bluuebunny/crossref_metadata_2025_split huggingface dataset:
P0550ISCHEMIC PRECONDITIONING ATTENUATES RENAL ISCHEMIA-REPERFUSION INJURY THROUGH ACTIVATING THE NRF2/HO-1 PATHWAY ENHANCED AUTOPHAGY
Authors: Hwang Jeong Kye , Choi HyunSu , Kim Mi-hyeong 
Published: June 2020

Abstract

Background and Aims
Ischemic preconditioning (IPC), which is a brief and nonlethal episode of ischemia, confers protection against subsequent ischemia-reperfusion (I/R) through the up-regulation of endogenous protective mechanisms. Recent studies have reported that the activation of autophagy is associated with IPC. However, the underlying mechanisms still need to be determined. In this study, we investigated the role of IPC in renal I/R injury and demonstrated that IPC could ameliorate renal I/R injury by activating the Nrf2/HO-1 pathway and induction of autophagy.

Method
In order to gain insights into IPC–induced alterations at the cellular level, an in vitro model for IPC was designed using the human proximal tubule epithelial cell line HK-2. In vitro I/R was induced by layering mineral oil (for 60 min) over a thinfilm of media covering the cells followed by 120 min of reperfusion in normal media. IPC was performed by a 10-min period of incubation of cells under mineral oil followed by a 30-min recovery period prior to the 120 min reperfusion. To further determine the role of autophagy in IPC-induced renoprotection, the cells were treated with bafilomycin A1 (200 nM), prior to I/R injury. In a renal I/R injury model, mice were subjected to 30 min of renal ischemia followed by 24 h of reperfusion. IPC was produced by 5 min of ischemia followed by 10 min of reperfusion prior to sustained ischemia.

Results
We found that IPC significantly attenuated I/R-induced kidney injury and suppressed oxidative stress and inflammatory responses. IPC also increased LC3-II and decreased SQSTM/p62 and cleaved caspase-3 during renal I/R injury, as well as increased the number of intracellular double-membrane vesicles in injured renal cells. IPC-induced renal protection was efficiently attenuated by pretreatment with Bafilomycin A1 (0.3 mg/kg, IP). Pretreatment with IPC also dynamically affected the expression of Nrf2/HO-1 signaling components. The beneficial effects of IPC were abolished by Brusatol (2 mg/kg, IP), potent inhibitors of Nrf2. Moreover, the Nrf2 agonist t-BHQ (50 mg/kg, IP) showed similar activity as IPC.

Conclusion
In summary, the present study shows that Nrf2 plays a critical role in regulating the HO-1 production induced by I/R. Also, upregulation of Nrf2 expression might represent one of the major mechanisms whereby IPC confers protection against I/R-induced kidney injury. The beneficial effects of IPC could be attributed to its antioxidative stress and anti-inflammatory properties
P0560POST-DISCHARGE FOLLOW UP AFTER AKI. AN EXTERNAL VALIDATION AND DECISION CURVE ANALYSIS OF TWO RISK MODELS
Authors: Sawhney Simon , Tan Zhi , Black Corri , Hemmelgarn Brenda , Marks Angharad , Mclernon David , James Matthew 
Published: June 2020

Abstract

Background and Aims
There is limited evidence to inform which people should receive follow up after AKI and for what reasons. Here we report the external validation (geographical and temporal) and potential clinical utility of two complementary models for predicting different post-discharge outcomes after AKI. We used decision curve analysis, a technique that enables visualisation of the trade-off (net benefit) between identifying true positives and avoiding false positives across a range of potential risk thresholds for a risk model. Based on decision curve analysis we compared model guided approaches to follow up after AKI with alternative strategies of standardised follow up – e.g. follow up of all people with AKI, severe AKI, or a discharge eGFR&lt;30.

