bluuebunny/crossref_metadata_2025_split huggingface dataset:
MO271: A Single Dose of Lithium Protects Against Renal Injury Following Bilateral Ureteral Obstruction
Authors: Heloisa Massola Shimizu Maria , Aparecido Volpini Rildo , Carolina de Braganca Ana , Moura Nascimento Mariana , Bernardo Desiree , Canale Daniele , Carlos Seguro Antonio 
Published: May 2022

Abstract

BACKGROUND AND AIMS
Obstructive nephropathy decreases renal blood flow (RBF) and glomerular filtration rate (GFR). Glycogen synthase kinase 3β (GSK3 β), an apoptotic enzyme, is increased in a model of unilateral obstruction. Treatment with a single dose of lithium, a selective inhibitor of GSK3β, accelerated recovery of renal function in models of cisplatin and ischemia-reperfusion induced acute kidney injury (AKI). The aim of this study was to evaluate the efficacy of a single dose of lithium in the treatment of AKI induced by bilateral ureteral obstruction (BUO)

METHOD
Adult male Wistar rats were divided in four groups: (i) sham (sham operated); (ii) lithium: rats treated with lithium chloride 80 mg/Kg BW Intraperitonially (IP); (iii) BUO during 24 h; (iv) BUO during 24 h and treated with the same dose immediately after ureteral desobstruction. The rats were anesthetized 48 h after desobstruction to measure inulin clearance and renal blood flow. At the end of the clearance experiments, the rats were euthanized and the kidneys were removed to measure GSK3 β renal expression.

RESULTS
As described in the Table 1, BUO showed markedly reduction of GFR and RBF associated with an increase of GSK3β. A single dose of lithium administration ameliorated all these alterations.

CONCLUSION
Lithium treatment attenuated renal dysfunction in this model of BUO-associated AKI by improving inulin clearance. These therapeutic effects were due to an inhibition of renal expression of GSK3β. This may be a new therapeutic approach for BUO-induced AKI.
MO272: Effect of the Hollow Fiber Diameter and Membrane Surface Area of the Polymethyl Methacrylate Membrane Filter Used in Continuous Renal Replacement Therapy on the Lifetime of the Filter
Authors: Kurihara Yoshitaka , Kobayashi Yuta , Ushiroda Yosuke , Ueki Shunichi , Tsukao Hiroshi , Kobayashi Kozue , Kokubo Kenichi , Kubota Masaru , Kobayashi Hirosuke 
Published: May 2022

Abstract

BACKGROUND AND AIMS
When polymethyl methacrylate (PMMA) membranes are used in renal replacement therapy, inflammatory cytokines and other substances are removed by adsorption. However, these filters are also prone to clogging and the filter lifetimes are likely to be short. In the present study, we investigated the effects of the hollow fiber inner diameter and membrane area of PMMA membranes on the filter lifetime and protein removal performance using an in vitro continuous hemofiltration (CHF) experimental model with porcine blood.

METHOD
Three filters with different hollow fiber inner diameters and membrane areas were used: CH-1.0N (membrane area, 1.0 m2; hollow fiber inner diameter, 200 µm), CH-1.0W (prototype: 1.0 m2; 240 µm), and CH-1.8W (1.8 m2; 240 µm). Blood samples from one pig were divided into three portions, and in vitro CHF experiments for each filter were performed at QB = 100 mL/min and QS = QF = 10 mL/min. The pressure changes, total protein concentration in the blood, and total protein amount in the filtrate were measured during the experiments. From the results of the pressure changes, the time for the TMP to reach 200 mmHg (corresponding to the time when the membrane pores were clogged) and the time for the pressure drop through the filter to reach 200 mmHg (corresponding to the time when the hollow fibers were clogged) were calculated as the filter lifetime for comparative evaluation.

