bluuebunny/crossref_metadata_2025_split huggingface dataset:
MO605INFLAMMATION-BASED MODIFIED GLASGOW PROGNOSTIC SCORE AND CHRONIC KIDNEY DISEASE PROGRESSION
Authors: Stefan Gabriel , Stancu Simona , Zugravu Adrian Dorin , Capusa Cristina-Stela 
Published: May 2021

Abstract

Background and Aims
The modified Glasgow prognostic score (mGPS), based on combination between albumin (sAlb) and C-reactive protein (CRP), has been derived from oncology and validated in multiple diseases. Since chronic kidney disease (CKD) progression is related to inflammation, we aimed to evaluate the relationship between the mGPS and CKD outcome.

Method
The present retrospective unicentric cohort study included 547 CKD patients (age 60.2 years, 53% male, eGFR 42.0 mL/min, mean change -2 mL/min/year) admitted between January 1, 2007 and December 31, 2012.
The mGPS assessment: zero points if CRP ≤10 mg/L and sAlb ≥3.5 g/dL; one point if CRP &gt;10 mg/L and sAlb ≥3.5 g/dL, two points if CRP &gt;10 mg/L and sAlb &lt;3.5 g/dL.
Patients records were reviewed from the CKD diagnosis to one of the four outcomes: end-stage kidney disease (ESKD), death, loss to follow-up, or until July 31, 2017.

Results
The mGPS score was 0 for 420 (78%), 1 for 110 (19%), and 2 for 17 (3%) patients. Rapid progression defined as a sustained decline in eGFR of more than 5 mL/min/year was found in 17% of the studied patients. More patients with rapid CKD progression were found in the group with the highest mGPS (30% vs 17%, vs 16%, p=0.05).
In the multivariate analysis, mGPS was associated with the eGFR slope (OR 1.42 (95%CI 0.29, 2.55), p 0.01). Moreover, mGPS was negatively correlated with baseline eGFR (OR -3.74 (95%CI 7.8, 0.33), p 0.05) and positively with albuminuria (0.87 (95%CI 0.51, 1.23), p 0.001).
During the study period, 130 patients (24%) died and 109 (20%) reached ESKD. The mean kidney survival time was 8.1 (95%CI 7.9, 8.4) years. Kidney survivals at 12, 24, 36, 48, 60, and 72 months were 96, 95, 89, 86, 83 and 82%, respectively.
In univariate time-dependent analysis, patients with zero mGPS had better kidney survival than those with the score of one and two (99.9 (95%CI 96.9, 102.9) vs 92.1 (95%CI 85.2, 99.0) vs 78.1 (95%CI 60.4, 95.4) months, log rank p=0.02). However, the kidney survival differences were not present after adjusting for CKD progression risk factors (HR 1.12 (95%CI 0.78, 1.62), p 0.5).

Conclusion
The inflammation-based mGPS score was associated with eGFR decline in CKD patients. Therefore, could prove useful in improving risk stratification of CKD patients.
MO606FUNCTIONAL CAPACITY AND NUTRITION-INFLAMMATION BINOMIUM IN PATIENTS WITH ADVANCED CHRONIC KIDNEY DISEASE (ACKD)
Authors: Nogueira Ángel , Alvarez Graciela , Barril Guillermina 
Published: May 2021

Abstract

Background and Aims
There are differents factors that will influence the functional capacity of ACKD patients, among them the nutritional condition.

Aim
to assess the functional capacity of ACKD patients with the Short Physical Performance test Battery (SPPB), and its relationship with the malnutrition-inflammation binomium.

Method
We have evaluated 216 ACKD patients, 66.2% (143) male. xage 70.85 ?12.01 years, being female older than male (72.58 ?13.19 vs 69.96 ?11.32, p = 0.129). We have determine plasma proteins indicators of nutritional status such as albumin, prealbumin and CRP as a marker of the status of inflammation. And we have applied malnutrition inflamation score (MIS).

