, 2007, Drew and Fraggos, 2007, Blackburn et al., 2005, Carthew et al., 2009 and Escher et al., 2010). While there

is no generally accepted TTC of local effects in the respiratory tract, TTC values for systemic toxicity may be applied and after modification take into account for route to route differences between the respiratory tract and other organ systems (e.g., absorption, metabolism). However, so far adequate TTC models for inhalation route are under development (Carthew et al., 2009) and may become relevant in future. The described common principles can be applied to safety assessment of cosmetic sprays based on classical elements of risk assessment. The approach described relies on understanding external, systemic and in particular respiratory tract exposure click here and dose, understanding assessing potential toxicities and determination of safe exposure levels. The safety assessors will benefit from having access to improved exposure models and to standardized safety assessment methodologies utilized for spray product evaluation without interfering with the flexibility of the individual safety assessors who are Sirolimus price responsible

for the safety of their products. This paper is intended to provide basic elements of a tiered safety assessment approach in order to increase transparency for regulators and reliability of results to the benefit of the consumer. It provides a recommendation to use these tools in the sense of a Weight-of-Evidence Approach when conducting the safety assessment. The Authors report no conflicts of interest. The Authors are employees of the companies Procter and Gamble,

KPSS-KAO Professional Salon Services GmbH, Beiersdorf AG, Henkel AG & Co. KGaA, L‘Oreal and the IKW (The German Cosmetic, Toiletry, Perfumery and Detergent Association). The Authors thank IKW for providing the discussion platform to develop this document. We thank K. Sarlo, and G. Nohynek as well as B. Hall, L. Merolla and PJ34 HCl W. Steiling as members of the Colipa Expert (ET) for Inhalation Toxicology & Exposure for the critical review of the manuscript. “
“Figure options Download full-size image Download as PowerPoint slide This Special Issue of Toxicology Letters is dedicated to Elsa Reiner in honor of her important contributions to the field of cholinesterases in their interactions with substrates, inhibitors and reactivators. Elsa Reiner had personal and scientific relationships with us and attended some of the International Medical Chemical Defence Conferences held at the Bundeswehr Medical Academy in Munich. Hence, we feel it highly appropriate to honor her memory at this occasion. Elsa Reiner was born in Osijek, Croatia, in 1930 where she spent her childhood before she moved with her parents to Zagreb. Here, she began to study chemistry and obtained her PhD degree in 1962.

A thrombus is formed by the aggregation of platelets on the fibrin clot mesh. Because of its ability to induce fibrinolysis, Batroxase reduced the size of an “in vitro” induced thrombus in a 50 μg treatment after 24 hours of incubation, and it completely degraded the thrombus in a 100 μg. With the same amounts, Leucurolysin-a from Bothrops leucurus ( Gremski et al., 2007) was also able

to dissolve a thrombus “in vitro”, with the maximal activity observed for a 100 μg treatment. Batroxase did not affect human platelet aggregation by the agonist ADP. This characteristic capacity has been reported for other PI-class SVMPs, such as Neuwiedase from Bothrops neuwiedi ( Rodrigues et al., 2001) because this class contains only a proteolytic domain. PII class SVMPs possess the proteolytic domain and a disintegrin domain that contains an RGD site that enables Selleck ZD1839 find more interactions with other integrins on platelet surface, thereby preventing platelet aggregation by agonists ( Calvette et al., 1991). In the PIII class SVMPs, such as in Basparin

A from Bothrops asper ( Loría et al., 2003), an additional cysteine-rich domain further facilitates platelet aggregation. Several snake venom metalloproteinases are capable of inducing an incoagulable plasma condition because of their ability to consume plasma coagulation factors (Kamigutti, 2005). Similar to other PI-class SVMPs, Batroxase did not induce plasma coagulation, which facilitates the hemorrhagic process. The primary sequence of Batroxase was determined by N-terminal amino acid sequencing by automatic Edman degradation, and the digested peptides CYTH4 obtained by trypsin proteolysis were sequenced by mass spectrometry. These analyses indicated that