RESULTS
The time for the TMP to reach 200 mmHg was significantly longer with CH-1.8W than that with CH-1.0N or CH-1.0W (Friedman test, P &lt; .05, n = 15). The time for the pressure drop through the filter to reach 200 mmHg was significantly longer with CH-1.8W than that with CH-1.0N or CH-1.0W (Friedman test, P &lt; 0.05, n = 15). The results suggest that an increased membrane surface area is an essential factor for extending the filter lifetime. The total protein adsorption was significantly higher for the CH-1.0W and CH-1.8W filters than for the CH-1.0N filter (two-way ANOVA and post hoc Tukey test, P &lt; 0.01, n = 15). Thus, the membranes with larger hollow fiber inner diameters (CH-1.8W and CH-1.0W) adsorbed more protein.

CONCLUSION
A larger membrane area contributes to a longer filter lifetime, whereas increase in the hollow fiber inner diameter does not. On the other hand, the protein removal performance, especially the adsorption performance, was higher for membranes with larger hollow fiber inner diameters.
MO274: Vancomycin Adsorption During In Vitro Model of Hemoperfusion with Mini-Module of HA380 Cartridge
Authors: Lorenzin Anna , de Cal Massimo , Sorbo David , Ronco Claudio , Zanella Monica 
Published: May 2022

Abstract

BACKGROUND AND AIMS
Septic shock is one of the most frequent causes in Intensive Care Unit (ICU) admission and is related to a very high risk of mortality. About one-third of patients with sepsis develops AKI which contributes to a worsening prognosis. AKI due to sepsis is the result of a dysregulated host immune response to infection, with the production of inflammatory mediators and cytokines that cause haemodynamic alterations, endothelial damage, apoptosis and, finally, immunoparalysis. The new Jafron HA380 cartridge has been specifically designed for use in clinical conditions characterized by cytokine storm such as sepsis. Given the growing application of these devices in cases of septic AKI in ICU, an unsolved problem is whether these polymers adsorb drugs, including antibiotics.
In vitro experiments were conducted to determine its adsorption capacity toward Vancomycin antibiotic.

METHOD
In vitro circulation was performed using a dedicated testing platform Galileo. A customized cartridge was built assembling mini-module components scaled in dimension toward HA380 and filled with 75 g of HA380 beads (25% of the regular size cartridge). Peristaltic pump was set at 250 mL/min. we performed two circulation containing extremely high quantity of Vancomycin (5 g in 500 mL and 10 g in 1000 mL) for 300 minutes. Samples were collected every 20 minutes. Vancomycin concentrations were measured.
The adsorption isotherm was represented using the equation: Massadsorbed = RR × Massinjected, where the RR in the Vancomycin removal ratio.

RESULTS
In vitro circulation confirms the affinity of beads material in binding Vancomycin molecules. The kinetics of vancomycin adsorption shows a rapid decay of the concentration in the first part of the experiments, after which we can observed a plateau (Fig. 1a). A total of 4500 mg of the 5000 mg were adsorbed in the end of the experiment (RR = 94%), of which 90% in the first 40 minutes (RR = 87%); after this period the curve became flat and the adsorption phenomenon negligible (Fig. 1b).
In the experiment with 10 000 mg, after 60 minutes of rapid adsorption (RR = 55%), the curve reached a plateau converging to a RR higher than 60% (Fig.). The sorbent beads were able to bind 6100 mg toward 10 000 mg injected. This amount saturated the mini-module binding sites.

