be analysed to establish their plasticity. Finally, lymphocyte compartments can be monitored after specific interventions, as has been shown useful when associating expansion of lymphocyte

subsets, in this case naive B cells, in peripheral blood of patients in whom better outcomes were noted [107]. In spite of the potential concerns and controversies outlined with regard to Treg isolation and expansion protocols and the optimal clinical protocol, clinical PAK5 trials are under way to test the therapeutic potential of Tregs. Beneficial effects of Treg infusions on allograft survival were first reported in bone marrow transplantation models in which donor Tregs reduced the incidence of GVHD. The first human trial using Treg cell therapy by Trzonkowski et al. [108] involved two patients. The first patient had chronic GVHD 2 years post-bone marrow transplantation. After receiving 0·1 × 106/kg FACS purified ex-vivo-expanded Tregs from the donor, the symptoms subsided and the patient was withdrawn successfully from immunosuppression without evidence of recurrence. The second patient had acute GVHD at 1 month post-transplantation, which was treated with several infusions of expanded donor Tregs. Despite initial and transitory improvement, the disease progressed and resulted ultimately in the patient’s death. This was the first report to show that adoptive transfer of Tregs is well tolerated and thus was a major breakthrough.

Even though there was no significant difference in BMI (P > 0·05) between the CRPS and control groups in this study, the percentage of CRPS patients in our pain clinic who are Trichostatin A price either overweight or obese is higher than the general population [42]. Sleep has been shown to decrease the number of CD14+CD16+ monocytes [40], and

although acute exercise causes a transient increase in CD14+CD16+ monocytes [43,44], individuals who are physically inactive demonstrate a significantly higher percentage of CD14+CD16+ monocytes compared to those who are physically active [41]. Sleeping difficulties and physical inactivity are reported commonly by individuals afflicted with CRPS [4,45]. In addition, we showed that CRPS patients taking antidepressants demonstrated a positive

correlation with elevation of CD14+CD16+ monocytes. Even though other studies have shown that the expression of CD14 and CD16 in monocytes is unchanged in patients with depression compared to normal individuals [46], we cannot rule out that depression or antidepressant use are contributory factors to the increase in CD14+CD16+ monocytes shown by patients with CRPS. Thus, obesity, sleeping difficulties, physical inactivity and possibly depression may be contributory factors leading to the increase in the percentage of CD14+CD16+ monocytes seen in patients with CRPS. Following injury, many individuals develop the signs and PLX4032 ic50 symptoms of CRPS (swelling, buy Hydroxychloroquine redness, allodynia, hyperalgesia, etc.); however, in most patients, normal healing occurs and these signs and symptoms resolve. The process by which a subject fails to undergo normal healing following an injury and progresses to a chronic pain condition as well as the process by which the pain is maintained with little or no chance of resolving are some of the most important

and perplexing questions in CRPS research. The following observations make our finding of elevated CD14+CD16+ proinflammatory monocytes in patients with CRPS relevant to both the initiation and the maintenance of the disease: (1) the activation of microglia and astrocytes has been shown to be both necessary and sufficient for enhanced nociception [13] and (2) blood-borne monocytes/macrophages infiltrate the CNS and differentiate into fully functional microglia [24]. Our data cannot determine whether CD14+CD16+ monocytes were elevated in the study subjects prior to developing CRPS or became elevated afterwards. In either case, independent of causative mechanism, the elevation of blood proinflammatory monocytes prior to the initiating event may predispose individuals for developing the syndrome, whereas the elevation of blood proinflammatory monocytes following the development of CRPS may be relevant for its maintenance. The strengths of this study are: (1) that all patients met strictly defined IASP criteria for CRPS and (2) all patients were diagnosed and examined by the same senior clinician.

