bluuebunny/crossref_metadata_2025_split huggingface dataset:
#5674 HYPERURICEMIA AND HIGH URINARY URIC ACID LEVELS ARE THE NEW EARLY PREDICTORS OF CONTRAST-ASSOCIATED ACUTE KIDNEY INJURY
Authors: Cadri Vilma , Toska Loriana , Strakosha Ariana , Rista Elvana , Pasko Nevi , Imeraj Matilda , Barbullushi Myftar , Dibra Alban 
Published: June 2023

Abstract

Background and Aims
Contrast associated acute kidney injury (CA-AKI) is recently evidenced with lower frequency although yet worldwide its incidence ranges from 0-24%. Recent studies and meta-analysis have reported that hyperuricemia seem to be a useful biomarker in the early prediction of CIN incidence. The role of urine PH and spot uric acid to creatinine ratio (UACR) provide controversial evidence on the occurrence of CA-AKI. This research aims to gather evidence on the effect of uricemia, urine PH and UACR on the development of CA-AKI in acute conditions like primary percutaneous coronary interventions (PCI).

Method
A sample of 100 patients who underwent emergency coronary angiography in Cardiology Intensive Care Unit/UHCN-Tirana/Albania from October 2021- March 2022 were enrolled. Among these patients CA-AKI incidence was monitored, while CA-AKI was defined as an increased creatinine levels of more 25% of the baseline in a time window of 48-72h after the contrast. The analyses of the results were performed using ANOVA test for differences in parameters among CA-AKI/Non – CA-AKI patients. In order to understand the effect of each factor on the probability of experiencing CA-AKI a binary logistic regression model was constructed. Statistical analyses were performed using R-software.

Results
The general incidence of CA-AKI is 40%, while being different for men and women, with men incidence being 60%. The mean age for the patients observed was age 64.7 years old. The ANOVA analyses showed that incidence of patients experiencing CA-AKI is significantly different for chronic kidney disease patients (p (0.001, OR = 32.67 (95%CL 9.65-110.55), patients with diabetes (P 0.0033, OR = 4.64 (95%Cl 1.69-12.68) and hypertension (p 0.055, OR = 7.80 (95%Cl 0.96-63.56). The binary logistic regression showed that probability to experience CIN is significantly impacted by UACR post contrast model 1 :3.123 (2,385) with marginal effect 22.72, BMI index model 1: (−0.850) 0.25 with marginal effect 1.28, Uricemia model 1: (1,128) 0.52 with marginal effect 1.68 and Natremia level before contrast model 1: (−1,831) 0.0011 with marginal effect 7.81. Statistical significance for these results is 99% (as manifested by p-value).

Conclusion
CA-AKI post PCI is still the Achilles Heel of interventional cardiology. The results confirm that the increase of uricemia and BMI doubles the risk for CA-AKI. Uricemia is confirmed as an important prognostic factor for development of CA-AKI. High urinary uric acid levels post contrast define UACR independent early risk factor for CA-AKI.
#5689 ASSOCIATION BETWEEN INTERLEUKIN-37 RS3811047 POLYMORPHISM AND LUPUS NEPHRITIS IN AN EGYPTIAN POPULATION
Authors: Ismaeel Samah , Omar Hamdy , Ellawindy Alia , Omar Hanan , Hashem Asma , Tawfeek Marwa 
Published: June 2023

Abstract

Background and Aims
Systemic lupus erythematosus (SLE) is a chronic, clinically heterogenous, autoimmune disorder with unpredictable course and features ranging from mild skin affection to life-threatening involvement of major organs. Interleukin 37 (IL-37) is a cytokine with anti-inflammatory and immune-suppressive effects; it suppresses both innate and adaptive immune responses, thus protecting against excessive inflammation-induced tissue damage.

Aim
investigate the association of IL-37 (rs3811047) polymorphism with lupus nephritis in Egyptian population.

Method
This case-control study comprised 3 groups: 109 SLE patients without nephritis, 97 SLE patients with LN, and 240 healthy controls. History taking, clinical examination, disease activity in SLE patients was assessed and routine laboratory tests were done. Genotyping of the IL-37 rs3811047 polymorphism was done using real time polymerase chain reaction (PCR).

Results
The AA genotype was more frequently represented in LN patients (21.6%) compared to SLE patients without LN (7.3%) (p = 0.007), and carriers of the AA genotype had four times increased susceptibility to acquire LN compared to GG and GA genotype carriers (OR: 4.1). Likewise, the A allele was more represented in LN patients (43%) than in SLE patients without LN (30%) (p = 0.004), and the carriers of the A allele had nearly two times more risk of developing LN compared to carriers of the G allele (OR: 1.79). Moreover, the AA genotype was associated with LN susceptibility under the recessive genetic model (OR = 3.49, CI: 1.47-8.30) (p = 0.002), but not under other genetic models.

