bluuebunny/crossref_metadata_2025 huggingface dataset:
P0528RENOPROTECTIVE EFFECT OF IL-34 INHIBITION ON CISPLATIN-INDUCED NEPHROTOXICITY IN MICE
Authors: Wada Yukihiro , Iyoda Masayuki , Matsumoto Kei , Suzuki Taihei , Iseri Ken , Tachibana Shohei , Kanazawa Nobuhiro , Sugiyama Motonori , Honda Hirokazu
Published: June 2020

Background and Aims

Interleukin (IL)-34, a macrophage (Mø) mediator, is expressed by tubular epithelial cells (TECs). However, the influence of IL-34 on TECs injury has not been fully elucidated. We investigated the physiological properties of IL-34 on TECs damage caused by cisplatin-nephrotoxicity (CP-N).

Method

7-week-old male C57BL/6 (B6) mice (n=16) were fasted for 8 hours and then induced CP-N by intraperitoneal injection (IP) of CP (25 mg/kg) on day 0. Groups of animals were given either anti-mouse IL-34 antibody (CP+anti-IL-34 Ab, 400 ng/kg, n=8) or vehicle (CP+V, equal volume of saline, n=8) daily by IP from day -1 to day 2. Three age-matched male B6 mice were used as normal control (NC). All mice were sacrificed on day 3. In addition, mouse renal proximal TECs (MRTEpiC) were cultured to analyze the inhibitory effects of IL-34 on CP-induced TEC apoptosis. Cells were stimulated with CP (2 μg/mL), then treated with or without anti-IL-34 Ab (1000 pg/mL).

Results

Compared to the NC, CP+V mice exhibited marked acute kidney injury (AKI) and upregulated expression of IL-34 and its two receptors, cFMS and PTP-ζ. Compared to the vehicle treatment, anti-IL-34 Ab treatment significantly suppressed the intrarenal expression levels of IL-34 and its two receptors in CP-N mice; it also significantly suppressed serum IL-34 levels (72.1 ± 5.6 vs. 40.4 ± 7.5 pg/mL, p=0.013). Additionally, treatment with anti-IL-34 Ab significantly improved serum Cr levels (1.3 ± 0.2 vs. 0.7 ± 0.1 mg/mL, p=0.033), ameliorated tubulointerstitial injury (numbers of casts/HPF: 11.9 ± 2.6 vs. 6.5 ± 1.8, p=0.048), and suppressed the number of F4/80+ Mø (17.5 ± 2.7 vs. 11.1 ± 1.1/HPF, p=0.041) and TUNEL+ apoptotic cells (29.2 ± 4.9 vs. 16.7 ± 2.7/HPF, p=0.036) in CP-N mice. The renal cortical transcript levels of Kim-1, MIP-1/CCL3, TNF-α, and Bax were significantly lower in the CP+anti-IL-34 Ab mice than in the CP+V mice. Furthermore, the CP+anti-IL-34 Ab mice showed significantly less renal infiltration of CD11b+F4/80+TNF-α+ cells. In vitro, stimulation with CP induced the expression of IL-34 and its two receptors in MRTEpiC. Treatment with anti-IL-34 Ab significantly suppressed CP-induced caspase-3 and Bax expression with degradation of ERK1/2 phosphorylation in the damaged MRTEpiC.

Conclusion

IL-34 secreted from damaged TECs was involved in the progression of CP-N. Inhibition of IL-34 with neutralizing antibody directly prevented CP-induced TEC apoptosis by inhibiting the phosphorylation of ERK1/2. Blocking of IL-34 might suppressed proliferation of cytotoxic Mø, which indirectly led to the attenuation of CP-N. Thus, IL-34 represents a potential as therapeutic target for AKI with TECs injury.
P0532CD8+CD103+ INDUCED REGULATORY T CELLS BUT NOT NATURE REGULATORY T CELLS AMELIORATE IR-INDUCED KIDNEY INJURY
Authors: Xu Tongtong , Xu Zhenjian , Chen Liling , Xu Anping
Published: June 2020

Background and Aims

Acute kidney injury (AKI) is one of the most common complications in clinical practice, but current approaches offer no cures for AKI. Inflammatory response is the key mechanism of ischemia reperfusion (IR)-induce AKI, known as hypoxia/reoxygenation injury. T lmphocytes are crucial mediators of IR-induced AKI. It is reported that regulatory T cell (Treg) has potential ability to ameliorate IR-induced AKI. Tregs consist of nature Treg (nTreg) and induced Treg (iTreg), which are well established to blunt immune responses. We confirmed that CD8+CD103+iTreg remain steadily and barely transfer into Th17, which produce proinflammatory response, under inflammatory response. It is studied that nTreg tends to transfer into Th17 under inflammatory condition, which clarifies the instability of nTreg. Thus, the instability of nTreg under inflammatory response hints us that nTreg are not suitable for recovery from IR-induced AKI. Accordingly, we studied the role of CD8+CD103+iTreg in repair after IR-induced kidney.

Method

In vitro study, we test the expression of CD103, Foxp3 and IL-17a in CD8+CD103+iTreg under 1% O2 concentration. In vivo study, SPF C57BL/6J male mice (8-10 weeks old, body weight 20-25g) were divided into four groups, sham-operated control group, AKI group, iTreg treatment group and nTreg treatment group, with 6 mice in each group. On the day of surgery, we anesthetize the mice (pen-tobarbital sodium, 50 mg/kg body weight). Mice in the AKI group were reperfused after 25 minutes of bilateral renal artery ischemia. We injected CD8+CD103+iTreg (2 × 106/mouse) or nTreg (2 × 106/mouse) intraperitoneally after 24 hours of modeling to the treatment group and euthanized the mice on the third day of anesthesia.

Results

We discovered that the expression of CD103 is stable in CD8+iTreg in vitro under 1% O2 concentration (Figure 1, 2). In addition, their inhibiting abilities of T cells proliferation in vitro remain steadily (Figure not shown). However, CD8+CD103+iTreg seldom transfer into Th17, but remain Foxp3 under hypoxic condition (Figure 2). Adoptively transferring CD8+CD103+iTregs, a new subpopulation of CD8+iTreg we have identified, to AKI mice, we found that these cells can ameliorate the development of AKI by mitigating the level of serum creatine, alleviating acute tubular necrosis (ATN) and decreasing the mortality of AKI.

