bluuebunny/crossref_metadata_2025_split huggingface dataset:
P0939THE ASSOCIATION BETWEEN MUSCULAR STRENGTH, MUSCLE MASS AND DEPRESSION IN KIDNEY TRANSPLANT RECIPIENTS: A CROSS-SECTIONAL ANALYSIS
Authors: Vučković Marijana , Raos Hrvoje , Kovačević Katja , Orešković Josip , Gelemanović Andrea , Roguljić Marija , Radic Josipa 
Published: June 2020

Abstract

Background and Aims
While kidney transplantation (Ktx) offers several advantages in terms of improved clinical outcomes and quality of life compared to dialysis modalities, depressive symptoms are still present in approximately 25% of patients, rates comparable to that of the hemodialysis population. Correlates of depressive symptoms include marital status, income, and kidney function, history of affective illness, malnutrition, and inflammation. The aim of this study was to evaluate possible correlations between nutritional status evaluated through body mass composition parameters, muscle strength and depression in kidney transplant recipients (KtR).

Method
115 KtR, 61 (53 %) men and 54 (47 %) women, aged 59.3 (range 25 - 83) years were included. For each patient data about duration after Ktx, duration of dialysis before Ktx, age, gender, body weight and height were collected and body mass index (BMI) was calculated. Tanita MC780 Multi Frequency segmental body composition analyser was used to measure content of body fat, muscle mass, and visceral fat each study subject measured in kilograms (kg) and percentage (%.) Peripheral muscle strength of KtR was measured by using a standardized handgrip dynamometry protocol. The Beck Depression Inventory-Second Edition (BDI-II) was used as an indicator of the severity of depression.

Results
Out of all 115 KtR patients, according BDI-II score 25 (21.7 %) were depressed; 15 (13 %) had mild, 6 (5.2 %) moderate and 4 (3.5 %) severe depression. Significantly negative correlations between BDI-II scores (higher score – more depressive symptoms) and muscle mass (kg and %) was found (R=-0.205, P=0.032), (R=-0.278, P=0.003), respectively. Therefore, significantly positive correlations between BDI-II scores (higher score – more depressive symptoms), fat mass (%) and age was found (R=-0.24, P=0.012), (R=-0.231, P=0.013), respectively. Those KtR patients with more depressive symptoms (higher BDI-II score) had statistically lower muscle strength (R=-0.205, P=0.032). Significantly correlation between duration after Ktx and duration of dialysis before Ktx with BDI-II score was not found.

Conclusion
Prevalence rates for depression in this study is similar with previous reports and results have shown that depressive KtR patients were older and had significantly lower muscle mass and muscle strength and significantly higher fat mass content. Possible explanation for this findings might be that depression in KtR is associated with unhealthy behaviours including lower activity levels and worse dietary habits, which may in turn impact body mass composition parameters and upon transplant-related outcomes. Efforts to detect and treat depression should be a priority if one is to improve treatment and dietary adherence, quality of life, and outcomes in KtR.
P0952NEUTROPHIL GELATINASE - ASSOCIATED LIPOCALIN LEVEL AS A MARKER OF MALNUTRITION IN HEMODIALYSIS PATIENTS
Authors: Sabry Alaa , Mahmoud Rasha , Alsaody Shimaa 
Published: June 2020

Abstract

Background and Aims
Among hemodialysis patients, malnutrition is a common health problem, it is a marker of poor prognosis in these patients, associated with increased risk of hospitalization and mortality. NGAL is an iron transporting factor which increases in the serum in acute and chronic kidney disease. The aim of our study is to assess the use of NGAL as a marker of malnutrition in patients with stage 5 CKD maintained on hemodialysis.

Method
This is a cross-sectional study of 80 regular hemodialysis (HD) patients (51 males and 29 females). All cases of this study were subjected to: Anthropometric measurements . Biochemical measurements: Neutrophil Gelatinase-associated Lipocalin Level in blood using commercially available ELIZA kits, Serum albumin, Blood urea, Complete blood count, Serum electrolytes .