Amyotrophic lateral sclerosis (ALS) is an adult-onset neurodegenerative disorder characterized by progressive degeneration of upper and lower motor neurons in the brain and spinal cord, leading to progressive paralysis and ultimately death within 3 to 5 years of symptom onset.[1-3] One of the pathological hallmarks of ALS is the presence of transactivation response (TAR) DNA-binding protein (TDP-43) in ubiquitinated neuronal cytoplasmic inclusions in lower motor neurons.[4-8] Recent identifications of mutations selleck chemical in two genes encoding TDP-43 and fused in sarcoma (FUS), both of which are multifunctional DNA/RNA-binding proteins that are involved

in transcriptional regulation, have opened a new era in ALS research.[9-12] Although the pathomechanisms of cytoplasmic mislocalization and inclusion formation of TDP-43 and FUS, and motor neuron death in ALS are largely unknown, impairment of protein degradation machineries that include proteasome, autophagy and endosome systems

has also been suggested in neurodegenerative disorders that include ALS.[13-15] For instance, deficiency of 26S proteasome in mouse brain neurons by conditional knockout of a proteasome component PSMC1 (Rpt2/S4) causes neuronal ITF2357 in vivo aggregate formation and neurodegeneration.[16] Depletion of autophagosome components ATG5 and ATG7 also causes aggregate formation and neuronal cell death.[17, 18] Depletion of endosomal sorting complexes required for transport (ESCRT) components TSG101 (VPS23) and VPS24 (CHMP3) by short interfering RNA (siRNA) induces cytoplasmic TDP43-positive aggregate formation.[19] In the present study we produced recombinant adenovirus vectors encoding wild type and mutant TDP-43 or FUS, and those encoding short hairpin RNAs (shRNAs) for proteasome (PSMC1), autophagy (ATG5) and endosome (VPS24) systems to investigate whether the coupled gene transductions in rodent motoneurons by these adenoviruses elicit ALS pathology in vitro and in vivo. For the construction of adenoviruses encoding DsRed-tagged human TDP-43 and FUS, the full length and

C-terminal fragment (CTF; 208–414 a.a.)[20] TDP-43 (GenBank accession number NM_007375), and the full-length FUS (NM_004960) cDNAs obtained from HEK 293 cells by RT-PCR were cloned into pDsRed-Monomer-C1 plasmid Cyclic nucleotide phosphodiesterase vector at the C-terminus (Clontech, Palo Alto, CA, USA). Point mutations of TDP-43 (G294A:g881c, G298S:g892a, A315T:g1077a, Q343R:a1028g) were created by QuikChange II Site-Directed Mutagenesis Kit (Agilent Technologies, Santa Clara, CA, USA). C-terminal point mutations of FUS (R521C:c1561t, R521G:c1561g, R522G:a1564g, P525L:c1574t) were introduced through conventional PCR primers using wild-type FUS as a template. The resulting wild-type and mutant DsRed-TDP43 and DsRed-FUS fragments were subsequently cloned into Swa I cloning site of cassette cosmids pAxCAwtit2 and pAxCALNLwtit2 (TaKaRa, Osaka, Japan), respectively.

These mice are subsequently challenged with TT (without adjuvant), which results in not only cytokine production, including IL-2 and IFN-γ, by TT-specific memory CD4+ T cells, but also stimulates the pre-activated OT-II T cells. Notably, the use of mice not exposed to a TT prime-boost regimen (thus not containing TT-specific memory CD4+ T cells) prior to adoptive transfer of pre-activated OT-II T cells or the adoptive transfer of naïve OT-II T cells into

TT-prime-boosted mice fails to induce I-BET-762 bystander activation of pre-activated or naïve OT-II T cells, respectively, following TT challenge. Interestingly, TT booster-induced bystander activation of pre-activated OT-II T cells correlates with IL-2 and IFN-γ production in TT-specific memory CD4+ T cells. Moreover, pre-activated OT-II T cells express high levels of IL-2 receptors α and β (CD25 and CD122, respectively), as well as high levels of IL-7Rα (CD127), and proliferate strongly in the presence of IL-2 or IL-7 in vitro. selleckchem These data suggest that TT challenge leads to marked IL-2 production by TT-specific memory CD4+ T cells, thus causing IL-2-mediated bystander proliferation of pre-activated OT-II CD4+ T cells. A question that arises is to what extent these results are applicable to the in vivo situation, especially in terms of the