Results
In the univariate analysis, we found an association between the functionality determined with the test and the age (RR95% 0.866 p = 0.000), sex (RR95% 0.387 p = 0.005). albumin (RR95% 2,222 p = 0.035), prealbumin (RR95% 1.065 p = 0.018), CRP (RR95% 0.733 p = 0.022) and the state nutritional value determined with the MIS scale (RR95% 0.791 p = 0.000). We donot any found any association with DM, transferrin and total lymphocytes. Albumin values were established as 3.8g / dl, and CRP at 1g / dl, obtaining 4 groups: (G1: alb&gt; 3,7-PCR &lt;1, G2: alb&gt; 3,7-PCR&gt; 1, G3: alb &lt;3,7-PCR &lt;1 and G4: alb &lt;3,7-PCR&gt; 1 ).
The table shows the results of the relationship between groups and the limitations determined with SPBB. Group 1 was the most numerous, also being the one with the best nutrition-inflammation profile, observing that in this group 68 patients (78.2%) presented minimal / no limitations.

Conclusions
1. The nutritional-inflammation status will influence the functional capacity of the patient with ERCA.
2. The SPPB test, in addition to being a good choice to evaluate the functional capacity of patients with ACKD, can provide guidance on the nutritional status of patients.
3. Maintaining a good nutritional status will also have a positive influence on the functional capacity of ACKD patients.
MO608INTUITIVE EATING CHANGES AFTER A BEHAVIORAL MULTI-SESSION GROUP INTERVENTION FOR DIETARY MANAGEMENT OF WOMEN WITH CKD
Authors: Antunes Pereira Raíssa , Alvarenga Marle , S. Andrade Laila , R. Teixeira Renata , C. Teixeira Paula , R. da Silva Wanderson , Cuppari Lilian 
Published: May 2021

Abstract

Background and Aims
Approaches promoting eating guided by internal cues, such as intuitive eating (IE), have emerged as an alternative to decrease the impact of external cues on eating behavior while simultaneously avoiding the risk for dysfunctional eating. IE helps to connect with internal cues (i.e. hunger and satiety) and feelings rather than relying on external strategies to regulate what, how much and when to eat. In obese women, IE-based approaches have shown to enhance motivation and adherence to lifestyle changes, hence improving metabolic and psychological parameters, quality of life and diet quality. However, studies evaluating IE in chronic kidney disease (CKD) patients are scarce. Thus, we aimed to evaluate the impact of a behavioral multi-session group intervention on IE scores of overweight non-dialysis-dependent (NDD) CKD women.

Method
This is a prospective non-controlled clinical trial of a behavioral multi-session group intervention for dietary management. It was conducted with overweight women with chronic kidney disease (CKD). Each group comprised 5-8 participants in fifteen weekly or biweekly sessions lasting about 90 minutes. Most of IE principles were discussed throughout the meetings. IE scale 2 (IES2) translated and adapted to Brazilian population and composed of 23 questions with 5-point Likert response scale ranging from 1=“strongly disagree” to 5=“strongly agree” and four-factor model (Unconditional Permission to Eat, Eating for Physical Rather than Emotional Reasons, Reliance on Hunger and Satiety Cues, and Body-Food Choice Congruence) was applied before and after the intervention. The higher the score, the higher the intuitive eating attitudes.

Results
Of the 33 patients that initiated the study, 23 patients [age=62.0 (58.0-68.0) years; schooling= 9.0 (7.0-12.0) years of study; BMI=32.6 (30.2-39.3); eGFR=28.0 (22.0-31.0) ml/min/1.73m²] completed the intervention. Figure 1 shows the results regarding IES2.

Conclusion
The intervention approaching IE principles was effective to improve IE attitudes in the studied patients. With exception for “body-food choice congruence”, all IE subscales improved after intervention. These results are promising and may contribute to a paradigm change in the strategies aiming to enhance motivation and adherence to dietary recommendations in CKD population.
MO592INTERLEUKIN-1A (IL-1A) IS A CENTRAL REGULATOR OF INFLAMMATION IN CARDIOVASCULAR AND KIDNEY DISEASES
Authors: Schunk Stefan , Sarah Triem , Kramann Rafael , Boor Peter , Ampofo Emmanuel , Fliser Danilo , Speer Thimoteus 
Published: May 2021

Abstract

Background and Aims
Cardiovascular diseases (CVD) and chronic kidney disease (CKD) are highly prevalent, aggravate each other, and account for substantial mortality. Both conditions are characterized by activation of the innate immune system. The alarmin IL-1α is expressed in a variety of cell types promoting (sterile) systemic inflammation. The aim of the present study is to examine the role of IL-1α in mediating inflammation in the setting of cardiorenal diseases.