Conclusion
The AA genotype of the IL-37 rs3811047 polymorphism contributes to the development of SLE in Egyptian patients with doubled risk of acquiring LN in carriers of the allele A.
#5705 EFFICACY AND SAFETY OF SACUBITRIL/VALSARTAN IN PATIENTS WITH STAGE 3B-5 CKD AND HYPERTENSION
Authors: Zhou Qin , Yu Wenjuan , Shao Xiaofei , Liu Qin , Wang Honglei , Chen Junzhe , Tang Ying 
Published: June 2023

Abstract

Background and Aims
Sacubitril/valsartan (SV) plays a key role in improving left ventricular remodeling and prognosis in patients with heart failure. However its effects on kidney function in people with moderate to severe chronic kidney disease (CKD3b-5) are unknown. The present study was designed to assess the efficacy and safety of sacubitril-valsartan in patients with stage 3b-5 CKD and hypertension.

Method
In this randomized, double-blind, 3-month trial, patients with stage 3b-5 CKD and hypertension were randomly assigned to sacubitril/valsartan treatment group (n = 44, the doses of SV were up-titrated to sacubitril/valsartan 400 mg), and conventional antihyperensive treatment group (n = 40). The primary outcome was reduction in GFR from baseline at week 12.

Results
In total, 44 participants were assigned to sacubitril/valsartan group and 40 to crontol group (conventional antihyperensive group). Baseline measured GFR was 29.94±11.83, 27.86±10.14 mL/min/1.73 m2, respectively. There was no difference in measured GFR (P = 0.064). At week 12, there was a reduction in measured GFR in control group: 27.86±9.15 versus 22.03±11.41, but there was no significant difference (P = 0.155). Sacubitril/ valsartan could improve eGFR: 29.94±11.83 versus 32.05±14.57 (P = 0.018). We also observed that, compared with control group, sacubitril/valsartan decreased albuminuria: reductions in urinary albumin:creatinine ratio (ACR) in sacubitril/valsartan group was 89.5mg/g and reductions in urinary ACR in control group was -44.55mg/g. At week 12, Sacubitril/valsartan provided a significantly greater reduction in office mean sitting (ms) systolic BP (msSBP) than control group (20.75mmHg vs 12.88mmHg, P = 0.046). There was no serious adverse events in both groups. The incidence of hyperkalemia (potassium≥5.5 mmol/L) was 4.5% in SV group and 7.5% in control group.

Conclusion
The present data suggested that, in patients with stage 3b-5 CKD and hypertension, Sacubitril-valsartan could improve kidney function and decrease albuminuria, and was generally safe and well tolerated.
#5772 ESTIMATING CKD PREVALENCE AND INCIDENCE USING CROSS-SECTIONAL GERMAN CLAIMS DATA IN PERSONS AGED 70+
Authors: Bothe Tim , Fietz Anne-Katrin , Pöhlmann Anna , Schaeffner Elke , Mielke Nina , Freitag Julia , Krage Birgit , Ebert Natalie 
Published: June 2023

Abstract

Background and Aims
Little is known about trends over time and anticipated improvements in CKD diagnosis after the implementation of the Kidney Disease – Improving Global Outcomes (KDIGO) guidelines in 2012. We investigated CKD prevalence and incidence over time using claims data in persons aged 70+.

Method
We assessed CKD prevalence and incidence biennially in cross-sectional claims data of the German health insurance fund “AOK Nordost” for persons aged 70+ between 2012 and 2018. Data are available for n = 62,200 persons per year and were sampled equally distributed for five age strata (70-74, 75–79, 80–84, 85–89, ≥90) and for sex. CKD prevalence and incidence were estimated in 2012, 2014, 2016, and 2018 using in- and outpatient ICD-10 diagnoses (N18.3, N18.4, N18.5, N18.8, N18.9, N19). Incidence was defined as prevalent cases without a diagnosis in the four quarters preceding their first CKD diagnosis over all persons at risk (i.e., who were not prevalent in the respective previous year). Results are shown in total (standardized by age and sex using nationwide demographic distributions for a respective year) as well as stratified by age and sex. Cochran-Armitage test was applied to test time trends for incidence and prevalence from 2012–2018.

