bluuebunny/crossref_metadata_2025_split huggingface dataset:
SO009MORTALITY AND HOSPITALIZATION IN A LARGE INTERNATIONAL PERITONEAL DIALYSIS INSTITUTION DURING 2018
Authors: Marrón Belén , Pearce Suzanne , Wollheim Charlotta , Lucas Carlos , Torok Marietta , Munteanu Dan , Roesch Michael , Ostrowski Janusz , Kochman Pawel , Orosz Attila , Pérez Daniel , Pacheco Alejandro , Macário Fernando 
Published: June 2020

Abstract

Background and Aims
With the exception of some national registries, data referred to mortality or hospitalization within a single large international peritoneal dialysis (PD) institution are seldom reported.
To study all-cause mortality, transplantation rate, hospitalizations and peritonitis rates in our large PD program during 2018.

Method
Observational, prospective registry in 8 countries. The following variables were tracked: crude mortality rate and causes, hospitalization variables (nº of hospitalization days per patient; nº of hospitalization episodes per patient; nº of days per hospitalization episode; causes of hospitalization), peritonitis rate (episodes/year at risk and patient months at risk to a peritonitis episode) and transplantation rate.

Results
By the end of December 2018, 1207 pt. were treated (11 countries) but only 8 countries submitted data. Evaluated population as “patients treated at risk during the year”: AR (319.5), RO (173.5), DE (137), HU (103), PL (97), UR (69.5), CL (27), KZ (7). Crude mortality rate was 13.1%, same if first 90 days on therapy were excluded. Lowest mortality was seen in HU (9.9%) and highest in DE (19.3%). Causes of death: cardiac 32%, all type infections 22% [Sepsis 78%, PD related 11% (as 0.7% of total mortality), pulmonary 3.7%, others 7.4%], vascular 10%, gastrointestinal 3.3%, unknown 10.7% (highest in DE, 23%), other known causes 21.5%. Hospitalization rates: 0.55 episodes/per patient-year and 7.6 days of hospitalization per patient-year. Nº of days per hospitalization episode was 13.7. Causes of hospitalization: PD related 38%, cardiovascular 17%, non-PD infection sepsis 10.7% (higher in LA, 16.6%), vascular access 2.1%, unknown 4.5%, others 23.3%. Global peritonitis rate was 0.18 episodes/pt-year at risk (1 episode every 66 m.). However, large differences were seen among countries. Transplantation rate was 6.5% (much higher in UR). PD was withdrawal in 35% of pt. Country specific data have been evaluated but are not shown here.

Conclusion
The use of a common registry in our institution increases quality and allows homogeneous comparisons across countries that if promptly addressed may increase patients’ outcomes. Our series may bring light into the PD community as one of the ever largest tracked in a single institution.
SO010URINARY LITHOGENIC RISK PROFILE IN ADPKD PATIENTS TREATED WITH TOLVAPTAN
Authors: Bargagli Matteo , Dhayat Nasser A , Anderegg Manuel , Semmo Mariam , Huynh-Do Uyen , Vogt Bruno , Ferraro Pietro Manuel , Fuster Daniel Guido 
Published: June 2020

Abstract

Background and Aims
Nephrolithiasis is a common health problem in autosomal dominant polycystic kidney disease (ADPKD) and significantly contributes to patient morbidity. In observational studies, prevalence rates of up to 36% have been reported. Kidney stones of ADPKD patients are typically composed of uric acid (UA) or calcium oxalate (CaOx), and hypocitraturia and low urinary pH have been reported as the main prolithogenic abnormalities. Recently, Tolvaptan has been introduced for the treatment of ADPKD, but its impact on the lithogenic risk profile in ADPKD patients remains unknown.