Method
We assessed the expression of IL-1α on the surface of monocytes from patients with acute myocardial infarction (AMI) and patients with CKD and determined its association with atherosclerotic CVD events during follow-up in an explorative clinical study. Furthermore, we assessed the inflammatory effects of IL-1α in several organ injury models in Il1a -/- and Il1b -/- mice and investigated the underlying mechanisms in vitro in monocytes and endothelial cells.

Results
IL-1α is strongly expressed on the surface of monocytes from patients with AMI and CKD compared to healthy controls. Higher IL-1α surface expression on monocytes from patients with AMI was associated with a higher risk for atherosclerotic CVD events, which underlines the clinical relevance of IL-1α. In mice, IL-1α, but not IL-1β, mediates leukocyte-endothelial adhesion as determined by intravital microscopy. IL-1α promotes accumulation of macrophages and neutrophils in inflamed tissue in-vivo . Furthermore, IL-1α on monocytes stimulates their homing at sites of vascular injury. A variety of stimuli such as free fatty acids or oxalate crystals induce IL-1α surface expression and release by monocytes, which then mediates their adhesion to the endothelium via IL-1 receptor-1. Besides, IL-1α promotes expression of the vascular cell adhesion molecule-1 (VCAM-1) on endothelial cells thereby fostering the adhesion of circulating leukocytes. IL-1α induces inflammatory injury after experimental AMI and abrogation of IL-1α prevents the development of CKD in oxalate or adenine-fed mice.

Conclusion
IL-1α represents a key mediator of leukocyte-endothelial adhesion and inflammation in cardiorenal diseases. Inhibition of IL-1α may serve as a novel anti-inflammatory treatment strategy.
MO596HYPERPHOSPHATEMIA INDUCES ENDOTHELIN-1 SYNTHESIS AND INFLAMMATION IN LUNG FIBROBLASTS
Authors: Asenjo-Bueno Ana , Alcalde-Estevez Elena , Olmos Gemma , Rodríguez-Puyol Diego , Ruiz-Torres Maria Piedad , López-Ongil Susana 
Published: May 2021

Abstract

Background and Aims
Hyperphosphatemia is an aging-related condition associated to chronic diseases such as chronic kidney disease (CKD). In both cases, aging and CKD, it has been described a decline lung function, however, relationship between high serum levels of phosphate and lung damage has not been described yet. The aim of this work was to evaluate if phosphate could induce inflammation in lung, studying the mechanisms implied.

Method
In vitro studies were performed on a cell line from human lung fibroblasts (Wi-38) which were treated with a phosphate donor termed β-glycerophosphate (BGP, 10 mM) and also with endothelin 1 (ET-1, 10 nM) at different times. To assess inflammation, the expression of several cytokines such as TNF-α,IL-1β, IL-6 and MCP-1 were measured by real time PCR. mRNA expressions of prepro-ET-1 and endothelin-converting enzyme-1 (ECE-1) were also analyzed by real time PCR. Reactive oxygen species (ROS) production was evaluated by confocal microscopy in live cells using the fluorogenic probe CellROX as oxidative stress reagent.

Results
Treatment with BGP induced a significant rise of the pro-inflammatory cytokines expression, TNF-α, IL-1β, IL-6 and MCP-1, on lung fibroblasts. Moreover, BGP was able to regulate ET-1 system, as we found a significant increase of mRNA expressions not only of prepro-ET-1 but also of ECE-1, reaching a peak around 2 and 6 hours, respectively. Later, it was checked whether ET-1 could induce inflammation itself in lung fibroblasts. Cells incubated with ET-1 show similar results as BGP, increasing expressions of all cytokines, TNF-α, IL-1β, IL-6 and MCP-1.ET-1 response was earlier than BGP, around at 2 hours with ET-1 instead of at 8 hours with BGP. In order to elucidate a possible mechanism, ROS production was assessed after BGP treatment. BGP induced ROS production at 15 min in lung fibroblasts.