CONCLUSION
The application of HA380 mini-modules allowed to determine the amount of Vancomycin necessary to reach the saturation of the sorbent material. Based on the obtained results, we estimated that the cartridge HA380 could retain more than 24 g of Vancomycin during HP circulation. Further investigation is needed to validate our results and to better understand HA380 performance in clinical practice.
MO280: Osteoblast-Specific Deletion of MEMO1 in Mice Severely Impairs the Expression of FGF23
Authors: Moor Matthias , Bartos Katalin 
Published: May 2022

Abstract

BACKGROUND AND AIMS
Memo deletion in mice caused a bone disease with diminished osteoblast and osteoclast biomarkers in serum [1], resembling the alterations occurring in adynamic bone disease in humans with renal failure, as well as those found in Klotho-deficient mice [2]. In addition, FGFR signaling is impaired in Memo-deficient osteoblasts [1]. We previously detected lower Fgf23 expression in cultured Memo-deficient osteoblasts, as the expression of FGF23 by bone cells requires autocrine or paracrine FGFR/Klotho signaling [3]. Here, we demonstrate that Memo1 in osteoblasts is required for Fgf23 expression in murine bone.

METHOD
Exon 2 of the Memo1 gene was deleted in the osteoblast–osteocyte lineage in Memo fl/fl mice using a Cre recombinase under the Col1a1 promotor to obtain osteoblast-specific knockout (obKO) mice. Memo obKO and Cre-negative littermate control mice were genotyped by tail genomic DNA. Organs were studied by microcomputed tomography, by qPCR and Western blot. Memo obKO and littermate control mice were challenged with acute kidney injury.

RESULTS
Memo obKO were viable without changes in gross anatomy. Weight at weaning age was transiently impaired in male but not in female Memo obKO compared with littermate controls (Fig. 1A). Memo1 expression was blunted in the femur of Memo obKO (Fig. 1B), whereas it remained comparable to controls in kidney (Fig. 1B) and liver tissues. Micro-CT revealed no differences between genotypes in trabecular or cortical bone of vertebrae, femur and tibia (Table 1). FGF23 gene expression by qPCR was undetectable in the femur of Memo obKO mice (Fig. 1C). Western blotting revealed a decrease of FGF23 protein in females and a tendency to lower expression in males of the Memo obKO genotype.

CONCLUSION
These findings demonstrate a role of Memo in the osteoblast–osteocyte lineage in contributing to the normal expression of FGF23. These data expand previous findings of FGFR-Klotho dependent regulation of FGF23 expression by the bone.
MO286: MIR-155 Deficiency Protects Renal Tubular Epithelial Cells from Telomeres and Genomic DNA Damage in Cisplatin-Induced Acute Kidney Injury
Authors: Yin Qing , Wang Bin , Liu Bicheng 
Published: May 2022

Abstract

BACKGROUND AND AIMS
Cisplatin nephrotoxicity is an important cause of acute kidney injury (AKI), limiting cisplatin application in cancer therapy. Growing evidence had suggested that genome instability, telomere dysfunction and DNA damage were involved in the tubular epithelial cells (TECs) damage in cisplatin-induced AKI (cAKI). However, the exact mechanism is largely unknown.

METHOD
We subjected miR-155-/- mice and wild-type controls, as well as human proximal tubule cells, to cisplatin-induced AKI models. We assessed kidney function and injury with standard techniques and measured telomere by the fluorescence in situ hybridization.

RESULTS
Our study demonstrated that miR-155 deficiency significantly improved renal function and attenuated pathological damage and mortality during cAKI. Furthermore, miR-155 inhibition reduced cisplatin-induced TECs apoptosis, genome instability, telomere dysfunction and DNA damage both in vivo and in vitro. The miR-155 inhibition mediated protective effects may be caused by increasing expression of telomere repeat binding factor 1 (TRF1) and cyclin-dependent kinase 12 (CDK12), thereby limiting the telomere dysfunction and the genome DNA damage in cAKI.