Results
According to the result we found in our study 100% of CKD having malnutrition according to SGA, MIS and our data however most of our patients are mild malnutrition.
We found also a significant decrease in some anthropometric parameters including BMI, fat mass, TSF, MAC, MAMC and MAMA with advanced malnutrition in hemodialysis patients. In this study, we use Twenty-four hours dietary recall and we found most of patients were with low protein (96.2%) and calorie (68.8%) contents. Dialysis adequacy (Kt/V) can affect the nutritional status of patients Kt/V was adequate in all malnutrition groups. These findings are consistent with an earlier report in which HD patients with Kt/V&gt;1.4 had a significantly higher rate of malnutrition than patients with Kt/V ≤1.4. in this study NGAL serum levels were significantly (P=0.018) reduced with the severity of malnutrition. In this study, Spearman correlation analysis revealed that NGAL serum levels were significantly correlated with SGA (r =o,247 P =0.027) and albumin serum levels (r =0.402, P &lt;0.001).
NGAL serum levels were significantly (P=0.018) reduced with the severity of malnutrition. Using ROC curve analysis, NGAL serum levels had a good ability (AUC=0.845) to predict severe malnutrition with good sensitivity (83.3%) and specificity (78.4%).

Conclusion
NGAL is well correlated with other standard markers used routinely in assessment of nutritional status of hemodialysis patients. Patients with high NGAL levels were closely related to good nutritional status. Its serum levels had a good diagnostic power for severe-malnourished patients, as it helps us for early prediction to malnutrition.
P0962CHRONIC KIDNEY DESEASE AND URINARY TRACT INFECTION IN PREGNANTS
Authors: Vetchinnikova Olga , Nikol`skaya Irina 
Published: June 2020

Abstract

Background and Aims
Pregnant women with chronic kidney disease (CKD) are at risk of developing/exacerbating urinary tract infection (UTI) due to the presence of additional (“specific”) risk factors. The aim of our study was estimation the features of UTI in women with CKD during pregnancy.

Method
The study included 139 women with CKD G1-G3 who had UTI during pregnancy. Most women (63) had chronic glomerulonephritis, 47 had with chronic pyelonephritis, and the rest had diabetic nephropathy (11), chronic tubulointerstitial nephritis (9), renal transplant (7) and lupus nephritis (2). An analysis of the bacteriological examination of urine, the sensitivity of pathogens to antibiotics, clinical manifestations and perinatal complications was performed.

Results
The following forms UTI are diagnosed: asymptomatic bacteriuria (50.4%), exacerbation of chronic pyelonephritis, including renal transplant (33.1%), acute pyelonephritis (16.5%). The true bacteriuria is determined identically at all stages of CKD, in those with chronic pyelonephritis in 70%, chronic glomerulonephritis in 45% of cases (p = 0.02). Gram-negative microorganisms become apparent in 73.6% of pregnant women with CKD, less often in patients with glomerular pathology than with chronic pyelonephritis (66% versus 81%). Escherichia coli among gram-negative microorganisms was 74.4%, a high frequency of detection of strains with the production of extended-spectrum β-lactamases was established. The course of asymptomatic bacteriuria in pregnant women with non-diabetic glomerulopathy was characterized by a moderate tendency to relapse and moderate release of resistant pathogens. The course of asymptomatic bacteriuria in patients with diabetic nephropathy and after kidney transplantation, on the contrary, had a pronounced tendency to relapse and the frequent release of resistant pathogens. Exacerbation of chronic pyelonephritis proceeded with minimal clinical manifestations, a vivid clinical picture of exacerbation of the disease was determined in one third of pregnant women. It was characterized by a high tendency to relapse and the development of systemic infection, a high frequency of release of resistant pathogens. Pregnant women with CKD who underwent UTI had a high risk of giving birth to premature babies (23% versus 11% p=0.01) who were required to carry out artificial lung ventilation and transfer to stage nursing (34% versus 16%, p=0.01).

Conclusion
The course of UTI in pregnant women with CKD is characterized by a high prevalence, dependence on primary renal disease, the release of resistant pathogens, and a high probability of an atypical clinical picture.
P0970EXOSOMAL MIR-92A-1-5P DERIVED FROM PROXIMAL TUBULAR EPITHELIAL CELLS INDUCES EPITHELIAL-MESENCHYMAL TRANSITION IN MESANGIAL CELLS IN DIABETIC NEPHROPATHY
Authors: Tsai Yi-Chun , Kuo Mei-Chuan , Hsu Ya-Ling 
Published: June 2020

Abstract

Background and Aims
Diabetic nephropathy (DN) has been the leading cause of end-stage renal disease in the world-wide. Exosomes play a key role in signal transduction between cell-cell communication in kidney pathophysiology. The aim of this study is to investigate that HK-2 cells-derived exosomal miR-92a-1-5p causes epithelial-mesenchymal transition (EMT) in mesangial cells (MCs), further leading to DN progression.