Conclusion
BGP induces the synthesis of pro-inflammatory cytokines as well as the system of synthesis of ET-1, besides to rise ROS production.ET-1 itself also increases pro-inflammatory cytokines expression. ET-1 could contribute to the inflammation observed in lung fibroblast after BGP treatment. We propose oxidative stress as a potential mechanism implied, as it is well known that ROS can mediate in inflammation and in the ET system. However, more studies are necessary to confirm this role. All in all, these results relate hyperphosphatemia with a higher inflammation in lung fibroblasts which could decline lung function in chronic diseases associated to aging as CKD.
MO439NATURAL IMMUNISATION AGAINST ATHEROSCLEROSIS IN BEARS DURING HIBERNATION*
Authors: Stenvinkel Peter , Shamal Shailesh , Fröbert Ole , Frostegård Johan 
Published: May 2021

Abstract

Background and Aims
Brown bears (Ursus arctos) hibernate for 5-6 months during winter, but in spite of kidney insufficiency, dyslipidemia, insulin resistance and inactivity they do not seem to develop atherosclerosis or cardiovascular disease (CVD). Antibodies against phosphorylcholine (anti-PC) are associated with protection in atherosclerosis, CVD and uremia. Potential underlying protective mechanisms include anti-inflammatory effects, inhibition of cell death, promotion of T regulatory cells, clearance of dead cells and inhibition of oxidized Low density lipoprotein (OxLDL)-uptake in macrophages in atherosclerotic plaques. PC is an important antigen on nematodes, parasites, some bacteria, dead and dying cells and OxLDL.

Method
Paired serum from 12 brown bears sampled during winter and summer were analyzed for metabolic parameters and for IgM, IgG, IgG1/2 and IgA anti-PC by enzyme linked immunosorbent assay (ELISA). Differences in antibody levels between winter and summer were determined by paired Student´s t test or Wilcoxon´s signed rank test (when not normally distributed).

Results
As expected, marked differences in metabolic parameters were found comparing median summer vs winter values; Cholesterol 5.9 vs 11.3 mmol/L; p&lt;0.001, triglycerides 1.9 vs 3.7 mmol/L; p&lt;0.001, glucose 5.4 vs 7.7 mmol/L; p&lt;0.05, S-creatinine 76 vs 203 µmol/L; p&lt;0.001, urea 12.1 vs 2.9 mmol/L; p&lt;0.002. When determined as arbitrary units (AU; median set at 100 at summer), marked and significant differences were observed between summer and winter.

Conclusion
Anti-PC (strikingly so for IgA and IgG1) are significantly raised during hibernation as compared to levels during summer. We hypothesize that these changes contribute to the protection of arteries, but also kidneys and other organs, during the metabolic vulnerable hibernation period. Our observation may represent a natural immunization with microorganisms, preventing atherosclerosis during a period of severe kidney insufficiency and could have therapeutic implications for patients with chronic kidney disease.
MO452CHRONIC KIDNEY DISEASE TEN YEARS AFTER PEDIATRIC ALLOGENEIC HEMATOPOIETIC STEM CELL TRANSPLANTATION
Authors: Bresters Dorine , Jol-van der Zijde Els , Dorresteijn Eiske , Louwerens Marloes , Jordans Carlijn , Lankester Arjan , Lugthart Gertjan , De Pagter Anne , Van Rooij-Kouwenhoven Roos , Sukhai Ram 
Published: May 2021

Abstract

Background and Aims
Chronic kidney disease (CKD) is an important sequela of hematopoietic stem cell transplantation (HSCT), but data regarding CKD after pediatric HSCT are limited.

Method
In this single center cohort study, we evaluated eGFR dynamics, proteinuria and hypertension in the first decade after HSCT and assessed risk factors for chronic kidney disease in 216 pediatric long term HSCT survivors, transplanted between 2002 and 2012.