cytokine signals implicated and the CD4+ T cells responding to them. Previous reports showed that bystander activation of CD4+ T cells was confined to the CD44high memory subset and that the kinetics of activation in the CD44high MP CD4+ cells was similar to that of the MP CD8+ T cells 1, 2, suggesting that the same cytokine, namely IL-15, might be implicated in both processes (Fig. 1). Indeed, CD44high MP CD4+ T cells express intermediate levels of CD122 7 and might thus respond not only to IL-15, but also to IL-2. Moreover, other data suggest that IL-2 might be implicated in bystander activation of CD8+ T cells

8, 12, which is consistent with the data of Di Genova et al. on CD4+ T cells 8, 12. As for the in tuclazepam vitro pre-activated CD4+ T cells used by Di Genova et al. 8, 12, these cells are clearly different from memory CD4+ T cells, the latter of which are known to express low levels of CD25, intermediate levels of CD122, and high levels of CD127 13, 14. Moreover, memory CD4+ T cells are known to be responsive to IL-7 and IL-15 signals under steady-state conditions in vivo 14, 15, while in vitro pre-activated CD4+ T cells are, by contrast, very sensitive to IL-2 and IL-7, but not IL-15 12. This discrepancy in the IL-2- and IL-15-responses further illustrates that in vitro pre-activated CD4+ T cells crucially depend on high surface expression of CD25, as the other two IL-2 receptor subunits, CD122 and γc should have been sufficient to confer responsiveness to IL-15.

5). Only the two subjects who received 1010 BMB72 had IgA responses against listeriolysin (data not shown). Responses to influenza nucleoprotein were not detected in these assays. These results were interpreted to represent low level mucosal immune response against the listerial vector only. Serological immune responses XL765 in vivo were modest at best, with isolated individuals having four-fold or greater titer increases in ELISAs directed against listeriolysin or sonicated listerial antigen (denoted in Table 2 as one or two positive assays). No individual seroconverted to the recombinant nucleoprotein antigen.

Virtually all individuals had relatively high titers directed against recombinant nucleoproteins at baseline, which did not change over time (i.e. ≥1:640). Sera from other species (mouse and rabbit) studied similarly in ELISAs did not have similarly high baseline values, so these were interpreted to ATM/ATR assay represent bona fide pre-existing immune responses to this influenza protein, rather than inadequate blocking or another technical problem with the assay. A high baseline is not unexpected, as most

subjects had evidence of cellular immunity to influenza A, and it is expected that most healthy young adults would have been exposed to influenza. Grouped by vaccine given, there was no statistically significant increase in IgG mean titers (GMT; pre-immune to peak value) directed against listerial sonicate, listeriolysin or nucleoprotein, as exemplified in Figure 6b (for listeriolysin). Baseline listeriolysin titers were high, which is not unexpected. Antibodies to streptolysins

present in commensal and pathogenic streptococci cross-react with listeriolysin (34). Our volunteers were required to have previously received penicillin Erythromycin or ampicillin, commonly administered to treat Group A streptococcal pharyngitis. Overall, mean serum IgA titers did increase modestly when considered as a group for both vaccine organisms (Fig. 6a). All subjects had positive control responses to the lectin PHA (usually TNTC), and all but one to the CEF control pool (subject No. 11 had both robust PHA responses and responses to sonicated listerial antigen, but no apparent response to CEF or influenza nucleoprotein peptides). Most subjects (17/22) had convincing baseline immune responses to at least one of the Influenza A nucleoprotein peptide test pools (tens to many hundreds of spots per million PBMC, see exemplary data in Fig. 7a). About two-thirds of the subjects (14/22) had some baseline responses to the listeriolysin peptide pools, with mean baseline value 21 (range 0–205) SFC/106 PBMC, comparable to others’ published work (35). ELISpot data were analyzed by individual and as a group by vaccine administered, irrespective of dose, as responses overall did not appear dose-related. Values were analyzed as pre-immune vs.