Conclusion

Therefore, we confirmed that CD8+CD103+iTreg is stable under inflammatory(hypoxic) environment. Thus, CD8+CD103+iTreg targeting may be a novel therapeutic approach to enhance recovery from IR-induced AKI.
P0537LINARIN PROTECTS KIDNEY AGAINST ISCHEMIA/REPERFUSION INJURY VIA INHIBITION OF ETS2
Authors: Yang Chengyu , Xu Yan
Published: June 2020

Background and Aims

Ischemia/reperfusion injury (IRI), a participant in acute kidney injury (AKI), can occur as a series of pathological processes such as inflammation. Linarin (LIN) has been widely used for different diseases. To confirm the anti-inflammatory value and relevant mechanism of LIN during IRI, in vivo and vitro model were established.

Method

LIN or isovolumetric DMSO was given, and histologic analysis, quantitative real-time reverse transcription polymerase chain reaction (qRT-PCR), serum creatinine (SCr) testing and blood urea nitrogen (BUN) were used to evaluate kidney injury. Microarray analysis, protein-protein interaction (PPI) analysis and molecular docking were used to identify target protein of LIN.

Results

At first, we find that LIN could inhabit the kidney injury in vivo IRI model and decrease the expression of IL-12 p40 in vitro IRI model. To explore the mechanism of LIN, we collected raw data from public microarray database and identified E26 oncogene homolog 2 (ETS2) as a target protein of LIN according to microarray analysis, PPI and molecular docking. The contact area is highly conserved and located on a protein-protein interaction domain of ETS2 which indicated that LIN may alter the interaction with synergistical protein in the regulation of IL-12 p40 expression.

Conclusion

Our study demonstrated the anti-inflammatory effect of LIN during IRI-triggered AKI, broadening the medicinal value of LIN and the therapeutic options for IRI-triggered AKI.
P0540EFFECT OF MEMBRANE MATERIALS ON VANCOMYCIN, TEICOPLANIN AND LINEZOLID REMOVAL DURING CONTINUOUS RENAL REPLACEMENT THERAPIES: AN IN VITRO STUDY
Authors: Godi Llaria , Lorenzin Anna , De Cal Massimo , Ronco Claudio
Published: June 2020

Background and Aims

In a continuous renal replacement therapy (CRRT) scenario, removal of anti-methicillin resistant Staphylococcus Aureus agents can be quantitatively important, thereby contributing to clinically relevant decreases in their plasma concentration during treatment. Extracorporeal elimination of antimicrobial agents is influenced by the dose and modality prescribed, as well as the sieving coefficient (SC) and adsorptive properties of the membrane used.The aim of this study was to document the specific SC and adsorptive capacity of three different membrane materials related to vancomycin, teicoplanin and linezolid.

Method

This in vitro study used a model of continuous veno-venous hemofiltration. 500 ml of whole blood from healthy donor spiked with one antibiotic under investigation was pumped (blood flow of 50 ml/min and ultrafiltrate flow of 10 ml/min) in a closed-circuit using polysulfone (PS), polymethylmethacrylate (PMMA) and polyacrylonitrile (PAN) membranes. Samples were collected from in-flow, out-flow and ultrafiltrate lines in a 360 min period. Antibiotic concentrations were measured to calculate SCs. Mass balance analysis was assessed to evaluate the adsorptive capacity of PS, PMMA and PAN membrane related to each antibiotic.

Results

The SCs were substantially affected by the hemodialyzers material in the case of Vancomycin, where PMMA membrane had higher SC (SC=0.89±0.01) compared to PAN (SC=0.79±0.02) and PS (SC=0.62±0.03) membranes. The effect of material was minor for Teicoplanin (Sc=0.12±0.05 for PS, Sc=0.17±0.05 for PMMA, Sc=0.19±0.00 for PAN) and no noticeable difference within hemodialyzers was found for Linezolid (Sc=0.92±0.03 for PS, Sc=0.95±0.01 for PMMA, Sc=0.95±0.00 for PAN). In terms of adsorptive capacity, PS and PMMA membranes showed higher interaction with Vancomycin and Teicoplanin compared with PAN membrane, while a small amount of Linezolid was adsorbed by all the three filters. The cumulative adsorbed amount of PS and PMMA of Teicoplanin were also clinically relevant (99.15 mg/m2 and 51.33 mg/m2 respectively) compared to PAN membrane (9.14 mg/m2).

Conclusion

PS, PMMA and PAN membranes behave differently in terms of sieving and adsorptive properties related to vancomycin, teicoplanin and linezolid. These differences may have a clinical influence on vancomycin and teicoplanin removal during CRRT, while linezolid variability during CRRT hasn’t to be ascribed for membrane material.
P0555HYPOTHERMIA ATTENUATES CHRONIC RENAL INJURY AFTER ISCHEMIA-REPERFUSION IN KIDNEY
Authors: Na Ki Ryang , CHOI DAE EUN , Lee Kang Wook , Kim Dabi , Kim Eunji , Jeong Jin Young , Ham Young Rok , Kim Haeri , Choi Wonjung , Chang Yoon-Kyung
Published: June 2020