Results
Claims data-based CKD prevalence showed a significant constant increase from 0.18 in 2012 to 0.26 in 2018 (p &lt;0.001). This time trend in CKD prevalence was consistent among all age and sex strata (Figure 1). Over the same time period, CKD incidence increased from 0.06 to 0.08 (p &lt;0.001), while the percentage of persons at risk decreased from 0.81 to 0.72 between 2012 and 2018 due to increasing prevalence (Table 1). Both prevalence and incidence estimates were higher in males compared to females in all age strata (Figure 1).

Conclusion
The present cross-sectional analysis in claims data allows novel insights of CKD prevalence and incidence among older adults in Germany. CKD prevalence increased constantly over time after the introduction of the KDIGO guidelines in 2012. For CKD incidence, we detected only a small increase over the observation period. The extent of time trends for CKD incidence might be underestimated due to increasing prevalence.
#5781 DRUG-INDUCED ACUTE INTERSTITIAL NEPHRITIS (D-AIN): HOW TO IDENTIFY THE RESPONSIBLE DRUG?
Authors: Moreno Javier Azores , Rivas Begoña , Cabrera Cristina Vega , Cabañas Rosario , Fernández Eugenia García , Yébenes Laura , Barceló Sara Aldana , Raso Irene Vázquez , Juarez Gema Maria Fernandez 
Published: June 2023

Abstract

Background and Aims
The mainstay of D-AIN treatment is the removal of the responsible drug. However, it is not always easy to identify the culprit drug as this entity mainly affects elderly patients on multiple medications, they rarely associate systemic symptoms (rash, fever), and the timeline regarding the diagnosis and the associated drug is not always clear. Therefore, the diagnosis and treatment are delayed, making full renal function recovery less likely. The lymphocyte transformation test (LTT) has demonstrated to be useful in the identification of the involved drug in other hypersensitivity-mediated lymphocyte T diseases such as Stevens-Johnson Syndrome or Dress Syndrome. For this reason, we wonder if this test could be relevant in identifying the responsible drug in D-AIN. The aim of this study is to test LTT in patients with clinical and histological diagnosis of D-AIN.

Method
We have conducted a retrospective observational study in which we have collected data from 2019 to 2022 from our electronic databases.
Results: We have registered 9 cases of D-AIN diagnosed with histological confirmation in whom the LTT had been performed. 22.2% of these patients were men. The mean age was 48.1 years (standard deviation of 15.8). None of them had previous chronic kidney disease (CKD). Mean peak creatinine at diagnosis was 4.66 mg/dl (standard deviation of 1.95). Regarding the typical symptoms of the D-AIN, three patients (33%) presented with fever and none of them suffered from rash. 6 patients had sterile pyuria (66%). All of them received steroid treatment. Concerning the LTT results, 7 cases were positive for one of the drugs the patient was taking, and 2 were negative. Among the positive cases, the identified drugs were 1 case of beta lactams (piperacillin), 1 case of PPIs (omeprazole), 1 case of metamizole, 1 case of paracetamol, 1 case of eslicarbazepine and 2 cases of NSAIDs (dexketoprofen), while the negative cases have not been suspected of taking any culprit drug.

Conclusion
LTT may be a useful test to identify the responsible drug for D-AIN, especially in patients taking multiple medications in which may be included some of great importance like immunotherapy (typical cause of D-AIN) in oncological treatments. In negative cases, it could be expected that the patient had taken medications difficult to be identified in the clinical history or, in some situations, the drug hapten responsible for kidney damage might be a drug metabolite and not the drug itself, which cannot be detected by the test.
#5785 ACUTE KIDNEY INJURY AS A RISK FACTOR FOR THE DEVELOPMENT OF CHRONIC KIDNEY DISEASE AND MORTALITY IN HOSPITALIZED PATIENTS
Authors: García Julio Francisco Colina , García-Galán Lucía Cordero , Martínez Marta Rivero , Hernández Paúl , González-García Celia , Lozano Sergio Huerga , Pérez Justo César Sandino , Auñón Pilar , Gutiérrez Eduardo , Morales Enrique 
Published: June 2023

Abstract

Background and Aims
Acute kidney injury (AKI) is a complication that affects more than 5% of all hospital admissions and up to one third of patients admitted to critical care units. This entity, whose incidence is on the rise, remains a major cause of morbidity and mortality. In addition, AKI has been linked as an independent risk factor for mortality, especially in severe forms, and of those patients who survive, a percentage will develop chronic kidney disease (CKD) during follow-up. We conducted this study to analyse the incidence of CKD at 6 and 12 months follow-up in hospitalized patients with AKI, to identify possible risk factors leading to its development and to determine mortality in this group of patients.