Upon CD95L and anti-CD95 treatment we observed significantly more viable thymocytes from vavFLIPR mice compared with the number of WT thymocytes (Fig. 3A and B). In contrast, dexamethasone (Dex)-induced cell death, which proceeds via the glucocorticoid receptor in a death receptor-independent pathway, was not affected by the c-FLIPR transgene (Fig. 3A and B). To have a closer look into the time-course of apoptosis, thymocytes from WT and vavFLIPR animals were stimulated with CD95L for

up to 8 h. After 4 h of CD95L-stimulation, more early apoptotic (AnnexinV+ 7AAD−) WT cells than vavFLIPR cells were identified (Fig. 3C and D). After 8 h of stimulation, higher frequencies of both late apoptotic (AnnexinV+ 7AAD+) and early apoptotic WT cells were observed in comparison to vavFLIPR LY2835219 thymocytes (Fig. 3C and D). Taken together, WT thymocytes were rapidly

undergoing apoptosis, whereas vavFLIPR thymocytes were more resistant to CD95-induced apoptosis. Next, we examined the apoptosis sensitivity of peripheral T and B Poziotinib cells. Sorted CD4+ and CD8+ T cells as well as CD19+ B cells were stimulated with CD95L and Dex. Significantly, more viable (AnnexinV− 7AAD−) vavFLIPR CD4+ and CD8+ cells were identified upon CD95L stimulation compared to WT cells, while the Dex-treated controls were comparable between WT and vavFLIPR cells (Fig. 4A and B). Furthermore, sorted CD19+ B cells were activated with lipopolysaccharide (LPS) for 2 days to induce expression of the CD95 receptor before CD95L- and Dex-stimulation. Although activated B cells were fairly insensitive toward both

CD95L- and Dex-induced apoptosis, we detected significantly lower specific apoptosis of vavFLIPR B cells than of WT B cells (Fig. 4C). Again, the specific apoptosis of Dex-treated B cells was comparable between WT and vavFLIPR samples (Fig. 4D). Reactivation Farnesyltransferase of the T-cell receptor leads to subsequent apoptosis via the death receptor pathway and the CD95 receptor has been shown to be involved in activation-induced cell death (AICD) [20-23]. To assay AICD, peripheral lymph node cells from WT and vavFLIPR mice were isolated and T cells were activated for 2 days with plate-bound anti-CD3 and anti-CD28 in presence of IL-2. Activated T cells were further expanded for 3 days in medium containing IL-2. Subsequently, AICD was assessed by restimulating T cells with plate-bound anti-CD3 to induce cell death on day 5. Also in this assay, cells from vavFLIPR mice showed significantly less specific apoptosis compared to WT cells (Fig. 4E). Thus, the c-FLIPR transgene is functional and protects primary immune cells against CD95-induced apoptosis and AICD. Next, we analyzed lymphocyte populations in vavFLIPR mice, since inhibition of CD95-induced apoptosis is often associated with alterations in lymphocyte numbers. However, total cellularity in spleen, peripheral lymph nodes, and thymus, was overall comparable between WT and vavFLIPR mice (Table 1).

Rhesus and human pDCs in PBMC cultures responded to stimulation by CpG C and TLR7/8-L by production of large amounts of IFN-α at levels comparable to previous reports.26,32,52 This is consistent with the constitutively high expression of IRF-7 reported in both human and rhesus pDCs.41 When IFN-α was measured by ELISA Abiraterone after 24 hr of stimulation, the IFN-α levels in both human and rhesus cultures were

higher in response to CpG C compared with TLR7/8-ligand. This may at least in part be because of the higher stability of CpG C, leading to more persistent stimulation. TLR7/8-ligand was shown to be most efficient as an adjuvant when administered in a conjugated form.19,53 Further, we found that IFN-α effectively enhanced B-cell function to TLR7/8 ligation both in human and rhesus B cells. This enhancing effect included proliferation, phenotypic differentiation and induction of IgM secretion. It is therefore plausible that both the human and