Background and Aims: Hypothermia attenuates the renal injury induced by ischemia-reperfusion(IR). However, the detailed molecular pathway remains unknown. Although there has been reported that hypothermia protects acute renal damage, there is little known that hypothermia reduce renal fibrosis in IR kidney injury. We evaluated hypothermic protection against renal fibrosis in renal IR injury. Method: C57Bl/6 mice were divided into the following groups: sham-operated (cold, 32C) vs normal temperature (37C); IR mice (32C vs 37C). Kidneys were harvested 10 and 27 minutes after induction of renal ischemia and 24, 72, 168 hours after iIR injury. Functional and molecular markers of kidney injury were evaluated. Results: The blood urea nitrogen and serum creatinine levels and the histologic renal injury scores were significantly lower in 32C IR than 37C IR kidneys (all P values < .05).In kidney harvested 10 and 27 min, the extent of renal AMPK,ERK, and HIF1 phosphorylation was significantly increased in the kidneys of 32C compared to 37C IR mice. In kidney harvested 27 min, 24hr, 72hr, and 168hr, the expression levels of SOX9, TGF beta, alpha SMA, collagen IV, and fibrinogen decreased in 32C IR compared to 37C IR mice. In addition, in kidney harvested 72hr, and 168hr, the stained area of TGF beta, alpha SMA, and masson trichrome, were significantly decreased in 32C IR compared to 37C IR mice. Conclusion: Hypothermia attenuates the renal fibrosis induced by Ischemia reperfusion.
P0557HYPERBARIC OXYGEN PRECONDITIONING INCREASES HEME OXYGENASE 1 EXPRESSION IN KIDNEY TISSUE AND IMPROVES KIDNEY FUNCTION IN SPONTANEOUSLY HYPERTENSIVE RATS WITH ISCHEMIC ACUTE KIDNEY INJURY
Authors: Ivanov Milan , Miloradovic Zoran , Mihailovic-Stanojevic Nevena , Jovovic Djurdjica , Karanovic Danijela , Vajic Una-Jovana , Jeremić Rada , Djelic Marina , Brkic Predrag
Published: June 2020

Background and Aims

Renal ischemia–reperfusion (RIR) injury is one of the factors in the development of acute kidney injury (AKI). AKI is multifactorially caused, but the mechanism of pathogenesis and development of this disease is still incompletely defined. AKI is characterized by the sudden appearance, rapid progression of disease and very uncertain and often fatal outcome. Heme oxygenase-1 (HO-1) is a cytoprotective enzyme that catalyzes the breakdown of heme to biliverdin, carbon monoxide, and iron. HO-1 is now recognized as a protection factor in acute kidney injury. The aim of this study was to determine the effect of preconditioning with hyperbaric oxygen (HBO) on HO-1 expression in kidney tissue and kidney function in spontaneously hypertensive rats (SHR) during kidney ischemia–reperfusion injury.

Method

An experiment was performed in anesthetized, adult six-month-old male SHR. The right kidney was removed and the renal ischemia was performed by clamping the left renal artery for 40 minutes. SHR were randomly selected in three experimental groups: sham operated group (SHAM; n=7); AKI control group (AKI; n=9); and AKI group with HBO (AKI+HBO; n=9). Treated group were placed into experimental HBO chambers and exposed to pure oxygen, twice a day (in a 12 hour period, 8AM and 8 PM) for two consecutive days in the following manner: 10 minutes slow compression, 2.026 bar for 60 minutes, 10 minutes slow decompression. Mean arterial pressure (MAP) and HO-1 expression in kidney tissue were measured 24h after reperfusion. Clearance of creatinine (CCr), urea (CUr) and phosphate (CPh) were calculated 24h after reperfusion.

Results

After AKI induction reduction of blood pressure was recorded in both groups with AKI. Preconditioning with HBO significantly improved kidney function in rats with AKI compared to control group. HO-1 expression in kidney tissue was significantly higher in the treated group (p<0,01) compared to SHAM and AKI control group.

Conclusion

Our results suggest that HBO treatment improves kidney function in the AKI+HBO vs. AKI control group. This implies that increased level of HO-1 due to preconditioning with hyperbaric oxygen may have beneficial effects on kidney function, and potentially protective effect in an ischemic model of AKI with hypertension.
P0558DICLOFENAC ENHANCES RENAL INFLAMMATION IN EXPERIMENTAL SUBCLINICAL ACUTE KIDNEY INJURY (AKI)
Authors: Störmer Johanna , Gueler Faikah , Rong Song , Jang Mi-Sun , Shushakova Nelli , Schmidt Sonja , Haller Hermann , Greite Robert
Published: June 2020

Background and Aims

Diclofenac is frequently used for pain control. In a previous study, we showed that already a single oral dose of diclofenac could reduce renal perfusion in healthy individuals. To investigate the influence of oral diclofenac administration on renal inflammation in the setting of pre-existing renal damage, we used a mouse model of subclinical acute kidney injury (AKI) induced by renal ischemia-reperfusion injury (IRI) followed by diclofenac administration.

Method

Male CD1 mice (7-8 weeks old) underwent unilateral renal pedicle clamping for 15min to induce subclinical AKI. After reperfusion mice received a single oral dose of 100 or 200mg/kg diclofenac via oral gavage. Vehicle treated mice with unilateral IRI served as control. At day 1, mice were placed into metabolic cages to collect urine. Histology was performed on day 1 and 14 for renal morphology. Inflammation and fibrosis were investigated by immunohistochemistry and qPCR.

Results

Diclofenac treated mice showed reduced urine production. Morphologically, signs of AKI were more pronounced in diclofenac treated kidneys which also showed more Cox-2 positive tubuli in the cortex. On mRNA expression level the pro-inflammatory markers IL-6 and CXCL2, the chemoattractant for neutrophils, were elevated in the diclofenac group. Early upregulation of the pro-fibrotic markers CTGF and PAI-1 was detected already on d1 after IRI in the diclofenac group and tubular atrophy was pronounced after two weeks.

Conclusion

Already, a single oral dose of diclofenac causes aggravation of renal inflammation and progressive renal fibrosis in the setting of pre-existing subclinical acute kidney injury.
P0567ACUTE KIDNEY INJURY IN OBSTRUCTIVE UROPATHY; EPIDEMIOLOGY, RENAL OUTCOME AND MORTALITY
Authors: Sun Bong Gyun , Min Hyeon-jin , Son Young-Bin , Choi Eunho , Yang Jihyun , Oh Se Won , Kim Myung-gyu , Jo Sang-Kyung , Cho Won-Yong
Published: June 2020

Background and Aims

Urinary tract obstruction (UTO) is a common clinical problem leading to acute or chronic renal impairment. Unlike pediatric population in which congenital anomalies of urinary tract account for a majority of UTO and contribute to end stage renal disease (ESRD), etiologies, clinical manifestation and outcome in adult UTO remain uncertain due to lack of large epidemiological data.