Method
We conducted a retrospective analysis of patients enrolled in the Bern ADPKD registry, an observational cohort study. Inclusion criteria were age ≥ 18 years, clinical diagnosis of ADPKD, and informed consent. The main exclusion criterion was need for renal replacement therapy. 24-h urine analyses were performed at baseline and then at yearly follow-ups. Relative supersaturation ratios (RSS) for CaOx, calcium phoshate (CaP) and UA were calculated with EQUIL2. Univariate and multivariate mixed-effects linear regression models, adjusted for age, sex, BMI, eGFR and endogenous acid production, estimated by net acid excretion, were used to assess the impact of Tolvaptan treatment on urinary composition.

Results
38 patients received Tolvaptan treatment (39.5% females) and were included in the analysis. Six patients (15.8%) had a history of symptomatic stone events. In multivariate analysis, Tolvaptan treatment was significantly associated with reductions of CaOx, CaP and UA RSS (p &lt; 0.01) and increased urinary citrate (p = 0.015) and calcium (p &lt; 0.01) excretion. In contrast, Tolvaptan treatment was not associated with alterations in urinary oxalate excretion or urinary pH.

Conclusion
Tolvaptan significantly reduces RSS for CaOx, CaP and UA. Future studies are needed to assess the impact of Tolvaptan treatment on stone recurrence in ADPKD patients.
SO011OXALATE-DEGRADING ACTIVITY IN FECAL MICROBIOTA ASSOCIATED WITH BLOOD LIPID PROFILE IN DIALYSIS PATIENTS
Authors: Stepanova Natalia , Tolstanova Ganna , Akulenko Iryna , Savchenko Olena , Lebid Larysa , Skovorodka Marharyta , Kolesnyk Mykola 
Published: June 2020

Abstract

Background and Aims
Cardiovascular disease (CVD) remains the leading cause of morbidity and death in end-stage renal disease (ESRD) patients. Thus, the accumulation of oxalate due to ESRD can increase the risk of CVD. Also, the ability of fecal oxalate-degrading activity (ODA) to reduce plasma oxalate levels has been discussed. On the other hand, despite a key role of atherogenic dyslipidemia in the development of CVD, only a few studies have shown a potential role of microbiota in the regulation of blood lipid profiles in the general population. However, at present, there is a general lack of research on this topic in dialysis patients.
The present study aimed to investigate the association between oxalate-degrading activity (ODA) in fecal microbiota and blood lipid profiles in ESRD patients.

Method
We represented the data of a cross-sectional pilot study examining ODA in fecal microbiota, plasma oxalate concentration (POx) and blood lipid profile markers in 32 ESRD patients. Among the patients, there were 21 hemodialysis (HD) patients and 11 peritoneal dialysis (PD) patients. The average age of the patients was 52.5 [39; 65] years.
The redoximetric titration with KMnO4 was adopted to evaluate total ODA in fecal microbiota. The results were expressed in % oxalate degradation per 0.01 g of feces. The blood lipid spectrum was determined in all patients: total cholesterol level (TC), high (HDL), low (LDL) and very low (VLDL) density cholesterol, triglycerides (TG) and atherogenic index of plasma (AIP).
The median (Me) and interquartile ranges [Q25; Q75] were calculated using the nonparametric Kruskal-Wallis test. The Spearman test was used for the correlation analysis. Chi-square tests were used for comparison of 2 proportions. All statistical analyses were performed using MedCalc.

Results
Dyslipidemia defined as an increase in atherogenic lipoprotein fractions and inhibition of HDL cholesterol was identified in 13/32 (40.6%) ESRD patients. Negative ODA in fecal microbiota (≤ 0 % /0.01 g) was observed in 14/32 (43.7%) patients. Among them, there were 5/21 (23.8%) HD patients and 7/11 (63.6%) PD patients (χ2=3.9, p=0.04).
Significantly lower ODA in fecal microbiota was observed in the patients with atherogenic dyslipidemia in comparison with dyslipidemia-free patients (-5.0 [-8.7; 3.7] vs 3.0 [0.5; 9] %/0.01 g of feces, p=0.02) (Fig. 1). Less ODA in fecal microbiota was, higher levels of TG (r=-0.5, p=0.004) (Fig. 2), VLDL (r=-0.34, p=0.05) (Fig. 3) and, accordingly, AIP (r=-0.38, p=0.03) (Fig. 4) occurred.