CONCLUSION
We demonstrated that inhibition of miR-155 ameliorates AKI involving the targeting and regulation of TRF1 and CDK12, indicating a novel regulatory mechanism and elucidating a potential target for cisplatin-induced AKI treatment.
MO299: Profile Of COVID-19 Patients who Developed Acute Kidney Injury in Intensive Care: Multicentre Study
Authors: Afifi Rania , Maazouzi C , Medkouri G , Elkhayat Ss , Mtioui N , Zamd M , Ramdani B , Benghanem M 
Published: May 2022

Abstract

BACKGROUND AND AIMS
The SARS-COV-2 acute respiratory distress fyndrome, which is the source of the infection known as coronavirus disease (COVID-19), spread rapidly, causing a pandemic that not only severely affected human health but also restricted the activities of daily living and weakens the global economy. Organs other than the lungs can be affected, including the kidneys. The incidence of acute kidney injury (AKI) in hospitalized patients with COVID-19 disease has been reported to range from 0.5% to 80%; thus, a better understanding of the pathophysiology of AKI during COVID-19 is crucial to manage and improve the survival of patients who develop an acute kidney injury (AKI) attributed to COVID-19 is a common complication of severe cases and is further associated with high mortality; and there is glomerular involvement associated with COVID-19, characterized in some cases by collapsing glomerulopathy or by tubular necrosis in other cases. The objectives of our study are to determine the incidence and describe the risk factors as well as the evolution of AKI in patients admitted for pulmonary infection with COVID-19 in intensive care unit.

METHOD

RESULTS
Our study included 4261 patients hospitalized in intensive care in the different cities of Morocco; among them, 1495 (1/3) presented an AKI or 35.09%, the average age of our patients was 68.5 years or (25–99), with a male predominance or a sex ratio of 3 men to a woman.
There is hypertension in 80% of cases, diabetes in 75% of cases, the association of hypertension and diabetes in 63% of cases, coronary heart disease in 10%, epilepsy in 1% and lymphoma in 0.5% of cases.

CONCLUSION
AKI is a complication that appears to be common in patients with severe SARS-CoV-2 infection, associated with a poor prognosis. Nephroprotection measures should be put in place to prevent the occurrence of AKI. Any patient hospitalized with SARS-CoV-2 should undergo an initial nephrologic evaluation, including proteinuria and urine sediment examination.
MO323: Effects of Patient Frailty and Comorbidity on Duration of Hospitalisation as an Outcome Among Adults With Acute Kidney Injury
Authors: Lobo Aquiline , Waters Christopher , Aspin Nicola , Dasgupta Tanaji 
Published: May 2022

Abstract

BACKGROUND AND AIMS
Acute kidney injury (AKI) is commonly associated with an adverse outcome in hospitalised patients. Frailty and comorbidity are risk factors for acute kidney injury. The aim of this study was to assess the strength of association between frailty and comorbidity as modifiers for duration of hospitalisation (LOS) as an outcome among inpatients with acute kidney injury in our institution.

METHOD
A retrospective observational study as part of a service assessment of adult inpatients, in a 1-month period, during the pre-pandemic phase was conducted to evaluate for changes needed to existing care pathways in our institution. AKI was identified with the help of the national algorithm endorsed by NHS England, which is incorporated in hospital reporting systems. Clinical frailty and comorbidity were estimated using the Rockwood Clinical Frailty Scale (CFS) and the Charlson comorbidity index (CCI). Pairwise correlations between LOS, CFS and CCI were estimated and tested for statistical significance using Bonferroni-adjusted significance levels. Ordinary least-squares linear regression was used to assess the prediction of LOS using CFS and CCI in separate models.