Method
The Alberta AKI risk model predicts the risk of stage G4 CKD at one year after AKI among those with a baseline GFR&gt;=45 and at least 90 days survival (2004-2014, n=9973). A trial is now underway using this tool at a 10% threshold to identify high risk people who may benefit from specialist nephrology follow up. The Aberdeen AKI risk model provides complementary predictions of early mortality or unplanned readmissions within 90 days of discharge (2003, n=16453), aimed at supporting non-specialists in discharge planning, with a threshold of 20-40% considered clinically appropriate in the study. For the Alberta model we externally validated using Grampian residents with hospital AKI in 2011-2013 (n=9382). For the Aberdeen model we externally validated using all people admitted to hospital in Grampian in 2012 (n=26575). Analysis code was shared between the sites to maximise reproducibility.

Results
Both models discriminated well in the external validation cohorts (AUC 0.855 for CKD G4, and AUC 0.774 for death and readmissions model), but as both models overpredicted risks, recalibration was performed. For both models, decision curve analysis showed that prioritisation of patients based on the presence or severity of AKI would be inferior to a model guided approach. For predicting CKD G4 progression at one year, a strategy guided by discharge eGFR&lt;30 was similar to a model guided approach at the prespecified 10% threshold (figure 1). In contrast for early unplanned admissions and mortality, model guided approaches were superior at the prespecified 20-40% threshold (figure 2).

Conclusion
In conclusion, prioritising AKI follow up is complex and standardised recommendations for all people may be an inefficient and inadequate way of guiding clinical follow-up. Guidelines for AKI follow up should consider suggesting an individualised approach both with respect to purpose and prioritisation.
P0575TIME TO NEPHROLOGY CONSULTATION AND MORTALITY RISK IN COMMMUNITY ACQUIRED AKI
Authors: Acosta-Ochoa Isabel , Coca Armando , Lorenzo Arturo , Mendiluce Alicia 
Published: June 2020

Abstract

Background and Aims
Acute Kidney Injury (AKI) is the most frequent cause of Nephrology consultation. Although time to nephrology consultation (TNC) has been object of study, few works focus on its influence on in-hospital mortality in patients with community acquired AKI (CA-AKI).

Method
We picked cases of CA-AKI, and divided individuals in dead in-hospital and survivors. We analyzed clinical and epidemiological variables, and categorized AKI with the KDIGO-2012 stages. We compared clinical outcomes and influence of TNC in mortality.

Results
We included 420 patients, 92 (22%) in the mortality group. These individuals were older, had higher Charlson’s Index, were hospitalized in critical care units, and were classified in KDIGO-2012 Stage 3 more frequently (Table 1). TNC was higher in the dead patients and was significantly associated with mortality HR 1.28 (CI 95% 1.03-1.55, P=0,009). In KDIGO Stages 1 and 2 TNC was shorter in the survivors group, and in Stage 3 we found no differences. In general wards (medical and surgical), TNC was higher in the mortality group, with no differences in the consults from critical units (Table 1). In the survival curves we observe a decline in survival in patients with TNC ≥2 days since admission (Figure 1).

Conclusion
We found that a longer TNC was associated with a poorer survival. This finding would indicate that earlier nephrology attention could impact in-hospital mortality. We interpret the longer TNC in less severe AKI stages as a warning of the unawareness and late recognition of AKI in other specialties. More well designed and larger studies are needed to prove that electronic alerts offer a survival benefit.
P0583RED CELL DISTRIBUTION WIDTH PREDICTS CONTRAST-INDUCED NEPHROPATHY IN PATIENTS UNDERGOING ENHANCED COMPUTED TOMOGRAPHY
Authors: Li Youqi , Shi Yongjun , Li KeXuan , Shen Jian , Xiao ShaoBing 
Published: June 2020

Abstract

Introduction
Contrast-induced nephropathy (CIN) is an major complication of enhanced computed tomography(CT) procedures.Development of CIN after enhanced CT may lead to worse clinical outcomes. Thus, markers are used to identify the risk of patients ,who undergo enhanced CT with CIN.Red cell distribution width(RDW) is a measurement of erythrocyte variability and heterogeneity, and it is obtained routinely in standard complete blood cell counts.Current researches indicate that RDW is the independent predictor of AKI after patients receiving percutaneous coronary intervention (PCI).However, the correlation of RDW and CIN after enhanced CT are yet to be determined.In this study we investigated whether RDW levels correlate with development of CIN in patients after enhanced CT.