Method
This is a retrospective study of a cohort of cases with AKI (baseline eGFR &gt;60 mL/min/1.73 m2 without previous structural damage) from our hospital, taking place from June 2020 to February 2021. Regarding the evolution of the AKI, four possibilities were considered: recovery of normal kidney function, development of CKD at 6 months, development of CKD at 12 months or death during follow-up.

Results
We studied 148 patients (55% male), with a median age of 83 years (74-87). Thirty-six patients (24.3%) developed CKD at 6 months follow-up and 30 patients (20.3%) at 12 months. Forty-one patients (27.7%) died within the first 12 months following de episode of AKI. The risk factors identified for development of CKD at 12 months were older age (85 vs 77; p = 0.03), higher serum lactate dehydrogenase levels at admission (246 U/L vs 201 U/L; p = 0.04) and at 3 months (252 U/L vs 192,5 U/L; p = 0.039), and eGFR &lt; 60 mL/min/1.73 m2 at 1 week (74,5 vs 57; p = 0.004) and at 3 months (79 vs 50; p &lt; 0.001) of follow-up. Identified risk factors and predictors of AKI-associated mortality were older age (84 vs 80,5; p = 0.018), concomitant oncological pathology (10,8% vs 7,4%; p = 0,018), higher Charlson index (6 vs 5, p &lt;0.001), higher AKI stage (p = 0.042), lower serum albumin levels at first (3.35 g/dL vs 3.90 g/dL; p = 0.014) and at third month (3,2 g/dL vs 4 g/dL; p &lt; 0.001) of follow-up.

Conclusion
Our study showed a high incidence of CKD in patients who have had an episode of AKI. Several risk factors for development of CKD were identified, being the older age and the greater length of recovery period from AKI the most useful predictors in the clinical practice. AKI-associated mortality was very high in those older patients with higher comorbidity and persistence of AKI. Despite advances, we need non-classical biomarkers for early diagnosis and more effective therapeutic measures to avoid this high prevalence of CKD and mortality.
#5790 IMPAIRED FATTY ACID METABOLISM PERPETUATES LIPOTOXICITY ALONG THE TRANSITION TO CHRONIC KIDNEY INJURY
Authors: Rinaldi Anna , Lazareth Helene , Poindessous Virginie , Nemazanyy Ivan , Lopes-Sampaio Julio , Malpetti Daniele , Bignon Yohan , Naesens Maarten , Rabant Marion , Anglicheau Dany , Cippà Pietro , Pallet Nicolas 
Published: June 2023

Abstract

Background and Aims
Understanding the cell-intrinsic mechanisms contributing to the maintenance of a dysfunctional cellular state in chronic kidney disease (CKD) and identifying therapeutic targets are research priorities in renal medicine. A key contributor to chronic kidney histological damage is acute kidney injury, especially ischemia-reperfusion injury (IRI). Persistent cell-extrinsic perturbations generated upon IRI, for example hypoxia, impair the energetic metabolism of Proximal Tubular Cells (PTC) participating in the process of transition from acute to chronic kidney injury. Here, we propose to investigate the PTC intrinsic factors involved in the perpetuation of an impaired cellular state which contribute to CKD progression

Method
We combined single nucleus transcriptomic, metabolomic and lipidomic approaches in experimental models and patient cohorts to investigate the molecular bases of the progression to chronic kidney allograft injury initiated by IRI.

Results
The urinary metabolome of kidney transplant recipients with chronic allograft injury and who experienced severe IRI was significantly enriched with long chain fatty acids (FA). We identified a renal FA-related gene signature with low levels of Cpt2 and Acsm5 and high levels of Acsl4 and Acsm5 associated with IRI, transition to chronic injury, and established CKD in mouse models and kidney transplant recipients. The findings were consistent with the presence of Cpt2-, Acsl4+, Acsl5+, Acsm5- PTC failing to recover from IRI as identified by single nucleus RNA sequencing. In vitro experiments indicated that endoplasmic reticulum (ER) stress contributes to CPT2 repression, which, in turn, promotes lipids accumulation, drives profibrogenic epithelial phenotypic changes, and activates the unfolded protein response.