Selleck GSK3235025 rhesus immune system have similar regulatory mechanisms for how B-cell responses evolve to virus infections or other conditions engaging TLR7/8 signalling. However, there were marked differences between human and rhesus B cells with regard to alterations of cell surface markers during differentiation. The distinct CD27high populations observed in human B-cell cultures associated with plasmablast formation2,3,45,54 was absent from rhesus

B-cell cultures under conditions when both human and rhesus B cells produced increased levels of IgM. Instead, rhesus B cells showed a distinct down-regulation of CD20, which correlated with the levels of IgM production. Hence, CD20 down-regulation may be a useful marker for monitoring rhesus B-cell differentiation. One cannot rule out that the lack of a CD27high plasmablast population in rhesus B-cell cultures reflects a functional difference between the two species. CD27 and its Farnesyltransferase ligand CD70, which is expressed on activated CD4+ T cells, B cells and DCs, play a critical role in T-cell-dependent B-cell responses. CD27 activation was shown to induce antibody production after an initial phase of cellular expansion that involves CD40 : CD40 ligand interactions.55,56 B cells with up-regulated CD27 expression therefore probably possess an increased ability to receive signals via this receptor. The impact of CD27 signalling in B cells on antibody production may therefore be greater in humans compared with in rhesus macaques. CD20 is expressed on almost all B cells and can be targeted by the mAb rituximab. Although this antibody is used for several applications including immunotherapy, knowledge about the biology of CD20 is relatively limited. CD20 has no known natural ligand and CD20 knockout mice display an almost normal phenotype.

9%). Among then, E. coli accounted for 54 episodes (12.7% of total). 18 episodes were caused by ESBL producing enterobacteriaceae and all of them were ESBL E. coli (4.2% of the total episodes and 33.3% of all E. coli). 6 Episodes check details were treated with IP Imipenen/cilastatin with a dose ranged from 100–200 mg/L continuously. 2 of them required T/C removal and no death reported. IP meropenem was attempted in 5 episodes with a continuous dose of 200 mg/L in 2 and intermittent dose of 200–400 mg daily in the remaining. 1 episode has relapse (200 mg daily dose) and no death reported. Overall, no severe adverse reaction was noted, especially neurological complications. Chi-square

test for T/C removal rate showed P value 0.15. Conclusion: It appeared the number was inadequate to provide a meaningful statistical analysis.

Although the total dose of IP Tienam/Meropenem (up to 1.6 gram/day) were quite high, there was no specific neurological complications reported. However, lower dose was attempted successfully (Meropenem 400 mg/day), thus it may be a safer alternative while retaining the efficacy. Detailed pharmacokinetic study of Meropenem and large scale outcome study with various dosages are needed. YABUUCHI BMS-777607 datasheet JUNKO, MAKIISHI TETSUYA, MAEDA SAYAKO Division of Nephrology, Department of Internal Medicine, Otsu Red Cross Hospital Introduction: Twenty-four hour quantification of urinary protein collection (24-h proteinuria) has been the foundation for monitoring SB-3CT patients with various kidney diseases including membranous nephropathy (MN). However, because of the accumulation studies showing good correlations between random single-void (spot) urine protein to creatinine (P/C) ratio and 24-h proteinuria, spot urine P/C ratio is widely used instead of 24-h urine collection.

In the management of patients with MN, the amount of urine excretion is a marker for early diagnosis of relapse. However, the accuracy of spot urine P/C ratio has not been validated in MN. We aimed to evaluate its accuracy in patients with MN. Methods: Among 19 patients with MN who were treated at our institution between 2008 and 2013, 5 patients with at least one paired result of 24-h urine P/C ratio and a random spot urine P/C ratio were identified, and a total 51 paired results were examined. As a control, a total of 124 paired results from patients with primary (IgA nephropathy, n = 10, 52 pairs; minimal change nephrotic syndrome, n = 2, 18 pairs; focal segmental glomerulonephritis, n = 2, 37 pairs) and secondary (lupus nephritis, n = 1, 12 pairs) glomerulonephritis were also examined. All spot urine samples were obtained at daytime. The correlation and agreement between the P/C ratios in the two methods were assessed by Pearson correlation and the Bland-Altman procedure, respectively.