Method
A total of 633 patients undergoing enhanced CT from June 2015 to June 2018 at Huizhou Central Municipal Hospital were enrolled. Patients were divided into CIN group and no-CIN group. The diagnostic criteria for CIN is an increase in serum creatinine(Scr) more than 44.2μmol/L or 25% higher than the baseline value within 72 hours after contrast administration.

Results
The study population consisted of 633 patients ,25(3.95%) patients developed into CIN. Patients who got CIN were older and had a higher prevalence of active smoking compared with those were without CIN. The range of the baseline serum creatinine and red cell distribution width was significantly higher in CIN groups.However,baseline eGFR,red blood cell counts,hemoglobin and albumin levels were significantly lower in patients who developed CIN(all P&lt;0.05).Multivariate logistic regression analysis revealed that baseline RDW level(OR=2.325,95% CI 1.521∼3.556,P&lt;0.001),albumin(OR=0.888,95%CI 0.803∼0.982, P=0.021)and eGFR(OR=0.921,95%CI 0.849∼0.999,P=0.047)were independent risk factors in the development of CIN in patients after enhanced computed tomography.The area under the ROC curve for RDW was 0.803(95% CI 0.706∼0.900,p&lt;0.001),and an RDW of 13.85% or higher predicted CIN with a sensitivity of 72% and specificity of 75.80%(Figure 1).

Conclusion
Increased baseline of RDW, decreased eGFR and lower albumin are independently related with a higher risk of CIN in patients undergoing enhanced CT.RDW is possibly a predictive biomarker for the early diagnosis of CIN.
P0584A COMPARATIVE STUDY ON THE INCIDENCE OF CONTRAST INDUCED NEPHROPATHY FOLLOWING INTRA-ARTERIAL VERSUS INTRAVENOUS CONTRAST ADMINISTRATION
Authors: Moideen Adel 
Published: June 2020

Abstract

BACKGROUND
Contrast-induced nephropathy (CIN) / Contrast induced-acute kidney injury (CI-AKI), defined as a relative increase of ≥25% or an absolute increase of ≥0.5 mg/dL in S.Cr levels assessed at 48 hours post procedure, is a well described following an administration of Intra-arterial (IA) iodinated contrast agent, but its occurrence after Intravenous (IV) contrast is being questioned.

AIMS
To compare the incidence of CIN following IV and IA contrast procedures and to identify its risk factors.

METHOD
This is a prospective, single center study of 774 patients (449 males and 325 females with mean age of 48.85 ± 14.05 years) who underwent contrast studies with nonionic, low-osmolar iodinated contrast agent (Iomeprol) via IV and IA routes were included in the study. We recorded baseline characteristics along with laboratory parameters; underlying renal injury risk factors; contrast administration volume, type, and route of administration; incidence of CIN and requirement of renal replacement therapy (RRT). Univariate and multivariate models were used to determine predictors of CIN.

RESULTS
The total incidence of CIN was 14.85% (115 patients). Baseline eGFR was lower for patients undergoing intra-arterial contrast procedures (66.02 ± 23.70 ml/min/1.73m2 vs 71.31±24.07 ml/min/1.73m2, p=0.002). Simple logistic regression showed a statistically significant difference in the rate of CIN in patients who received IV vs. IA iomeprol (6.2% vs 25.1%). The total risk of RRT was 1.7% with the incidence being more in the IA group than the IV group (3.1% vs 0.5%, p=0.005). Advanced age, dehydration and hypotension, CCF, anemia, proteinuria, diabetes mellitus, preexisting renal disease (i.e. baseline serum creatinine&gt;1.5mg/dl), baseline eGFR&lt;60ml/min/1.73m2), use of nephrotoxic antibiotics and route of contrast correlated significantly with CIN. Proteinuria ≥1 g/day and hypoalbuminemia was significantly higher in the intra-arterial group than the intravenous group (p=0.001).