RESULTS
In 148 patients in our cohort, the mean age was 76.4 [95% confidence interval (95% CI) 74.1–78.8] years. Of these, 54% were male, 24.3% were diabetic, 29.7% had at least one criterion for prior vascular disease and 16.2% had a history of cancer. A total of 22.3% had a prior history of chronic kidney disease. In terms of severity at presentation, 67.6% had stage 1 AKI, 18.9% had stage 2, and 13.5% had stage 3 AKI.
The mean CCI was 5.4 (95% CI 5.06–5.81) and the mean RFI was 4.6 (95% CI 4.3–5.0). 50% were both at least moderately frail (CFS ≥ 5) and had a CCI of &gt;5.
The mean duration of hospitalisation was 8.7 days.
Spearman's correlation coefficient constant for CFS with LOS was 0.23 and was 0.11 with CCI, with only the correlation between LOS and CFS being statistically significant at the 5% level after Bonferroni correction. As expected, there was a statistically significant correlation between CCI and CFS (0.49). Beta coefficients for ordinary least-squares linear regression individual models with LOS as the outcome variable were 0.69 (95% CI 0.18–1.19; P &lt; .007) for CFS and 0.27 (95% CI –0.16 to 0.70; P = .22) for CCI.

CONCLUSION
Compared with patient comorbidity, clinical frailty has a stronger and statistically significant association with the duration of hospitalisation among hospitalised adults with AKI. This study quantifies the magnitude of factors over and above those resulting from patient comorbidity that are contributory to frailty in adult inpatients with AKI. Further studies are required to improve understanding of how clinical frailty affects duration of hospitalisation in patients with AKI, to help inform future clinical care pathways and improve duration of hospitalisation as a clinical outcome.
MO368: Study of Relationship Between Some Biomarkers of Inflammation and Microbiomal Status in Patients With Chronic Kidney Disease
Authors: Olimkhonova Komilakhon 
Published: May 2022

Abstract

BACKGROUND AND AIMS
In view of the fact that the human microbiota varies depending on many factors, including comorbid pathology, it seems reasonable to investigate the intestinal microbiota in patients with chronic kidney disease and its likely relationship with markers of systemic inflammation.

PURPOSE OF THE STUDY
To reveal the relationship between some biomarkers of inflammation with changes in the composition of the intestinal microbiota in patients with chronic kidney disease.

METHOD
The study included 85 patients with CKD C 2–4. The average age of the patients was 52 ± 4 years (48 men and 37 women). The control group consisted of 30 healthy volunteers aged 50 ± 3 years, 15 men and 15 women, comparable to the main group in terms of gender and age. Blood samples were taken using standard methods. GFR was assessed using the CKD-EPI formula (2011). In addition, biomarkers such as interleukin-6 (IL-6), tumor necrosis factor alpha (TNF-α) were evaluated. Bacteriological examination of feces was carried out in the bacteriological laboratory of the third clinic of the TMA. Markers of systemic inflammation were assessed on the basis of an increase in the level of leukocytes (&gt;11 × 109/L), C-reactive protein (&gt;5.0 mg/L) by the immunoturbodimetric method, fibrinogen (&gt;4.0 g/L), as well as interleukin-6 by enzyme immunoassay. Differences between groups were considered statistically significant at P&lt;0.05; correlation analysis was performed using Spearman’s nonparametric rank correlation method.

RESULTS
Analysis of fecal matter showed a deficiency of Bifidobacterium bacteria (&lt;108 CFU) in the examined patients. In addition, the examined patients showed an increase in the number of Escherichia (&gt;108 CFU). According to the results of the study, in the group of CKD patients, the level of inflammatory markers was higher (CRP: 55%, IL-6: 60%, leukocytes 62%) than in the control group (CRP: 45%, IL-6: 40%, leukocytes: 38%).
In men, the IL-6 index was higher than in women. The results of the study demonstrated that in patients with CKD, an imbalance of the intestinal microbiota is combined with an increased level of CRP, IL-6 and leukocytes.