Results
The eGFR decreased from median 148 to 116 ml/min/1.73m2 between pre-HSCT and ten years after HSCT. CKD, defined as an eGFR &lt;90 ml/min/1.73m2 and/or proteinuria (KDIGO stage ≥G2 or ≥A2) occurred in 21% of patients. In multivariate analysis, hematological malignancy as HSCT indication (HR 5.5, 95% CI 1.2-25) and cytomegalovirus reactivation (HR 2.4, 95% CI 1.1-5.4) were independent risk factors for CKD. One third of patients with CKD had both an eGFR &lt;90 ml/min/1.73m2 as well as proteinuria, one third had isolated eGFR reduction and one third only had proteinuria. Hypertension was observed in 27% of patients with CKD compared to 4.4% of patients without CKD. Tubular proteinuria was present in 7% of the subgroup of patients (n=71) in which β2-microglobulinuria was measured.

Conclusion
In conclusion, a significant proportion of pediatric HSCT recipients developed chronic kidney disease within ten years after HSCT. Our data stress the importance of structural long term monitoring of eGFR, urine and blood pressure after HSCT to identify patients with beginning CKD who could benefit most from nephroprotective interventions.
MO456DOES PHOSPHORUS EXCRETION PER NEPHRON AFFECT THE PROGNOSIS OF CHRONIC KIDNEY DISEASE?
Authors: Fujii Takayuki , Koshizaka Junya , Yamauchi Nobuaki , Matsunaga Takahiro , Morimoto Mayu , Terasaki Noriko , Tanaka Hiroaki , Suzuki Satoshi 
Published: May 2021

Abstract

Background and Aims
Serum phosphorus is an important factor associated with mortality and cardiovascular disease in dialysis patients as well as in non-dialysis patients with chronic kidney disease (CKD) and healthy individuals. One observational study reported that elevated phosphorus is a risk factor for end-stage renal disease and is linked to reduced renal function, even within the normal range. Although the mechanism is unknown, an excessive load of phosphorus to the kidney is presumed to cause renal damage via phosphorus-containing nanoparticles. In this study, we examined the association between phosphorus excretion per nephron and the prognosis of CKD.

Method
A single-center, retrospective cohort study was conducted in 276 patients with CKD category G3 to G5 who were admitted to our hospital and received an inpatient educational program on CKD between June 2016 and November 2019 and who could be followed up for at least 1 year or started on dialysis within 1 year after hospitalization. Phosphorus excretion per nephron was defined as daily phosphorus excretion divided by creatinine clearance (Ccr), and its association with the annual rate of decline in estimated glomerular filtration rate (eGFR) was investigated for each CKD category. For statistical analysis, multiple regression analysis was performed using the following covariates: age, sex, presence/absence of diabetes mellitus, mean arterial blood pressure, amount of daily urine protein, serum phosphorus level, and use of a renin-angiotensin system inhibitor.

Results
There were 108 patients with CKD G3, 106 patients with CKD G4, and 62 patients with CKD G5. Daily phosphorus excretion was 442 mg in G3, 350 mg in G4, and 350 mg in G5 patients. Phosphorus excretion per nephron was 8.4 mg/Ccr in G3, 14.0 mg/Ccr in G4, and 24.2 mg/Ccr in G5 patients. It increased with the progression of renal damage. In G4 patients, phosphorus excretion per nephron was significantly negatively correlated with the rate of decline in eGFR (p = 0.004); however, no correlation was found between the two in G3 and G5 patients (p = 0.09 and p = 0.16, respectively). Multiple regression analysis showed that phosphorus excretion per nephron was not a significant worsening factor for renal function in G3, G4, and G5 patients (p = 0.09, p = 0.36, and p = 0.41, respectively). On the other hand, serum phosphorus level was a significant worsening factor for renal function in G3 and G5 patients (p = 0.03 and p = 0.01, respectively).