CONCLUSION
We found that administration of both IV and IA iodinated contrast agents is associated with a risk of CIN with a significant higher risk of CIN as well as RRT following IA contrast. Proteinuria may be a new risk factor for the development of CIN.
P0596LONG TERM FOLLOW UP OF CONTRAST INDUCED ACUTE KIDNEY INJURY IN A TERTIARY JORDANIAN HOSPITAL
Authors: Oweis Ashraf , Alshelleh Sameeha 
Published: June 2020

Abstract

Background and Aims
Contrast induced acute kidney injury (CI-AKI) is potentially preventable and reversable cause of acute kidney injury (AKI).
Multiple factors are associated with the development of CI-AKI, some are modifiable such as drugs, type and amount of contrast, others are not like preexisting chronic kidney disease (CKD), heart failure.
Though it’s usually a reversable condition, there is increasing evidence of adverse long-term outcome (increasing morbidity and mortality).
The aim of this study to evaluate the long-term outcome of CI-AKI on mortality, the rate of re-catheterization and the development of CKD.

Method
In a prospective observational study design, we evaluated all patients admitted for cardiac catheterization between June 2015 and January 2016. A total of 326 patients signed the consent to participate in the study.
Patients had blood withdrawn 48 hours after the procedure for their creatinine level.
CI-AKI was defined as an increase in serum creatinine by &gt;25% or 44 mmol/l from the baseline level (48-72) hours after contrast administration, without any other obvious cause.
We used only low osmolality contrast media (CM) (Lopamidol, Bayer, Germany).
Of the 326 patients included, 202 patients had their second sample taken, thus, were eligible to continue in the study.
Patients were followed for at least 3 years.

Results
The incidence of CI-AKI was 14.8% (30 patients), for baseline characteristics see table 1.
At the end of follow up; a total of 7 patients died; 6 in the non CI-AKI group vs. 1 in the CI-AKI group (p= ), though the difference between the mean eGFR was not statistically significant by the end of the follow up (85.4ml/min for the CI-AKI vs. 79.2ml/min for the other group (P=0.31)), but the decline in eGFR for the CI-AKI was significant ( a drop from 105.4 ml/min to 85.4ml/min vs. 85.2ml/min to 79.2ml/min, P=0.004).
The rate of re-catheterization was not statistically significant between the two groups (61 for the non CI-AKI vs. 12 for the other group; P=0.63).

Conclusion
CI-AKI carries a higher negative long-term effect on eGFR, while did not affect the mortality in our cohort.
P0619POINT OF CARE CREATININE FOR EARLY DIAGNOSIS OF COMMUNITY ACQUIRED ACUTE KIDNEY INJURY IN NIGERIA. TECHNOLOGY EVALUATION AND DESIGN OF QUALITY IMPROVEMENT PROJECT
Authors: Poulikakos Dimitrios , Erekosima Ibi , Emem-Chioma Pedro , Fakrogha Prelador , Oko-Jaja R I , Utein Nkoyo , Wokoma F S , David-West Manda , Ndu Victor , Ugochukwu Duru Stephen , Ohiri John , Harry Agba M , Kalra Philip A , Lewis David 
Published: June 2020

Abstract

Background and Aims
Acute Kidney Injury (AKI) in low- and middle-income countries is mostly a community-acquired potentially reversible syndrome and has high morbidity and mortality. Due to limited laboratory infrastructure diagnosis of AKI is often delayed until life threatening complications have developed and dialysis treatment is largely unavailable. Decisions for hospital referral from primary health care centers and triage decisions for hospital admission are not based on laboratory results in Port Harcourt Nigeria. To address the need for early diagnosis and treatment of AKI we established a collaboration between the Renal Unit of the University of Port Harcourt Teaching Hospital, Primary Health Care Board Rivers State and the Renal Department of Salford Royal NHS Foundation Trust, aiming at the evaluation of the use of point of care (POC) Creatinine (Cr) for early detection and management of community acquired AKI.