Method

We performed a multi-center, retrospective study analyzing 1,711 patients who underwent percutaneous nephrostomy (PCN) from 2001 to 2015.

Results

The most common cause of UTO was malignancies (55.6%) followed by urolithiasis (28.5%) and others. Metastatic colorectal cancer were the most common type of malignancies. Patients with UTO caused by malignancies were significantly older, had more advanced stage acute kidney injury (AKI) and higher mortality rate, while those with urolithiasis had higher prevalence of hypertension, diabetes, cardio-cerebro-vascular diseases. Eighty two percentage of patients developed AKI and 15.2% of patients needed a temporary dialysis. Older age, malignancy associated UTO and high uric acid level were independently associated with AKI. Among patients with AKI, 38.2% patients showed a renal functional recovery defined as eGFR ≥60ml/min/1.73m2 on day 7 after PCN. Multivariate analysis showed that older age and lower hemoglobin level were independent factors predicting a nonrecovery of renal function. During the median follow up period of ∼∼months, overall mortality rate was 33.9% with the highest rate was found in malignancy associated UTO (51.9%), followed by other causes (15.9%) and urolithiasis (8.8%). Malignancy associated UTO (OR 4.754, 95% CI 3.151-7.174, p<0.001), lower albumin level (OR 0.731, 95% CI 0.568-0.942, p<0.001) and stage 3 AKI (OR 2.529, 95% CI 1.332-4.803, p=0.005) were found to be independently associated with mortality. However, the impact of AKI on overall mortality was more prominent in non-malignancy associated UTO with stepwise increase of mortality as KDIGO stage increased.

Conclusion

In conclusion, malignancy is the most common cause of upper UTO in adults and AKI is frequently associated. Short term renal recovery after PCN was observed only in 38.2% patients and older age, lower hemoglobin level were associated with nonrecovery of renal function. Malignancy associated UTO showed the highest mortality rate compared to urolithiasis or other causes and stage 3 AKI as well as lower hemoglobin and lower albumin level were found to be independent predictors of mortality in UTO.
P0568INCIDENCE AND RISK FACTORS OF ACUTE KIDNEY INJURY AND TUMOR LYSIS SYNDROME IN PATIENTS WITH MULTIPLE MYELOMA TREATED WITH BORTEZOMIB
Authors: SONG SEUNGMIN , Boo Hyo jin , Jang Hye Ryoun , Huh Wooseong , Kim Dae Joong , Kim Yoon-Goo , Lee Jung Eun
Published: June 2020

Background and Aims

Nephrotoxicity of bortezomib, a proteasome inhibitor, has not yet been described frequently, while tumor lysis syndrome (TLS) associated with multiple myeloma (MM) has been increased after introduction of the drug. This study compared the incidence and risk factors of acute kidney injury (AKI) and TLS in patients with MM after bortezomib-based chemotherapy to investigate the drug-related nephrotoxicity.

Method

From 2006 to 2017, 276 patients who underwent first cycle of bortezomib-based chemotherapy for MM were identified in single tertiary hospital. Laboratory TLS was defined according to the Cairo-Bishop definition. Development of AKI was assessed by AKI Network (AKIN) criteria within 7 days after first chemotherapy.

Results

The age was 65 [56-72] years old, and 47% (n=131) of participants were female and baseline estimated glomerular filtration rate (eGFR) was 61.3 [34.1-89.1] mL/min/1.73m2. The incidences of AKI and laboratory TLS were 17% (n=47) and 13% (n=36), respectively. Ten (3.6%) subjects corresponded to the both AKI and TLS criteria. Multivariate analyses showed that lower eGFR category (30∼59, odds ratio [OR]=3.063 [1.278-7.339]; 15∼29, OR=3.417 [1.088-10.726]; <15, OR=10.080 [2.677-37.951] vs ≥ 60), lower serum albumin level (OR=0.491 [0.278-0.868], P=0.0144) and renal amyloidosis (OR=11.174 [3.974-31.420], P<0.0001) were predictors of development of AKI. MM stages and β2-microglobulin were not associated with AKI occurrence.

Regarding laboratory TLS, MM stage and β2-microglobulin were higher in those with TLS. In multivariate analyses, β2-microglobulin levels (OR=1.194 [1.066-1.337], P=0.0021) and any chromosomes abnormalities at high risk (OR=0.115 [0.026-0.503], P=0.0041) were associated with higher risk of TLS.

Conclusion

Development of AKI was often observed without being accompanied by TLS in patients with MM after treatment of bortezomib. In addition, risk factors of AKI and TLS were widely different. These findings implicated the potential nephrotoxicity of bortezomib besides TLS in patients with decreased kidney function. The efforts to prevent bortezomib associated AKI are needed in patients at high risk.
P0571EPIDEMIOLOGY AND OUTCOMES OF ACUTE KIDNEY INJURY IN CHILDREN IN UKRAINE
Authors: Fomina Svitlana , Lavrenchuk Olga , Bagdasarova Ingretta
Published: June 2020

Background and Aims

The problem of acute kidney injury (AKI) in children continues to be relevant for pediatric nephrology and pediatrics due to the increasing frequency and the lack of a unified approach to management and further monitoring of these patients. The aim of our study was to determine the etiology and outcomes of acute kidney damage in children.

Method

101 patients (aged from 3 months) were studied in referral center from early period after AKI (first month) to 18 years old. They were observed every 6 months during first year of disease course, and once per year till transfer to adult clinic. The outcomes were identified as complete recovery, isolated albuminuria and chronic kidney disease (CKD). The AKI outcomes were analyzed up to 1.5-3, 5-10 and 15 years of follow up (stage 1, 2 and 3, respectively).

Results

The predominant patients were males (72/71.3%). The most of the children were younger than 3 years old at the time of AKI (58/57.4%), and only a small part of patients were adolescents (7/6.9%).

The hemolytic uremic syndrome (HUS) related to diarrhea was the main cause of the AKI (64/63.4%), and children of the first years of life formed the basis of this clinical group (0-3 years old: 44/68.8%). Sepsis and complicated acute viral and bacterial infections have also been confirmed as common AKI causes (12/11.9% and 8/7.9%, respectively). In some cases AKI were associated with hemolytic anemia (5/5.0%), acute glomerulonephritis (5/5.0%), vaccination (1/1.0%), contrast nephrotoxicity (1/1.0%) or unknown cause (3/3.0%).