Method
The function of HK-2 cells-derived exosomes under normal glucose (NG) and high glucose (HG) was analyzed in mouse MCs model. Total RNAs were extracted from renal proximal tubular epithelial cells (RPTECs) of normal individual and type 2 diabetes for small RNA expression profiling using next-generation sequencing (NGS), then analyzed using systematic bioinformatics analyses. The expression of miR-92a-1-5p was examined in HK-2 cells-derived exosomes and MCs treated with HK-2 cells-derived exosomes under HG. The role of miR-92a-1-5p in EMT was evaluated using MCs model under NG and HG conditions. Urinary exosomal miR-92a-1-5p levels were measured in 50 type 2 diabetic patients and 34 healthy volunteers who were enrolled to determine the relationship between urinary exosomal miR-92a-1-5p and kidney function.

Results
Decreased E-cadherin, and increased N-cadherin and Vimentin expression were found in mouse MCs treated with HK-2 cells-derived exosomes under HG. Transcriptome analysis of RPTECs of normal individual and type 2 diabetic patient indicated that miR-92a-1-5p contributes to HG-induced renal proliferation. HG elevated miR-92a-1-5p expression in HK-2 cells and exosomes derived from-HK-2 cells, at meanwhile exosomal miR-92a-1-5p derived from-HK-2 cells under HG leads to EMT in mouse MCs. miR-92a-1-5p mimic increased EMT in mouse MCs under NG, and miR-92a-1-5p inhibitor reversed EMT in mouse MCs induced by exosomes derived from HK-2 cells under HG. EMT of mouse MCs was enhanced in the presence of exosomes isolated from the urine of type 2 diabetic patients with high levels of exosomal miR-92a-1-5p. Type 2 diabetic patients had higher urinary exosomal miR-92a-1-5p levels than normal individuals. Higher urinary exosomal miR-92a-1-5p levels were significantly correlated with lower renal function and higher albuminuria in human model.

Conclusion
Exosomal miR-92a-1-5p derived from HK-2 cells under HG induces EMT in mesangial cells. Blocking miR-92a-1-5p epigenetic regulatory network might be a potential therapeutic strategy to prevent EMT in DN.
P0977LOW EXPRESSION OF AUTOPHAGY-RELATED PROTEIN 5 (ATG5) LEADS TO SUPPRESSION OF AUTOPHAGY IN PATIENTS WITH DIABETIC NEPROPATHY AND RETINOPATHY
Authors: Nakhoul Nakhoul , Nakhoul Rula , Abass Remah , Farber Evgeny , Tadmor Hagar , Nakhoul Farid 
Published: June 2020

Abstract

Background and Aims
Autophagy is a catabolic mechanism that involves lysosomal-dependent degradation of unnecessary or dysfunctional intracellular components. Autophagy plays role in many biological processes, including diabetic nephropathy (DN) and diabetic retinopathy (DR). Autophagy-related gene 5 (ATG5) is one of the most important participants in the autophagy mechanism. Deficiencies in ATG5 protein levels are associated with several diseases by influencing the level of autophagy pathway. Our study's aim was to investigate if aberrant expression of ATG5 protein or Atg5 gene is associated with DN or DR.

Method
The study included 120 human participants in 4 groups – Healthy, diabetic (DM), DN and DR; and 10 mice in 2 groups – healthy and DN. Western blot analyses of ATG5 and its downstream collaborator LC3B were performed on human white blood cell (WBC) lysates and murine renal lysates. Immunohistochemical analysis was performed on mice renal tissues. Quantitative real-time PCR analysis of ATG5 was performed on total mRNA isolated from human WBC.

Results

Conclusion
P0979BENEFICIAL EFFECT OF CHLOROQUINE AND AMODIAQUINE ON DIABETIC TUBULOPATHY BY ATTENUATING MITOCHONDRIAL NOX4 AND ENDOPLASMIC RETICULUM STRESS
Authors: Lee So-Young , Yang Dong Ho , Lee Yu Ho , Lee Mi Jung , Kim Hyung-Jong , Sung MinJi , An Hyun-Ju , Lee Sang-Ho 
Published: June 2020

Abstract

Background and Aims
Oxidative stress induced by chronic hyperglycemia is recognized as a significant mechanistic contributor to the development of diabetic kidney disease (DKD). Nonphagocytic nicotinamide adenine dinucleotide phosphate oxidase 4 (Nox4) is a major source of reactive oxygen species (ROS) in many cell types and in the kidney tissue of diabetic animals. We designed this study to explore the therapeutic potential of chloroquine and amodiaquine for inhibiting mitochondrial Nox4 and diabetic tubular injury.