Method
The first stage of the project evaluated the accuracy of POC Cr technology. Following informed consent patients underwent concurrent measurement of Cr using the central laboratory (Lab) assay (Jaffe) from a venous sample and a point of care Cr measurement using a capillary sample (fingerstick) with the NOVA Stasensor Xpress Cr analyser. Pearson Correlation and Bland-Altman plots were used to assess correlation and agreement between the two methods. During the second stage, the results were discussed at a focused AKI workshop and guidance for the use of POC Cr was developed.

Results
During the first phase 96 concurrent POC Cr capillary and venous Lab Cr samples were analysed. Mean age was 49±14 years and 66 subjects were females. POC Cr values were 127±122 umol/l and Lab Cr values were 100 ±85 umol/L, mean positive bias of 27.2±47.94 umol/L. Overall, correlation between POC Cr and Lab Cr was very good, with Pearson correlation r=0.956) Figure 1A. All 4 out of 96 values that were outside the limits of agreement (set at mean ±2 standard deviations) were for Lab Cr values &gt;200 umol/L. A Bland-Altman Plot is presented for paired samples with Lab Cr values &lt;200 umol/L (Figure 1B).
P0645EDARAVONE MAY DECREASE THE INCIDENCE OF CONTRAST INDUCED ACUTE KIDNEY INJURY (CI-AKI)
Authors: Ivanov Dmytro , Ivanova Mariia , Burlachenko Illia 
Published: June 2020

Abstract

Background and Aims
Edaravone is a low-molecular-weight antioxidant drug targeting peroxyl radicals of reactive oxygen species and has shown clinical efficacy in patients with acute ischemic stroke.
We have conducted a multicenter open prospective randomized controlled study to evaluate the efficacy of edaravone in preventing AKI in patients with CKD 3b-4 stages.

Method
The study included 2 groups of patients aged 46 to 68 (55 ± 3): group A (n=16) with CKD stage 3b or 4 (eGFR EPI 32 ± 4 ml/min) that received intravenous edaravone 30 mg bid on 0,1,2 day of contrast media infusion and control group B (n=20) with CKD stage 3b or 4 (eGFR EPI 33 ± 3 ml/min) with no edaravone intervention during CT coronarography. Patients of both groups received intravenous hydration with 0.9% sodium before CT. Primary endpoint: CIN onset in 48 hours after contrast media infusion and need for RRT. Secondary endpoint: serum potassium level above 5.5 mmol/l.

Results
CIN onset was obtained in 4 patients of group A and 12 patients of group B (p&gt;0,05, RR 0.417, RRR 0.583, RD 0.350, NNT 2.857). Other results are presented in table
P0653THE USE OF URINARY EPIDERMAL GROWTH FACTOR FOR EVALUATION OF KIDNEY GRAFT FUNCTION
Authors: Chan Joe , Eide Ivar Anders , Jenssen Trond Geir , Waldum-Grevbo Bård , Tannæs Tone Møller , Svensson My 
Published: June 2020

Abstract

Background and Aims
Follow-up after kidney transplantation requires repeated, reliable glomerular filtration rate (GFR) measurements. Measured GFR (mGFR), using urinary or plasma clearance of an exogenous filtration marker such as iohexol, provides precise measurements but are expensive and time consuming. Instead, estimated GFR (eGFR) based on serum creatinine is most commonly used in clinical practice. Epidermal growth factor is produced in the kidney and promotes tubular cell regeneration and recovery of kidney function after injury. Low levels of urinary epidermal growth factor (uEGF) are linked to progression of chronic kidney disease and increased risk of kidney graft failure. The aim of this study was to investigate uEGF as an additional marker to evaluate graft function in kidney transplant recipients (KTRs).