At stage 1 (1.5-3 years after event, n=60) complete remission were documented in

24/40.0%, albuminuria from 45 to 601 mg/day without other clinical signs – in 22/36.7%, and CKD 2-4 – in 12/23.3%.

At stage 2 (5-10 years after event, n=54) complete remission were confirmed in 29/53.7%, persisted albuminuria – in 6/14.8%, and CKD 2-4 – in 19/31.5%.

At stage 3 (15 years after event, n=12) CKD 2-4 were founded in all patients with arterial hypertension (n=7), focal-segmental glomerulosclerosis (n=2) and kidney cysts (n=3).

Conclusion

AKI was the most often in children of the first 3 years old, mainly in boys. The development of disease was firstly associated with HUS and severe infections. The long-term outcomes of AKI with distance from the event (AKI) to CKD even with recovery renal function and absence of clinical symptoms were difficult to predict. The prolongation of the observation period, the collaboration between the pediatric and adult centers, the widest usage of verified prognostic markers (i. g. albuminuria) and search for new ones are the most important options in post-AKI management.
P0578QUININE EXPOSURE AND THE RISK OF ACUTE KIDNEY INJURY: A POPULATION BASED OBSERVATIONAL STUDY OF OLDER PEOPLE
Authors: Duncan Andrew , Hapca Simona , De Souza Nicosha , Morales Daniel , Bell Samira
Published: June 2020

Background and Aims

Quinine can precipitate Acute Kidney Injury (AKI) by immune-mediated reactions. Cramps, for which quinine is traditionally prescribed, may be a symptom of conditions that are risk factors for AKI. The relationship between quinine and AKI at a population level is unclear. The aim of this study was to establish and quantify any observable association between the exposure to community prescriptions for quinine and AKI events in a population of older adults.

Method

We performed two observational studies of older adults (60+ years) who received quinine prescriptions in Tayside, Scotland, between January 2004 and December 2015. The first study was a retrospective longitudinal cohort study with the primary outcome AKI. Creatinine measurements less than seven days apart were grouped as episodes of care. Multivariable logistic regression was used to calculate odds ratios (OR) for AKI comparing between episodes with and without recent quinine exposure after adjustment for demographics, comorbidities and concomitant medications. A self-controlled case series (SCCS) was then conducted with follow-up divided into periods “on” and “off” quinine for the same individual, calculating incidence rate ratios (IRR) for AKI adjusting for age.

Results

The first study included 12,744 individuals who experienced 13,616 AKI events during cohort follow-up (crude incidence 12.5 per 100 person-years). Exposure to quinine before an episode of care was significantly associated with an increased probability of AKI (adjusted OR=1.27, 95% CI 1.21-1.33). The SCCS cohort included 5,907 people with quinine exposure with ≥1 AKI event. Exposure to quinine was associated with an increased relative incidence of AKI compared to unexposed periods (IRR=1.20, 95% CI 1.15-1.26), with the greatest risk observed within 30 days of quinine initiation (IRR=1.48, 95% CI 1.35-1.61).

Conclusion

Exposure to quinine in patients aged 60 years and over was associated with an increased risk of AKI, the incidence of which is unlikely to simply be explained be immune-mediated reactions only. Further research is required to determine exact reasons for the increased risk of AKI.
P0587CLINICAL PROFILE AND SHORT-TERM OUTCOMES OF ACUTE KIDNEY INJURY IN PATIENTS WITH PRE-ECLAMPSIA AND ECLAMPSIA
Authors: Sharma Manjuri , MAZUMDER MASTAKIM AHMED , Mahanta Pranab Jyoti , Doley Prodip Kumar , Pegu Gayatri , Alam Shahzad
Published: June 2020

Background and Aims

Acute kidney injury (AKI) is rare in women during pregnancy and puerperium. Although sepsis remains the predominant cause of AKI in pregnancy in developing countries, pre-eclampsia and eclampsia are important causes and can be life threatening. The primary focus of this study was to analyze the clinical profile as well as maternal and fetal outcomes of AKI in pregnant females with pre-eclampsia and eclampsia.

Method

A prospective study of patients admitted with pre-eclampsia or eclampsia and AKI in Gauhati Medical College Hospital from June 2018 to June 2019. Clinical profiles and outcome data were recorded. AKI was defined according to the Kidney Disease Improving Global Outcomes (KDIGO) criteria.

Results

A total of 26 cases were recorded. The mean maternal age at delivery was 27.5 ± 5.1 years. At least one recorded preexisting medical condition, including hypertension, diabetes mellitus, or chronic kidney disease was present in 5 cases (19.2%). Cesarean section was performed in 9 cases (34.6%). Eighteen patients (69.2%) developed AKI in third trimester and 6 (23.1%) within 12 weeks postpartum. Four patients (15.4%) were treated with dialysis. Four women (15.4%) died and 2 (7.7%) remained dialysis dependent 12 weeks after delivery. Low birth weight (<2500 g), small for gestational age or preterm birth (<37 weeks gestation) occurred in 11 pregnancies (42.3%). There were 2 (7.7%) neonatal deaths. AKI occurring before 34 weeks of gestation had worse fetal outcomes as compared to those after 34 weeks (p<0.05).

Conclusion

AKI in pregnancies with pre-eclampsia or eclampsia can not only lead to maternal mortality and morbidity but also poor perinatal outcomes. Preeclampsia or eclampsia presenting with AKI early during gestation had worse fetal outcomes.
P0589ACUTE KIDNEY INJURY IN PATIENTS UNDERGOING LIVING DONOR LIVER TRANSPLANT-INCIDENCE ,RISK FACTORS AND SHORT TERM PATIENT OUTCOMES ,A PROSPECTIVE SINGLE CENTER STUDY
Authors: Rana Abhyudaysingh , Gadde Ashwini , Mahapatra Amit , Saraf Neeraj , Soin Arvinder , Bansal Shyam
Published: June 2020

Background and Aims

AKI is a major concern in the management of candidates for liver transplantation. Post-LT AKI is associated with worse short- and long-term recipient and graft outcomes and the subsequent development of chronic kidney disease (CKD ).Most of the studies done on this are on deceased donor Liver transplant ,or if done on Living donor are retrospective in nature & there is inconsistency in studies regarding definition of AKI

To assess incidence, risk factor and outcomes of patient developing acute kidney injury(AKI) in patients undergoing living donor liver transplant(LT).