CONCLUSION
The study of markers responsible for proinflammatory effects in the body showed that such indicators as IL-6, CRP, fibrinogen showed a significant correlation with the composition of the microbiota in patients with CKD.
MO374: Urinary Cell Transcriptomics Provides a Non-Invasive Readout of Kidney Genes Essential to Renal Health and Disease
Authors: Eales James , Bogdanski Pawel , Wystrychowski Wojciech , Zukowska-Szczechowska Ewa , Zywiec Joanna , Woolf Adrian S , Samani Nilesh J , Keavney Bernard , Charchar Fadi , Tomaszewski Maciej 
Published: May 2022

Abstract

BACKGROUND AND AIMS
Chronic kidney disease affects up to 15% of adults, current diagnostic methods for assessing kidney health and early detection of renal disease lack sensitivity and/or can be highly invasive. The kidney sheds cells into the urine and harvesting these cells and their transcriptomic profile could yield non-invasive insights into genes responsible for maintenance of kidney health and early detection of kidney disease.

METHOD
Cell pellets were isolated from 200 mL of fresh morning urine from 33 participants, samples were spun at 3000 g for 10 min, washed and then resuspended in PBS. Each urinary cell pellet was then profiled by standard Illumina poly-A RNA-sequencing, generating an average of 30 million paired reads per sample. These were quantified using the standard GTEx quantification pipeline and were compared against 43 different human tissues and other bodily fluids.

RESULTS
Detailed RNA-sequencing metric analysis revealed that urinary cell pellets can generate reliable data of comparable or better quality than saliva and cerebrospinal fluid at similar read coverage. The one hundred most highly expressed urinary cell genes show an enrichment for immunity (P = 1.2 × 10–7), glucose metabolism (P = 1.3 × 10–5) and renal mineral absorption (P = 9.8 × 10–4); themes shared with the renal transcriptome. Across all protein-coding genes, kidney cortex (r2 = 0.65) and kidney medulla (r2 = 0.64) showed the highest level of correlation with the urinary transcriptome in an analysis of 43 human tissues. The correlation between urinary cells and the kidney was particularly strong (r2 = 0.72) in an analysis restricted to highly specific kidney genes (including UMOD, KCNJ1 and SLC12A1 all known for their role in kidney health and disease).

CONCLUSION
Poly-A RNA-sequencing of cells harvested from human urine can yield high quality gene expression profiles that correlate with transcriptional activity of the kidney. RNA-sequencing-based profiling of urinary cells offers a completely non-invasive route to assessing the expression of kidney genes of key relevance to renal health and disease.
MO379: Collagen-Derived Peptides in CKD: A Link to Fibrosis
Authors: Mavrogeorgis Emmmanouil , Mischak Harald , Latosinska Agnieszka , Vlahou Antonia , Schanstra Joost , Siwy Justyna , Jankowski Vera , Beige Joachim , Jankowski Joachim 
Published: May 2022

Abstract

BACKGROUND AND AIMS
Collagen is a major component of the extracellular matrix (ECM) and has an essential role in the onset and progression of fibrosis and chronic kidney disease (CKD). Collagen alpha-1(I) (col1a1) is the most abundant collagen type in humans and the involvement of col1a1in CKD onset and progression is well established. We aimed to assess in detail the association of urinary col1a1 fragments with the progression of CKD and ageing.

METHOD
About 5000 urinary peptidomic datasets from healthy participants and CKD patients were retrieved from the ‘Human Urinary Proteome Database’. Inclusion criteria were age &gt;18 years and eGFR being available. Urinary col1a1 fragments were identified and their abundance and correlation with eGFR and age were investigated.

RESULTS
Of 707 specific col1a1 peptides, 63 were significantly and highly positively associated with eGFR, while only six peptides showed a significant and strong negative association. A similar tendency was observed for ageing, where the abundance of most of the 244 peptides significantly associated with age, decreased with increasing age. The ten most significantly correlated peptides associated with eGFR corrected for age or age in a cohort matched for eGFR are listed in the table.

CONCLUSION
The results show a strong association between the reduced abundance of urinary collagen peptides and loss of kidney function as well as ageing. The data suggest that the col1a1 peptides indicate reduced degradation of collagen in CKD and aging. The results further suggest that fibrosis, potentially also of other organs, may be the consequence of attenuation of collagen degradation, and not increased synthesis.