Batroxase is composed of 202 amino acids. Additionally, a primary structure analysis showed that Batroxase lacks N-glycosylation sites (N-X-S/T); its zinc-binding motif (HELGHNLGISH) is fully conserved when compared with that of other SVMPs; and it contains a C164I165 M166 motif associated with a “Met-turn”. PI-class SVMPs may be sub-characterized according to disulfide bridge content (Fox and Serrano, 2005); PIa proteins such as HT-2 from Crotalus ruber ruber, have two disulfide bridges, whereas PIb proteins such as Fibrolase from Agkistrodon contortrix contortrix and Lebetase from Vipera lebetina ( Bello et al., 2006) have three disulfide bridges. Batroxase presented seven cysteine residues that are fully conserved with those in the other metalloproteinases, with matching such as Cys117–Cys197, Cys157–Cys181 and Cys159–Cys164. According to our tertiary structure analyses, Batroxase forms an α-β-α fold that is stabilized by three disulfide bridges (above) similar to those of other class PI SVMPs (Gomis-Rüth et al., 1994, Gong et al., 1998 and Akao et al., 2010) (Fig. 8).

It was created through a collaborative effort by Fisheries and Oceans Canada, the Inuvialuit, private industry and local stakeholders, made possible with enactment of Canada’s Oceans Act in 1997 (Fast et al., 2001 and Fast et al., 2005). The TNMPA consists of three MPAs within, Niaqunnaq in the west, Okeevik in East Mackenzie Bay and Kittigaryuit in Kugmallit Bay (Fig. 1).

The purpose of the TNMPA is to conserve and protect the biological resources within the Mackenzie Estuary, ensuring the viability of a healthy population of beluga whales (Delphinapterus AG-014699 datasheet leucas) and their habitats. While in the Mackenzie Estuary, these belugas have long been, and continue to be, the subject of an important traditional anti-EGFR antibody subsistence hunt conducted annually by the Inuvialuit of the western Canadian Arctic ( Nuligak, 1966, McGhee, 1988 and FJMC, 2013), a harvest which has been assessed by DFO as sustainable ( DFO, 2000). Collection

of, and access to accurate scientific information about beluga behaviour and habitat use in the TNMPA is crucial to ensure the conservation objectives are met, and that management decisions are evidence-based (Fast et al., 2001). Specifically, a better understanding is needed of outcomes of harvesting; the sources, extent and impacts of pollution and loss of habitat; and the implications of climate change and loss of biodiversity (Fast et al., 2001). Consulting with the stakeholders throughout the planning process (Fast et al., 2005), Canada finalized the monitoring protocols, indicators and strategies for the TNMPA in 2010 (Loseto

et al., 2010). Belugas aggregate in the warm, shallow waters of the Mackenzie River estuary during summer (Fraker et al., 1979 and Norton and Harwood, 1986) (Fig. 1). Use of the Estuary peaks in early to mid-July, and declines in late July (Fraker and Fraker, 1979, Norton and Harwood, 1986, Day, 2002 and Richard et al., 2001), as the distribution shifts to largely offshore in August (Norton and Harwood, 1985, Harwood et al., 1996 and Richard et al., 2001). The stock was last assessed as stable or increasing (DFO, 2000), numbering an estimated 39 258, with a coefficient of variation (CV) of 0.229 Histone demethylase (Hill and DeMaster, 1999). The belugas moult while they are in the TNMPA (St. Aubin et al., 1990 and Harwood et al., 2002), although the specific geographic locations within the TNMPA which promote moulting are not known. Identification and protection of protected marine areas encompassing critical habitats such as estuaries is a practice that is well-established globally (Hoyt, 2011 and WDC, 2014), with strategies that target ‘hot spots’ conferring the greatest conservation benefits (Ashe et al., 2009 and DFO, 2009). This has been undertaken for other stocks of belugas, in both Alaska (e.g., Cook Inlet: Hobbs et al., 2005; Carter and Nielsen, 2011; NOAA, 2014; Goetz et al., 2012, Ashford et al., 2013 and Ezer et al., 2013) and Canada (Gulf of St. Lawrence, Mosnier et al.