Method

This is a single center prospective study. Patients over age of 18 years undergoing living donor liver transplant were selected consecutively from Jan 19 to April 19, prospectively followed for 1 month post op to assess incidence of AKI(Early-<=7,Late >7 to <30) & reassessed at 3 months for persistence of renal dysfunction .Patients with fulminant liver failure, those undergoing combined liver kidney transplant & who died within first 72 hour post-LT were excluded .AKI was defined by KDIGO criteria. Preoperative, Intraoperative & Post operative variables were analysed for risk factor & patient outcomes by regression analysis.

Results

62 patients underwent LDLT between period of Jan 2019 to April 2019 .22(35%) patients developed AKI .15 (68%) had stage 1 AKI ,5 (23%) Stage 2 & 2(9%) had stage 3 AKI requiring CRRT.14 (64 %) patients had early AKI ,8 (36%) had late AKI.Acute CNI toxicity (3,14%) was most common cause of early AKI.Most common cause of Late AKI was Sepsis (7,11%).Use of vasopressors intra op & Past history of AKI (HRS) were the only statistically significant(p <0.001) risk factors for AKI .The mean ICU stay among patients with AKI was 7.2 ±4.2 days vs 4.5±1.2 days in patients without AKI .Median days to normalization of liver enzymes in non AKI group was 10 days vs 20 days in AKI group.2 (3.2%)patient had persistence of renal dysfunction at 3 month. 7(11.2%) patients died during analysis period, 2(3%) of them from AKI group.

Conclusion

- Incidence of AKI (35%) was higher in our study as compared to other cohort but lead to CKD in 2 patients . Past history of AKI (HRS) was a significant risk factor for Post op AKI though pre transplant e GFR did not differ in both group. Although AKI was transient but it lead to increase ventilator stay ,ICU stay and prolonged normalization of graft function in patients undergoing Living donor liver transplant.
P0590ADVERSE RENAL OUTCOME FOLLOWING ADMINISTRATION OF INTRAVITREAL ANTI-VASCULAR ENDOTHELIAL GROWTH FACTOR INHIBITORS IN A SINGLE TERTIARY CENTRE IN MALAYSIA
Authors: Jalalonmuhali Maisarah , Tengku Kamalden Tengku Ain Fathlun , Ismail Nurul 'Ain Sham , Yong See Yen , Teo Wei Ting , Lim Soo Kun
Published: June 2020

Background and Aims

Intravenous (IV) anti-vascular endothelial growth factor(VEGF) is a potent anti-angiogenic factor for the treatment of solid tumours. While, intravitreal anti-VEGF injection is used in the treatment for macular and retinal diseases. The effects of IV anti-VEGF agents are well documented to cause hypertension, renal impairment and proteinuria. However only few reports showed the significance of intravitreal anti-VEGF injection causing minimal change disease (MCD) and acute kidney injury (AKI). Hence, this study is to determine the outcome of renal function following intravitreal anti-VEGF injection.

Method

This is a prospective, cross sectional study recruiting patients from ophthalmology day-care operation theatre that were scheduled for intravitreal anti-VEGF injection in University Malaya Medical Centre (UMMC). On the day of the injection of anti-VEGF, patients’ demographic data (age, gender, medical background, medications), blood pressure, height, weight and investigations for serum creatinine and urine protein creatinine ratio (PCR) were collected. Following these, they will receive the intravitreal anti-VEGF as per schedule. All these patients were given a follow-up within 72hours to reassess blood pressure, serum creatinine and urine PCR.

Results

A total of 90 patients were recruited. However, 15 patients were subsequently excluded as there was no repeated serum creatinine at 72-hours post treatment. Their mean age was 67.25 ± 10.41. Among all, 3 patients had significance increased in serum creatinine (4%) with significance changed of urine PCR post treatment. Table 1 showed baseline parameters prior to treatment and table 2 was post treatment parameters.

Higher serum creatinine and proteinuria pre intravitreal anti-VEGF were identified to have higher OR of 1.018 (95% CI 1.001-1.035) (p=0.043) and OR 1.004 (1.000-1.007) (p=0.025) respectively among those who developed AKI. In assessing the association between higher pre-treatment creatinine and proteinuria (independent variable) and development of AKI (dependent variable) estimated by logistic regression with no AKI as a reference group we found that there were no significance.

Conclusion

Following intravitreal anti-VEGF administration, there were no significant changes in blood pressure. However, 4% from our cohort had AKI and worsening proteinuria at 72 hours post treatment. These patients had higher serum creatinine and proteinuria prior to treatment. However, our study is underpowered to establish the relationship between intravitreal anti-VEGF and development of AKI. Further study with larger sample size and longer-term outcome is needed.
P0592RISK FACTORS FOR SEPSIS ASSCOCIATED-ACUTE KIDNEY INJURY IN INTENSIVE CARE UNIT PATIENTS
Authors: Wang Xin , Zhou Jiaojiao , Yang Jia , Wang Siwen , Yang Lichuan
Published: June 2020

Background and Aims

To explore the risk factors of acute kidney injury in patients with sepsis in intensive care unit (ICU).

Method

The medical records of patients diagnosed with sepsis in ICU of west China hospital of Sichuan university from March 2009 to June 2016 were retrospectively analyzed. Differences between AKI group and Non-AKI group in general data, background disease, ICU entry and exit dates, complications, laboratory data and other related data were analyzed through univariate and multivariate statistical methods.