Method
Human renal proximal tubular epithelial cells (hRPTCs) were cultured in high-glucose media (30 mM D-glucose), and diabetes was induced with streptozotocin (STZ, 50 mg/kg i.p. for 5 days) in male C57/BL6J mice. Chloroquine and amodiaquine were administered to the mice via intraperitoneal injection for 14 weeks.

Results
Chloroquine and amodiaquine inhibited mitochondrial Nox4 and increased mitochondrial mass in hRPTCs under high-glucose conditions. Reduced mitochondrial ROS production after treatment with the drugs resulted in decreased endoplasmic reticulum (ER) stress, suppressed inflammatory protein expression and reduced cell apoptosis in hRPTCs under high-glucose conditions. Notably, chloroquine and amodiaquine treatment diminished Nox4 activation and ER stress in the kidneys of STZ-induced diabetic mice. In addition, we observed attenuated inflammatory protein expression and albuminuria in STZ-induced diabetic mice after chloroquine and amodiaquine treatment.

Conclusion
We substantiated the protective actions of chloroquine and amodiaquine in diabetic tubulopathy associated with reduced mitochondrial Nox4 activation and ER stress alleviation. Further studies exploring the roles of mitochondrial Nox4 in the pathogenesis of DKD could suggest new therapeutic targets for patients with DKD.

Figure
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P0989VDR/ATG3 AXIS REGULATES SLIT DIAGRAM TO TIGHT JUNCTION TRANSITION VIA P62-MEDIATED AUTOPHAGY PATHWAY IN DIABETIC NEPHROPATHY
Authors: Qian Jingyi , Wang Bin , Liu Bicheng 
Published: June 2020

Abstract

Background and Aims
Vitamin D receptor (VDR) loss, slit diagram (SD) to tight junction (TJ) transition and impaired autophagic flux contribute to podocyte injury in diabetic nephrology. This study aims to examine the effect and mechanism of VDR on autophagic flux and SD-TJ transition in diabetic nephropathy.

Method
Renal biopsy tissues from DN patients at stage IIa, IIb, III, IV and patients with minimal lesions were used to evaluate the expression of VDR, autophagic flux and SD-TJ transition glomeruli. In vitro, cultured podocytes were treated with serum starvation (SS), autophagic inhibitors (3-methyladenine 3-MA or chloroquine CQ) to determine the degradation pathway of TJ marker ZO-1. Meanwhile, db/db mice and STZ-induced rats were used to explore the therapeutic effect and mechanism of VDR agonist in diabetic nephropathy.

Results
SD-TJ transition between foot processes could be observed under electron microscopy in DN patients at all stages, whereas foot processes were separated by the filtration slit and appeared to be single cross-strands in the normal glomeruli. There was a trend of increasing expression of autophagic marker p62 and ZO-1 and the expression of p62 is positively correlated with the changes of ZO-1 in the glomeruli of DN patients. In vitro, inhibiting autophagy with 3-MA and CQ resulted in the accumulation of ZO-1 in cultured podocytes. In addition, Co-IP experiments further convinced the interaction between p62 and ZO-1, which was enhanced by the activation of autophagy. Podocytes apoptosis and the activity of caspase 3 and caspase 8 were significantly increased in the presence of 3-MA or CQ, while these effects were rescued by silencing p62. According to VDR gene expression data in GEO database, VDR expression was decreased in diabetic nephropathy patients compared with normal people. Knocking down VDR lowered the expression of atg3 and leaded to the blockage of autophagy, which could be reversed by over-expressing Atg3. Podocytes treated with high glucose resulted in the decrease of VDR and Atg3, impaired autophagic flux and aggravated podocytes injury. However, VDR agonist treatment partially reversed all the changes. In vivo, db/db mice and STZ-induced rats (DN animal models) exhibited SD-TJ transition, massive proteinuria, decreased expression of VDR and podocin and the increased accumulation of p62 and ZO-1, all of which could be partially reversed by VDR agonist.