The wave direction was determined in the 8-rhumb system (directional resolution 45°) as the approach direction of the largest wave components. In order to remove the bias caused by a systematically larger number of observations per day during relatively

calm spring and summer seasons on the Estonian coasts, the analysis in the cited sources is based on the set of daily mean wave heights. Spatial patterns of wave properties and their changes in the course of time have been extensively studied during recent years based on numerical simulations and realistic wind patterns for the entire Baltic Sea (Cieślikiewicz & Paplińska-Swerpel 2008, Kriezi & Broman 2008, Räämet et al. 2009, 2010, Räämet & Soomere 2010a,b, Soomere et al. 2011). This research selleck kinase inhibitor has been complemented by studies of local wave properties and their temporal changes using simplified one-point wave models and locally measured winds (Suursaar & Kullas 2009a,b, Zaitseva-Pärnaste et al. 2009). A

combination of these approaches (a rapid method of calculation of the wave climate in small areas using high-resolution spectral wave models covering the entire Baltic Sea and one-point high-quality marine winds) has been developed selleckchem in Soomere (2005) and Laanearu et al. (2007). Relatively simple models (in particular, the so-called SMB model, also called the significant wave method, based on the fetch-limited equations of Sverdrup, Munk and Bretschneider (Seymour 1977) and forced by one-point wind data) have been applied in a number of recent studies. Such models calculate the basic wave properties under the assumption that the wind properties are

constant over the entire fetch area. As strong winds are frequently highly homogeneous in the Baltic Proper and both the reaction and memory time of a large part of the wave fields in this basin are relatively short (Soomere 2005), such simple models are valuable tools for rapid estimates of the wave statistics Rucaparib purchase and for deriving first approximations of the wave time series in this water body. The models usually need a certain tuning in order to compensate for the difference between the measured wind speeds from those on the open sea (Suursaar & Kullas 2009a,b, Suursaar 2010). They usually reproduce not only the basic wave statistics but also the time series of the wave properties at the calibration site (Zaitseva-Pärnaste et al. 2009). Such models only fail to reproduce remote swell and extreme wave conditions (which are rare in the Baltic Sea, Soomere 2008, Räämet et al. 2010) and some refraction-caused effects. The identification of spatial patterns in variations of wave properties generally requires the use of contemporary spectral wave models that are able to adequately follow the wave patterns over the entire sea. In general, the WAM model gives good results in the Baltic Sea if the model resolution is appropriate and the wind information is correct (Tuomi et al. 1999).

5B). Next, whether the increase in cell proliferation induced by NE was also mediated by β-ARs was assessed.

SCC9 cells were treated with propranolol before stimulation with 10 μM NE at 6 h, and cell proliferation was assayed by MTT. Inhibition of β-ARs produced significant decrease in NE-induced cell proliferation, showing that this event is β-AR-dependent (Fig. 5C). This decreasing in NE-induced cell proliferation after β-ARs inhibition also was found in the SCC15 cells (results not shown). Since NE may stimulate PLX4032 IL-6 production by OSCC, whether NE-induced OSCC proliferation is mediated by IL-6 was subsequently tested. To this end, anti-IL-6 ab was used to neutralize the action of IL-6 in SCC9 cells. As illustrated in Fig. 5C, treatment of SCC9 cells with 10 μg/mL of anti-IL-6 induced significant inhibition of NE-induced proliferation (p < 0.05). Anti-IL-6

in lower concentration (1 μg/mL) was not able to inhibit NE-induced proliferation ( Fig. 5C). Recombinant IL-6 increased SCC9 cell proliferation (data not shown). To determine the clinical relevance of our results, expression of β1- and β2-ARs mRNAs were examined in 20 tumor specimens of OSCC and compared with the expression in 17 specimens of oral leukoplakia and 15 specimens of normal oral mucosa. Clinical characteristics of patients from whom samples were obtained are summarized in Table 1. β1- and β2-AR mRNAs were expressed in all 20 cases of OSCC. Of the 17 cases of leukoplakia, five

were negative for β1-AR and one was negative for β2-AR. Of the 15 specimens of normal mucosa, three did not express β1-AR and one was negative for β2-AR. Quantitatively, the mean expression Akt inhibition of the β1-AR mRNA levels in OSCC specimens was 2.7-fold higher compared to normal mucosa (p < 0.05), while in specimens of leukoplakia the expression was 1.6-fold higher (p > 0.05) ( Fig. 6A). In contrast, β2-AR mRNA mean expression was lower in leukoplakia compared to normal mucosa and OSCC, but these results were not significant ( Fig. 6A). The β-AR expression for each studied case can be better seen in Fig. 6B and C. This study provides strong evidence that OSCC cells are influenced by neurohormonal mediators. The results demonstrated that stress-related mediators (NE and isoproterenol) mafosfamide can enhance the production of the pro-angiogenic cytokine IL-6 in human OSCC cell lines. IL-6, originally identified as a B-cell growth factor, is produced by many cell types, including T-cells, macrophages, and stromal cells. As seen in this study, OSCC cells are also capable of producing IL-6, and basal levels are already detectable at 1 h. Secreted cytokine products, including IL-6, are available to interact with cellular receptors; thus, they are able to exert paracrine or autocrine effects. The concentrations of IL-6 secreted by OSCC cells in this study, even by non-stimulated cells, are clearly within the range expected to have biological activity.