Results

A total of 2331 patients with sepsis were included in the study, including 626 patients in the AKI group and 1695 patients in the Non-AKI group. The multivariate logistic regression analysis confirmed that age >40 yr. [odds ratio (OR) =2.811], diabetes (OR=2.818), hypertension/coronary heart disease (OR=1.781), CKD (OR=13.221), the length of ICU stay ≥14 days (OR=3.327), heart failure (OR=2.316), ARDS (OR=2.105), SAP (OR=2.566), hypotension (OR=2.048), hypoproteinemia (OR=1.607), lactic acidosis (OR=2.380), hypoproteinemia (OR=1.607), organ failure >1 (OR=4.604),WBC > 10 ×109/L (OR=4.197), serum creatinine (OR=4.535), PCT (OR=1.808), Cys-C (OR=7.066), mild anemia (OR=2.321), moderate anemia (OR=4.047), and severe anemia (OR=6.100) were all independent risk factors of SA-AKI.

Conclusion

A variety of risk factors are related to the occurrence of SA-AKI. Early identification and monitoring of risk factors for SA-AKI and early prevention of AKI can improve the prognosis of sepsis patients.
P0595CHANGING EPIDEMIOLOGY AND OUTCOME OF AKI PATIENTS IN TEACHING HOSPITAL FROM A DEVELOPING COUNTRY: A POPULATION-BASED COHORT STUDY
Authors: Ponce Daniela , Zamoner Welder , Batistoco Marci , Balbi Andre
Published: June 2020

Background and Aims

While considerable information is available on acute kidney injury (AKI) in North America and Europe, large comprehensive epidemiologic studies of AKI from Latin America and Asia are still lacking. The present study aimed to evaluate the epidemiology and outcome of AKI in patients evaluated by nephrologists in a teaching Brazilian hospital.

Method

We performed a large retrospective observational study that looked into epidemiology for AKI and its effect on patient outcome across time periods. For comparison purposes, patients were divided into two groups according to the year of follow up: 2011-2014 and 2015-2018.

Results

We enrolled 7,976 AKI patients and after excluding patients with Chronic Kidney Disease stages 3 to 5, kidney transplanted and those with incomplete data, 5,428 AKI patients were included (68%). The maximum AKI stage was 3 (50.6%) and mortality rate occurred in 1865 patients (34.3%). Dialysis treatment was indicated in 928 patients (17.1%). Patient survival improved along study periods: patients treated at 2015-2018 had a relative risk death reduction of 0.89 (95% CI 0.81–0.98, p=0.02). The independent risk factors for mortality were sepsis, older >65 anos, admission to ICU, AKI-KDIGO 3, recurrent AKI, no metabolic and fluid demand to capacity imbalance as dialysis indication and the period of treatment.

Conclusion

We observed an improvement in AKI patient survival along the years even after correction for several confounders and using a competing risk approach. Identification of risk factors for mortality can help in decision making for timely intervention, leading to better clinical outcomes.
P0598COMPARISION OF OUTCOMES ACCORDING TO URINE CHEMISTRY TESTING TIME FOR THE CAUSES OF ACUTE KIDNEY INJURY PATIENTS ADMITTED TO THE EMERGENCY ROOM
Authors: Hwang Won Min , Yun Sung Ro , Yoon Se Hei
Published: June 2020

Background and Aims

Rapid identification and treatment of acute kidney injury can help to restore kidney function. In order to differentiate between prerenal AKI and intrinsic AKI, we perform a urine chemistry test to determine the function of the renal tubule. However, there is no report that it is helpful to arrive at the hospital as early as possible and to perform these urine chemistry tests as soon as possible.

Method

We analyzed the timing of urinary chemistry in AKI patients who were admitted to our hospital through the emergency room for 3 years and divided into two groups. Early group was defined as patients who performed the test within 3 h of arrival in the emergency room. Late group was defined as patients who were late or not. The prognostic factors were change in 30 day eGFR and duration of hospital stay. We also compared the usefulness of urine chemistry test between pre renal AKI and intrinsic AKI in each group.

Results

The changes of eGFR after 30 days in each group are 41.6 ± 27.6 mL/min/1.73 m2 (Early group, n = 92) vs 30.4 ± 26.8 mL/min/1.73 m2 (Late group, n = 180) (P = 0.0013). Early group patients were discharged more quickly than patients in the late group (Hospital day: 11.5 ± 10.1 vs 13.8 ± 10.5, P = 0.0450). When analyzed according to the causes of AKI, these changes showed differences in prerenal AKI rather than intrinsic AKI(Figure).

Conclusion

A urine chemistry test is a test to help determine the cause of AKI. Based on the results of urine chemistry performed within 3 h after arrival at the hospital, patients with AKI who visited the emergency room had better improved kidney function and less hospitalization.
P0600LONG-TERM PROGNOSIS OF PATIENTS WITH METFORMIN -ASSOCIATED LACTIC ACIDOSIS(MALA) AND ACUTE KIDNEY FAILURE
Authors: Melero Martin Maria Rosa , Muñoz de Morales Alejandra , Tejedor Jorge Alberto , Patrocinio Rodriguez benitez , Bascuñana Arturo , Gueorguieva Antonia , Goicoechea Marian
Published: June 2020

Background and Aims

Although metformin-associated lactic acidosis (MALA) is a very rare event, is frequently seen in patients on metformin with risk factors for developing acute kidney injury (AKI). The long-term prognosis in patients with metformin-associated lactic acidosis (MALA) and renal failure remains unknown.

To describe the characteristics and prognosis of AKI in patients with MALA and investigate whether prescription of RRT and previous renal function are associated with long-term outcomes.

Method

A retrospective single-centre case series. One hundred and nine patients affected with MALA and AKI admitted between Marx 2007 and February 2019 were included. We analysed comorbidities, laboratory tests, clinical parameters and prescription pattern of RRT at admission. After discharging, renal outcomes (doubling serum creatinine or starting dialysis) and mortality were assessed in the long-term.

Results

We included 109 patients (59 males and 50 females), mean age of 74.2±8.6 years and mean Charlson comorbidity index of 8.0±2.4. 54 out of 109 patients had previous chronic kidney disease (eGFR < 60 ml/min/1.72 m2). Precipitating causes of AKI associated MALA included; acute dehydration (84.4%), exposure to iodinated contrast (7.3%) and non-specified causes (8.3%). During the admission, renal replacement therapy (RRT) was performed in 72 patients (continuous renal replacement therapy in 47 and dialysis in 25). RRT requirements was significantly associated with lactate, acidosis and serum creatinine levels, but not was associated with higher mortality rate during admission.