Method
Participants in the Omega-3 fatty acids in Renal Transplantation (ORENTRA) trial were examined with mGFR by iohexol clearance at 1 year after kidney transplantation. The concentration of iohexol in serum was measured 3 and 4 hours after iv injection. On the same day, fasting blood and urine samples were obtained in the morning. Serum creatinine was measured and eGFR calculated with the MDRD formula. uEGF and a pre-specified selection of inflammation and fibrosis markers were measured with multiplex immunoassay technique and normalized with urinary creatinine. Principal component analysis (PCA) was used to explore clustering of markers. Correlations were calculated with Pearson’s correlation coefficient R.

Results
Fifty-nine participants had complete measurements of mGFR (57.2 ± 15.2 mL/min/1.73m2), eGFR (68.6 ± 23.0 mL/min/1.73m2) and uEGF. The correlation between mGFR and eGFR was strong (R=0.783, P&lt;0.001). Measurements of uEGF had a coefficient of variation below 10% for all participants, with a mean value of 22.0 ± 12.1 μg/g creatinine. There was a significant correlation between mGFR and uEGF (R=0.678, P&lt;0.001). The component score of uEGF and eGFR calculated with PCA (74% of variance) had the strongest correlation with mGFR (R=0.845, P&lt;0.001).

Conclusion
Combining uEGF with eGFR into one component score by PCA gives a greater correlation with mGFR compared to eGFR alone in this cohort of KTRs. These findings need to be validated in other patient populations.
P0660COMPARISON OF BIAS AND ACCURACY OF CREATININE AND CYSTATIN C-BASED CKD-EPI EQUATIONS FOR GFR ESTIMATION
Authors: Sun Ling , Zou Luxi , Nicholas Susanne B , Lu Yan , Sinha K Satyesh , Hua Ruixue 
Published: June 2020

Abstract

Background and Aims
Glomerular filtrate rate (GFR) is a key index of kidney function, and directly measured GFR (mGFR) is the gold standard, but it is invasive and costly. The Chronic Kidney Disease Epidemiology Collaboration (CKD-EPI) equations have been widely used to estimate GFR with high accuracy. However, the comparative accuracy of estimated GFR (eGFR) using creatinine and cystatin C in CKD-EPI equations remains unclear. This study aimed to systematically assess the bias and accuracy of eGFR using equations of CKD-EPIcrea, CKD-EPIcys, and CKD-EPIcrea/cys in adult populations relevant to primary health care.

Method
Pubmed, Web of Science, EMBASE, and the Cochrane Library were searched from inception until December 2019 for studies comparing mGFR with simultaneous eGFR using CKD-EPI calculated from standardized serum creatinine and cystatin C. We pooled data on bias (difference between mGFR and eGFR), accuracy (P30; proportion of eGFR within 30% of mGFR), and correlation coefficient (R; between mGFR and eGFR), using random-effects models.

Results
A total of 35 studies with 23,667 participants, which reported the data on the bias, and/or P30, and/or R were included (Figure 1). The difference in the bias of eGFR using CKD-EPIcys was 4.84 mL/min/1.73 m2 (95% CI, 1.88∼7.80) lower than using CKD-EPIcrea, and 1.50 mL/min/1.73 m2 (95% CI, 0.05∼2.95) lower than using CKD-EPIcrea/cys. These gaps increased in subgroups of low mGFR (&lt;60 mL/min/1.73 m2) (Figure 2). CKD-EPIcrea/cys eGFR achieved the highest accuracy (Figure 3), 7.50% higher than CKD-EPIcrea (95% CI, 4.81∼10.18), and 3.21% higher than CKD-EPIcys (95% CI, -0.43∼6.85) (Figure 4); and the best correlation with mGFR, with Fisher's z transformed R of 1.20 (95% CI, 0.89-1.50) (Figure 5).

Conclusion
CKD-EPIcrea/cys and CKD-EPIcys equations gave less bias and more accurate estimates of mGFR than CKD-EPIcrea equation. Our findings validated and strengthened the use of cystatin C alone or in combination with creatinine in CKD-EPI equations. More variables and coefficients could be added in CKD-EPI equations to achieve less bias and more accuracy in future research.