Conclusion
ER stress through CPT2 inhibition and lipid accumulation, engages an auto-amplification loop leading to lipotoxicity and self-sustained cellular stress. Thus, IRI imprints a persistent FA metabolism disturbance in the proximal tubule sustaining the progression to chronic kidney allograft injury.
#5802 ASSESSMENT OF THE INTERNATIONAL IGA NEPHROPATHY PREDICTION TOOL AFTER IGAN TREATMENT: A CASE-SERIES STUDY
Authors: DI Maso Vittorio , Perencin Brigitta , Yazbek Ahmad , Marcantoni Carmelita , Zacchi Alberto , Zanconati Fabrizio , Bianco Francesco 
Published: June 2023

Abstract

Background and Aims
IgAN have a variable clinical course and a considerable risk of ESKD. The 2021 KDIGO guidelines recognize the International IgAN Prediction Tool (IIgAN-PT) as a quantifier of progression risk at the time of kidney biopsy. The possible application of the IIgAN-PT to re-evaluate the risk after treatment and during follow-up is debated. We analyzed the possible association between treatment response and changes of IIgAN-PT risk estimation.

Method
Retrospective study including patients with IgAN undergone kidney biopsy from Jan 2010 to Dec 2020. Inclusion criteria: treatment with glucocorticoids, age&gt;18, follow-up at 3-6-12-24 months, availability of risk
assessment. Progression risk evaluated by IIgAN-PT at time 0 (biopsy) and after 6-12 months. Two risk groups were identified based on the IIgAN-PT at time 0: Low-Intermediate risk group (Low-risk, IIgAN-PT&lt;23%) and High-risk group (High-risk; IIgAN-PT risk≥23%).

Results
A total of 22 patients were included (59% Low-risk; 31% High-risk). Patients at low- risk had significantly higher eGFR with respect to high-risk group (78 vs 40 ml/min/1.73 m² respectively) (p&lt;0.001). Age, MAP, and RASi use at biopsy did not differ significantly. Proteinuria was comparable among groups: 3.14 g/24 h in High-risk and 2.49 g/24h in Low-risk (p = 0.17). In the Low-risk group the median proteinuria swiftly decays below 1.0 g/day already at three months, and below 0.5 g/day after six. Conversely, in the high-risk group, it remained above 1 g/day until 12 months (Fig. 1). Regarding risk progression assessment: 89% of patients at higher risk at baseline became at lower risk at 6 months (Fig 2; Table 1).

Conclusion
Treatment response was associated with a reduction in the IgAN progression risk as demonstrated by changing of IIgAN-PT already after 6 months. These data suggest a possible dynamic use of IIgAN-PT for IgAN progression risk re-evaluation even in the short follow-up period.
#5811 URINARY CXCL9 AND CXCL10 CONCENTRATIONS AND KIDNEY TRANSPLANT INJURY
Authors: Macioniene Ernesta , Miglinas Marius , Simanavicius Martynas , Vitkauskaite Monika 
Published: June 2023

Abstract

Background and Aims
Kidney transplant rejection is diagnosed by the kidney biopsy which is an invasive diagnostic method, however, non-invasive biomarkers, distinguishing normal kidney transplant from transplant rejection would be prefered but are lacking. CXC chemokine ligand 9 (CXCL9) and CXC chemokine ligand 10 (CXCL10) are gamma interferon inducible small cytokines. The aim of this study was to evaluate urinary CXCL9 and CXCL10 as potential biomarkers of allograft rejection.

Method
117 kidney transplant recipients undergoing kidney transplant biopsy (surveillance or indication) were included into this study. Spot urine samples were collected before kidney biopsy for urinary creatinine, CXCL9 and CXCL10 measurement. The ratios of CXCL9 over urinary creatinine and CXCL10 over urinary creatinine were calculated. Kidney biopsies were analyzed according to Banff criteria by an experienced pathologist.

Results
26 (22.2%) of kidney biopsies were defined as normal histology, 24 (20.5%) – antibody mediated rejection, 9 (7.7%) – T cell mediated rejection, 10 (8.6%) mixed rejection, 5 (4.3%) BK virus nephopathy and 43 (36.8%) were defined as other histological lesions. Average CXCL9/creatinine was 0.39 ng/mmol in normal histology group and 12.1 ng/mmol in allograft rejection groups (p&lt;0.01). Average CXCL10/creatinine was 0.26 ng/mmol in normal histology and 4.55 ng/mmol in allograft rejection group (p&lt;0.01). CXCL9/creatinine and CXCL10 moderately correlated to proteinuria at the time of kidney biopsy (accordingly r = 0.595, p&lt;0.01 and r = 0.408, p&lt;0.01). ROC curve for CXCL9/creatinine detecting antibody mediated rejection was 0.79, CI 0.67 to 0.90, p&lt;0.01. ROC curve for CXCL10/creatinine detecting antibody mediated rejection was 0.79, CI 0.64 to 0.94, p&lt;0.01.

Conclusion
Urinary biomarkers CXCL9/creatinine and CXCL10/creatinine has a potential to distinguish normal renal histology from allograft rejection and correlates to proteinuria at the time of the biopsy.