The patients were followed a median time of 33 (10-65) months after discharging. 33 patients had a renal event and 55 patients died. The patients with CKD before admission had higher number of renal events (log Rank 6.346, p=0.012) and higher mortality (log Rank 12.943, p<0.001). In a model adjusted by age and RRT at admission, women were less likely to develop (HR 0.315(0.136-0.730, p=0.007) long-term renal events and previous CKD increased this probability (HR 2,532 (1.190-5.385), p=0.016). Previous CKD and RRT during admission increased mortality in a model adjusted by age, gender and comorbidity (HR 2.315(1.177-4.553), p=0.015 and HR 1.895(1.003-3.580), p=0.049, respectively).

Conclusion

The renal function prior to the episode of AKI associated to MALA and the RRT at admission are the main factors related to renal outcomes and mortality in the long-term.
P0609THE INCIDENCE AND RISK OF CONTRAST INDUCED ACUTE KIDNEY INJURY IN THE ELDERLY UNDERGOING PULMONARY COMPUTED TOMOGRAPHY ANGIOGRAPHY
Authors: Fadel Alrowaie , Almatham Khalid , Almousa Saud , Abonab Majed , AlJaser Abdullah , Alqahtani Ali , Alsaif Said , Alkadi Ammar , Alquefil Khalid
Published: June 2020

Background and Aims

Contrast-induced acute kidney injury nephropathy (CI-AKI) is a leading cause of acquired acute kidney injury and has been associated with prolonged hospitalization and adverse clinical outcomes. Advanced age has been reported as risk factor for CI-AKI. However, limited studies available to determine the exact incidence of CI-AKI in elderly patient. The aim of this study was to investigate the incidence of, risk factors for developing CI-AKI in patient above 65 years old who underwent Pulmonary Computed Tomography Angiography (PCTA).

Method

This single center retrospective study, performed in a large, tertiary care hospital in Riyadh, Saudi Arabia. It is a sub-study of (3 P-CIAKI) The Practice Pattern of Preventive Measures for Contrast Induced Acute Kidney Injury in Patients Undergoing Pulmonary Computed Tomography Angiography. Patients > 65 years of age, who underwent PCTA during a 5-year period (2014 to 2018) were included. Patients receiving long-term hemodialysis or peritoneal dialysis, and those without repeated serum creatinine 48-72 hours post procedure were excluded from the analysis. CI-AKI defined as raise of serum creatinine by 44 mmol/l 48-72 hours post PCTA.

Results

272 out of 908 patients, with a mean age of 74.93 ± 7.09 years, 58.1% having diabetes mellitus (DM) and estimated GFR of 74.92 ± 23.57 ml/min per 1.73 m2 were enrolled. 201 patients (73.9%) had eGFR > 60 ml/min. Diuretics was used by 37.1% of the patients, while 33.1 % of the patients on ACEI / ARBs. Prophylactic measures used in 35.7 % of the procedures. CI-AKI occurred in 19 cases (7.0 %) as compared with 4.7 % in the original 3 P-CIAKI study with mean age of 52 years and eGFR 97 ml/min. Renal replacement therapy required in 3 patients who had CI-AKI. DM status was only significant predictor for the development of CI-AKI.

Conclusion

Elderly patients are at greater risk for the development of CI-AKI even with eGFR above 60 ml/min specially in DM patient .The Incidence of CI-AKI in patients > 65 years of age is up to 7 %, that is less than the reported in the literature and this can be explained by higher base line eGFR in our study .
P0610ACUTE KIDNEY INJURY IN CRITICALLY ILL PATIENTS IN THE ICU
Authors: Markovic Mira , Knezevic Violeta , Azasevac Tijana , Knezevic Aleksandar , Stojkovic Svetlana , Celic Dejan
Published: June 2020

Background and Aims

Acute kidney injury (AKI) is common and serious complication in critically ill patients in intensive care unit (ICU). The rapid increase in aging populations with more comorbidities contribute to high incidence AKI in ICU. Incidence varies from 20% to as high as 70%. AKI in the ICU frequently requires costly supportive therapies, has high morbidity and it’s associated with poor outcomes.

We aimed to determine incidence of AKI, causes, risk factors, treatment and outcomes of AKI in critically ill patients in ICU.

Method

We collected data prospectively from case records of adult patients (older than 18 years of age) admitted to the ICU at the Department of Internal medicine, Emergency Center, Clinical center of Vojvodina in Novi Sad, Serbia, during 3 months. We included patients who had at least two measurements of serum creatinine. Data on patient demographics, diagnosis at the time of ICU admission, complete blood count, biochemistry, comorbidities (diabetes mellitus, arterial hypertension, other cardiovascular diseases, renal disease, prostate diseases, dehydration, burns, gastrointestinal bleeding, pancreatitis, peritonitis, sepsis), use of nephrotoxic agents, radiological procedures and treatment of AKI were recorded. We excluded patients with chronic renal disease who were on hemodialysis. There were no interventions.

Results

Of the 44 patients included in the study, median age was 67+/-13,20 years (range: 21 to 88). Of those 44 patients 20% developed AKI. De novo AKI was diagnosed in 51,22% of those patients and 48,78% had chronic renal failure in acutisation. The most frequent etiology was pre-renal, in 80,95% of patients. Renal origin and obstructive (post-renal) causes were detected in the same number of patients, 9,52%. Comorbidities were present present in all patients. Most common comorbidity was arterial hypertension, in 52,4% of patients, other cardiovascular diseases in 47,6 % of patients, sepsis also in 47,6% of patients and gastrointestinal bleeding in 33,3% of patients. Complete recovery of kidney function was detected in 42,86% of patients. Mortality was 28,57%. During the hospitalisation 90,48% of patients were treated conservative and 9,52% of patients required renal replacement therapy.

Conclusion

De novo AKI occurred in approximately half of the critically ill patients in ICU. The most frequent etiology was pre-renal. AKI was mainly detected in older patients with comorbidities. Age and comorbidities were also associated with the poor outcome. Mortality was high.