The proportion of cells with loss of membrane integrity and fragmented DNA was determined by flow cytometry using a FACSCalibur equipment (Becton and Dickinson System, San Juan, California, USA), as previously described (Jaroszeski and Radcliff, 1999 and de Lima et al., 2007). ECV-304 cells were treated with FA for 24 h, than the slides were washed, fixed and stained with

oil red O as previously described (Pearse, 1960). The slides were examined by light microscopy at 510 nm (Carl Zeiss Vision, Munchen-Hallbergmoos, Germany). Images were taken at 20× magnification www.selleckchem.com/products/MDV3100.html and a representative image is shown (Fig. 2 and Fig. 4C). Cells were treated with the FA for 30 min. After treatment, the cells were incubated with hydroethydine (1 μM) for 30 min at room temperature in the dark. Cells were visualized in a fluorescence microscope (Carl Zeiss Vision, Munchen-Hallbergmoos, Germany), using the 590/46 nm filter and analyzed by fluorescence intensity using the KS 300 software. For quantification of ROS production images were taken at 20× magnification from 10 random fields of view for each well and were analyzed by fluorescence intensity using the KS 300 software. Values of the areas were http://www.selleckchem.com/products/BEZ235.html averaged to obtain the mean values. A representative

image is shown (Fig. 2 and Fig. 4D). Results are presented as means ± SEM of 6–9 determinations from 2 to 3 experiments. Statistical analysis was performed by using one-way ANOVA and Tukey’s test (Graph Pad Prism 5; Graph Pad software) as indicated. 3-oxoacyl-(acyl-carrier-protein) reductase The level of significance was set at p < 0.05. Treatment with SA for 24 h decreased the proportion of viable cells by 18% at 150 μM, 9% at 200 μM and 11% at 250 μM, as compared to vehicle (Fig. 1A). The proportion of cells with DNA fragmentation was increased by 3-fold due to treatment with SA at 150 μM, by 3.5-fold at 200 μM and 4-fold at 250 μM for 24 h, as compared to vehicle (Fig. 1B). The treatment with SA at 150 and 200 μM for 24 h did not change the content of lipids but at 250 μM decreased it by 25% compared to

vehicle (Fig. 1C). ROS Production was increased by approximately 2-fold due to SA treatment either at 150, 200 and 250 μM, as compared to vehicle (Fig. 1D). Treatment with SA and the association with PUFA (ω-3 and ω-6) for 2 and 6 h did not alter the viability and the percentage of cells with DNA fragmentation compared to vehicle (data not shown). Treatment with SA for 24 h decreased the proportion of viable cells by 18% at 150 μM as compared to vehicle (Fig. 2A). The combination of SA with DHA at 100 μM decreased still further the proportion of viable cells by 19% as compared to SA. On the other hand, the association of SA with EPA at 50 and 100 μM increased the proportion of viable cells by 12% and 9%, respectively, compared to SA. ω-6 FA (LA and γA, at 50 and 100 μM) increased the proportion of viable cells in the presence of SA by 20% as compared to SA (Fig. 2A).

, 2004a; De Castro Bastos et al., 2004, Bohrer

et al., 2007 and Nascimento-Silva et al., 2012). Despite understanding the mechanisms involved in the hemorrhagic syndrome, little is known about the systemic physiopathological click here effects induced by L. obliqua venom. Although venom components have been detected in several organs (including the kidneys, lungs, liver, spleen, heart and skeletal muscle) of rats following a single subcutaneous injection of the venom, the systemic tissue damage in these organs remains poorly characterized ( Rocha-Campos et al., 2001 and Da Silva et al., 2004b). For example, the current level of knowledge regarding the kidney damage is based only on a few clinical case reports in which hematuria and high levels of serum creatinine are described as the main features of L. obliqua-induced AKI ( Burdmann et al., 1996). The venom-induced pathology in other organs remains completely unknown. In human patients, the impossibility of conducting early tissue biopsies, due to the coagulation disturbances inherent to the envenomation, has made it difficult to analyze the acute anatomopathological alterations. For these reasons, we believe that animal models of envenomation may be useful not only to characterize the underlying physiopathology but also to identify previously