Conclusion
VDR loss contributed to the impairment of autophagic flux and SD-TJ transition via down-regulation Atg3 in diabetic nephropathy. Here, we identified a new mechanism and evidence for VDR agonist to treat diabetic nephropathy.
P0999URINARY EXCRETION OF ADENYLATE AND URIDYLATE NUCLEOTIDES IN STREPTOZOTOCIN-INDUCED DIABETIC RATS
Authors: Sałaga-Zaleska Kornelia , Pikuł Piotr , Kreft Ewelina , Chyła Gabriela , Kuchta Agnieszka , Jankowski Maciej 
Published: June 2020

Abstract

Background and Aims
Extracellular nucleotides (ATP, ADP, UTP, UDP) acting through P2-receptors regulate renal vascular tone and glomerular permeability tor albumin. Both phenomenons are dysregulated in diabetes and are conducive to development of diabetic nephropathy. The aim of study was to investigate the urinary excretion of adenylate and uridynate nucleotides and the effects of suramin, P2-receptors antagonist and non-competitive inhibitor of ectoATPase, on those parameters in streptozotocin-induced diabetic rats.

Method
Diabetes in Wistar rats was induced by streptozotocin injection (65 mg/kg, i.p, day 0) and suramin was injected (10 mg/kg, i.p) on day 7 and 14. Nucleotides concentration in urine collected in metabolic cages on day 21 (3-weeks diabetes) were measured using HPLC method wit UV detector. All values are expressed as mean ± SEM.

Results
The excretion of ATP, UTP, ADP and UDP in diabetes were increased i.e. ATP: 34.99±1.73 vs 18.56±1.59 μmol/24h (p&lt;0.001); UTP: 0,72±0.06 vs 0.47±0,08 vs μmol/24h (p=0.03); ADP: 0,70±0.56 vs 0.28±0,04 vs μmol/24h (p=0.001); UDP: 9.08±1.28 vs 5.06±0,83 vs μmol/24h (p=0.02). UMP excretion was decreased 7.04±0.89 vs 11.36±0,621 μmol/24h (p=0.002) but AMP excretion was not affected by diabetes i.e. 0.86±0.09 vs 0.89±0.12 μmol/24h (p=0.08). Suramin administration did not affect urinary excretion of investigated nucleotides.

Conclusion
diabetes increases the urinary excretion of ATP, ADP, UTP and UDP and this effect is not modified by suramin. The changes in extracellular metabolism of nucleotides may affect the renal function during diabetes. This work was supported by National Science Centre Poland Grant (2016/23/B/NZ5/02632) to MJ.
P1001RENAL DAMAGE ASSOCIATED WITH INTRAVITREAL ADMINISTRATION OF ANTI-VEGF DRUGS
Authors: Fernandez-Vidal Maria , Moliz Candela , Redondo Beatriz , Bada Bosch Teresa , Aubert Lucia , Sandino Justo , Praga Manuel , Garcia Florencio , Morales Enrique 
Published: June 2020

Abstract

Background and Aims
Vascular endothelial growth factor inhibitors (anti-VEGF) have been shown to be effective in the treatment of macular degeneration and diabetic macular edema. It is known that systemic administration of these drugs can produce adverse renal effects, such as decreased glomerular filtration rate (eFGR), proteinuria, hypertension or thrombotic microangiopathy. However, there is little information about it when the administration is intravitreal. The aim of this study was analyzed the effect of anti-VEGF drugs on renal function and proteinuria.

Method
Observational and prospective study on diabetic patients, which were divided into two groups: non-cronic kidney disease (CKD) (group 1) and CKD (group 2). We analyzed clinical and analytical variables during follow-up.

Results
We included 45 diabetic patients (55.6% males) with a median age of 75 (50-91) years. Forty one patients (91.1%) were hypertensive and thirty three (73.3%) were CKD patients. Twenty six (57.8%) received bevazicumab, while the rest (42.2%) received ranibizumab, with a median dose of 6 (1-22). The median follow-up was 25 (9-94) months.
The evolution of eFGR and albuminuria are described in Figure 1, where it stands out the increase in albuminuria in group 2. Regarding the drug type, there were no differences. Within the CKD group, one patient presented two episodes of decompensation of heart failure after the administration of an anti-VEGF drug, and two required the initiation of renal replacement therapy.

Conclusion
Based on the results of our cohort, we believe that it would be advisable to establish a closer monitoring in diabetic patients who are administered an intravitreal anti-VEGF drug, with determination of renal function as well as albuminuria to establish an early diagnosis of possible complications.