Conclusion
No association was found between phosphorus excretion per nephron and the rate of the subsequent decline in renal function.
MO457PREVALENCE OF NON-ALCOHOLIC FATTY LIVER DISEASE IN PATIENTS WITH CHRONIC KIDNEY DISEASE: A CASE-CONTROL STUDY
Authors: Adrian Therese , Hornum Mads , Soerensen Ida Maria Hjelm , Freese Ballegaard Ellen Linnea , Bro Susanne , Kühl Joergen Tobias , Sigvardsen Per Ejlstrup , Fuchs Andreas , Kofoed Klaus F , Knop Filip K , Feldt-Rasmussen Bo 
Published: May 2021

Abstract

Background and Aims
Non-alcoholic fatty liver disease (NAFLD) is the most common liver disease and is characterised by hepatic accumulation of lipids. NAFLD represents a wide spectrum ranging from mild steatosis over non-alcoholic steatohepatitis with and without fibrosis to overt cirrhosis. Patients with NAFLD have a high risk of developing cardiovascular disease and chronic kidney disease (CKD). So far, there is scarce evidence of the prevalence of NAFLD among patients with CKD. The aim of this study was to investigate the prevalence of moderate to severe steatosis in a cohort with patients with different stages of CKD not on dialysis.

Method
A total of 291 patients from the Copenhagen Chronic Kidney Disease Study were included. For comparison, 866 participants with normal kidney function from the Copenhagen General Population Study were identified as controls. Blood samples, clinical demographics, information about smoking and alcohol were collected. Hepatic liver fat fraction was evaluated in all participants by computed tomography (CT). Liver attenuation density &lt;48 Hounsfield Units was used as cut-off value for moderate to severe steatosis corresponding to 10% liver fat after transformation of the CT attenuation.

Results
The prevalence of moderate to severe steatosis was 7.9% and 10.7% among patients with CKD and controls, respectively. Data of the continuous Hounsfield Units showed lower values among patients with CKD compared with the control group. No significant association between liver fat fraction and CKD stage was found. Pooled data from both cohorts showed that adjusted odds ratios (OR) for steatosis were strongly significant among persons with diabetes (OR 3.1, 95% confidence interval (CI) 1.6-5.9), overweight (OR 14.8, 95% CI 4.6-47.9) and obesity (OR 42.0, 95% CI 12.9-136.6), respectively.

Conclusion
In the present cohort of 291 patients with CKD, kidney function was not associated with the prevalence of hepatic steatosis as assessed by CT scan.
MO458URINARY GROWTH DIFFERENTIATION FACTOR-15 (GDF15) LEVELS AS BIOMARKER OF ADVERSE OUTCOMES AND BIOPSY FINDINGS IN CHRONIC KIDNEY DISEASE
Authors: Perez Gomez Maria Vanessa , Gomá-Garcés Elena , Pizarro Sanchez Maria Soledad , Gracia-Iguacel Carolina , Cano Santiago , Cannata-Ortiz Pablo , Sánchez-Rodríguez Jinny , Sanz Ana , Sanchez-Nino Maria Dolores , Ortiz Alberto 
Published: May 2021

Abstract

Background and Aims
Growth differentiation factor-15 (GDF15) is a member of the TGF-β superfamily. Increased serum GDF15 has been associated with increased risk of CKD progression. However, no prior study had addressed the significance of urinary GDF15 in adult CKD.

Method
We have now assessed serum and urinary GDF15 in a prospective cohort of 84 patients who underwent kidney biopsy and then were followed for 29±17 months.

Results
There was a statistically significant correlation between serum and urine GDF15 values. However, while serum GDF15 values increased with decreasing glomerular filtration rate, urinary GDF15 did not. Immunohistochemistry located kidney GDF15 expression mainly to tubular cells and kidney GDF15 staining correlated with urinary GDF15 values. Urine GDF15 was significantly higher in patients with a histological diagnosis of diabetic nephropathy than in diabetic patients without diabetic nephropathy. This was not the case for serum GDF15. Both serum and urine GDF15 were associated with patient survival in multivariate models. However, when both urine and serum GDF15 were present in the model, lower urine GDF15 predicted patient survival [B coefficient (SEM) -0.395 (0.182) p 0.03], and higher urine GDF15 predicted a composite of mortality or renal replacement therapy [0.191 (0.06) p 0.002] while serum GDF15 was not predictive. Decision tree analysis yielded similar results. The AUC of the ROC for urine GDF15 as a predictor of mortality was 0.95 (95% CI 0.89-1.00, p &lt;0.001).

Conclusion
In conclusion, urine GDF15 is associated with kidney histology patterns, mortality and need for renal replacement therapy in biopsied CKD patients.