unknown toxic activities of the venom. Therefore, the aim of the present work was PD-1 antibody inhibitor to develop a rat model to study systemic tissue damage during L. obliqua envenomation. An array of acute effects of the venom was characterized, including biochemical, hematological, histopathological, myotoxic and genotoxic alterations. In summary, our data indicate that in addition to hemostatic abnormalities, there are Ribose-5-phosphate isomerase also signs of multi-organ damage, mainly in the lungs,

heart, kidneys and spleen. Treatment with ALS is only effective at counteracting the systemic physiopathological effects if it is administered during the initial phase of envenomation. In addition, this study provides the first experimental evidence of the cardiotoxic, myotoxic and genotoxic activities of L. obliqua venom. L. obliqua caterpillars were kindly provided by the Centro de Informações Toxicológicas (CIT), Porto Alegre, Rio Grande do Sul, Brazil. The specimens used in this study were collected in the cities of Bom Princípio (Rio Grande do Sul, Brazil) and Videira (Santa Catarina, Brazil). L. obliqua venom was obtained by cutting the bristles at the caterpillar’s tegument insertion, and the excised material was kept at 4 °C prior to the preparation of the extract, which occurred immediately after dissection. The bristles were macerated in cold phosphate-buffered saline (PBS), pH = 7.4, and centrifuged at 9600 × g for 20 min.

Histological examination showed signs of acute cellular rejection in the allografts of both WT and Vav1AA/AA recipient mice, but enhanced fibrosis present in the Vav1AA/AA allografts indicates progression to a more

chronic stage of rejection compared to acutely rejected WT allografts (Fig. 6). This is in line with the observed histological features including acute cellular rejection and interstitial fibrosis for Vav1−/− mice with an allograft survival time below 100 days [23]. Antibody-mediated rejection seems to require Vav1 GEF activity, as the formation of alloantibodies is almost absent in transplanted Vav1AA/AA mice (Fig. 5). Antibody levels do not correlate with graft survival times in individual Selleck GSK1120212 animals, suggesting that the variations in graft survival time are caused by different mechanisms. Vav1 has been implicated in T cell dependent antibody formation, and it would be interesting to PR-171 see if the GEF function

of Vav1 is required for general antibody responses [30] and [31]. Correct migration and localization of activated T cells to antigenic tissue are essential for developing an immune response. Vav1 has been implicated in SDF-1-dependent cell migration, and has been shown to be important for the retention of T cells at the sites of inflammation [32] and [33]. Vav1−/− T cells fail to form sustained interactions with local APCs which reduce their ability to initiate a local immune response. Integrin-mediated adhesion and APC–T cell Forskolin purchase conjugate formation require Vav1 and its GEF activity, which may be a mechanism by which Vav1 GEF activity contributes to allograft rejection [20]. Costimulation is an important factor for allogeneic T cell activation, and blockade of costimulatory

pathways has shown promising results in preventing transplant rejection [5]. Vav1 has been shown to link CD28 costimulation to T cell activation [34], [35] and [36]. The GEF function of Vav1 could contribute to its role downstream of CD28, as Vav1 can enhance CD28-induced activation of transcription factors like NFκB via a Rac-dependent pathway [37]. In addition, CD3/CD28-induced proliferation and activation of T cells in vitro requires Vav1 GEF activity (Fig. 1) [20]. However, other costimulatory signals like ICOS, complement or OX40 contribute to T cell activation during graft rejection [5]. Whether Vav1 and its GEF function are involved in these different costimulatory signaling events has not been clarified yet. It is possible that Vav1 transmits different costimulatory signals independently of its GEF activity, which may partially account for the difference in graft survival between Vav1−/− and Vav1AA/AA mice.

, 2000 and Ferdinandusse et al., 2002). We have also to take into account that a considerable fraction of the supplemented exogenous Prist was possibly bound to proteins

present in the incubation medium, leaving a smaller portion of this acid compound free to react and exert its effects. On the other hand, we have recently described that phytanic acid (Phyt), which also accumulates in some peroxisomal disorders, provokes oxidative damage to lipids and proteins and reduces the non-enzymatic antioxidant defenses, Selleckchem Buparlisib besides impairing bioenergetics in rat brain (Busanello et al., 2010 and Leipnitz et al., 2010). However, the oxidative effects exerted by Phyt were moderate and occurred with higher doses supplemented to the incubation medium Angiogenesis inhibitor as compared to those caused by Prist. This is in line with previous findings obtained in cultured neural cells demonstrating that induction of reactive oxygen species generation by Prist is greater than that provoked by Phyt (Ronicke et al., 2009). In conclusion, to our knowledge, this is the first report showing that Prist that accumulates in some peroxisomal disorders provokes lipid and protein oxidative damage and diminishes the

antioxidant defenses in the cerebral cortex. However, additional studies performed in intact neural cells and in animal models of peroxisomal disorders are required to confirm the role of oxidative stress in the pathophysiology of these diseases.

In case the in vitro effects detected in the present study are confirmed in vivo and also in tissues from affected patients, it is tempting to speculate that the administration of antioxidants should be considered as an adjuvant therapy for these patients. Wistar male rats of 30 days of life obtained from the Central Animal House of the Department of Biochemistry, ICBS, Universidade Federal do Rio Grande do Sul, Porto Alegre, RS, Brazil, were used. The animals were maintained on a 12:12 h light/dark cycle (lights on 07.00–19.00 h) in air conditioned constant temperature (22 ± 1 °C) colony room, with free access to water and 20% (w/w) protein commercial chow (SUPRA, Porto Alegre, RS, Brazil). The experimental Urocanase protocol was approved by the Ethics Committee for animal research of the Federal University of Rio Grande do Sul, Porto Alegre, Brazil and followed the Principles of Laboratory Animal Care (NIH publication 85-23, revised 1996). All efforts were made to minimize the number of animals used and their suffering. All chemicals were purchased from Sigma (St. Louis, MO, USA). Prist solution was prepared on the day of the experiments in the incubation medium used for each technique and pH was adjusted to 7.4.

We calculated height-for-age Z-score according to the United States Centers for Disease Control standards of recumbent length Z-scores, birth to 24 months, and stature

Z-scores, 2–20 years in centimeters, by gender and age. 10 Fourteen eGFR equations were included and their respective values for 81 patients were compared against the mGFRs. This retrospective study was approved by the Lurie Children’s Hospital of Chicago Institutional Review Board. We measured iohexol in Navitoclax serum by a validated liquid chromatography tandem mass spectroscopy method from 4 serial blood samples collected at 10, 30, 120, and 300 minutes postiohexol injection with the clearance calculated using the concentration of iohexol as a function of time in 2 curves (fast and slow plasma disappearance).9 Scr was measured using an isotope-dilution mass spectrometry (IDMS)-traceable enzymatic method on the Roche Cobas

6000, following the Food and Drug Administration cleared procedure for Roche or Hitachi Cobas C systems. Blood urea nitrogen and cystatin C were analyzed in serum on the Roche Cobas 6000, following the Food and Drug Administration cleared procedures for Roche or Hitachi Cobas AP24534 research buy C systems. The cystatin C method on the Roche Cobas 6000 uses an automated particle-enhanced immunoturbidimetric assay (PETIA). A total of 14 eGFR equations were selected to calculate eGFR (Table I). These include 5 equations based on Scr alone, 5 based on Scys alone, and 4 based on combinations of both. The method of testing Scys was particle-enhanced nephelometric immunoassay (PENIA) in Filler et al,16 Bouvet et al,17

Chehade et al,18 and Schwartz et al4 and 11 equations. The others used the PETIA method. The method of testing Scr was Jaffe method in Gao et al,12 Bouvet et al,17 and Chehade et al18 equations. The others used the enzymatic assay. Continuous data were described as the mean ± standard deviation, median, and interquartile range (IQR), and categorical variables were expressed as cases or percentages. Differences between eGFR and mGFR were analyzed by the nonparametric Wilcoxon test, because the data were not normally Nintedanib (BIBF 1120) distributed. Correlations between eGFR and mGFR were established based on the Spearman correlation. Bland-Altman analysis was used to compare eGFR with mGFR using the average of the overall mean ± standard deviation and the precision was represented as the width between the 95% limits of agreement, wherein the smaller the limits of agreement, the greater the precision. Regression analysis and scatterplot analysis were used to compare the agreement between eGFR and mGFR. Three parameters used to assess the performance of eGFR equations relative to mGFR were as follows: • Bias (median difference between mGFR and eGFR) and absolute bias (median difference in |mGFR − eGFR|; We selected P < 0.05 a priori to be statistically significant.