Conclusion
The results of our study have provided preliminary evidence on the fact that a decrease in total ODA in fecal microbiota is associated with atherogenic dyslipidemia. Further studies are needed to determine the role of fecal ODA in the formation of dyslipidemia.
SO012RENOPROTECTIVE EFFECTS OF FEBUXOSTAT AND ALLOPURINOL IN PATIENTS WITH HYPERURICEMIA AND CHRONIC KIDNEY DISEASES: A META-ANALYSIS
Authors: Edding Sherida , Cabral Brian Michael , Cating-Cabral Monica Therese 
Published: June 2020

Abstract

Background and Aims
Hyperuricemia is associated with rapid deterioration of renal function in patients with chronic kidney disease (CKD). The two most common urate-lowering drugs available in the market are allopurinol and febuxostat. Randomized controlled trials (RTCs) have shown that the individual drugs have potential to slow down progression of renal function in patients with chronic kidney disease (CKD) and hyperuricemia. However, it is unclear which drug is more effective because of insufficient direct comparison between the two. Hence our study aims to perform a meta-analysis of RCTs to assess the renoprotective and urate-lowering effects between the two drugs in patients with CKD and hyperuricemia.

Method
A comprehensive literature search of randomized controlled trials using PubMed was performed with the following search terms: febuxostat, allopurinol, chronic kidney disease, renoprotection. Four prospective RCTs were selected and analyzed using Cochrane Revman v5.3. Outcomes assessed were change in serum creatinine, estimated glomerular filtration rate (eGFR), proteinuria and serum uric acid levels from baseline to 3 months post-initiation of therapy.

Results
Four relevant trials comprising of 486 patients were selected - 247 patients treated with febuxostat and 239 patients with allopurinol. No significant differences were found in the changes in serum creatinine (mean difference -0.04; CI -0.15, 0.07; P = 0.51) and eGFR (mean difference 1.57; CI -0.83, 3.97; P = 0.20) from baseline to 3 months between the febuxostat and allopurinol group. Decrease in proteinuria was significantly observed more in the febuxostat group (mean difference -50.13; CI -90.54; -9.71, P = 0.02). Similarly, serum uric acid levels were significantly more reduced in the febuxostat group (mean difference -1.11; CI -1.53, -0.68, P &lt; 0.00001).

Conclusion
Our study showed that febuxostat is non-inferior in terms of delaying renal function decline (as measured by eGFR) but it offers a better anti-proteinuric as well as a urate-lowering effect. However, more studies are needed to assess the efficacy of febuxostat across the spectrum of chronic kidney disease, including those requiring hemodialysis.
SO013CRUCIAL ROLE OF SERUM RESPONSE FACTOR IN EPITHELIAL-MESENCHYMAL TRANSITION OF RENAL TUBULAR EPITHELIAL CELLS IN HYPERUREICEMIC NEPHROPATHY
Authors: Zhao Long , Xu Yan 
Published: June 2020

Abstract

Background and Aims
To investigate the role of serum response factor (SRF) in epithelial-mesenchymal transition (EMT) of renal tubular epithelial cells (TECs) in hyperuricemic nephropathy (HN).

Method
The expression of SRF, epithelial markers (E-cadherin and ZO-1) and mesenchymal markers (fibronectin, α-SMA, FSP-1) was examined in rat renal tubular epithelial cells (NRK-52E cells) or renal medulla tissues following uric acid (UA). SRF was upregulated by SRF plasmids and downregulated by CCG-1423(a small molecule inhibitor of SRF) to investigate how SRF influenced EMT in TECs of HN. Oxonic acid (OA) was used to generate HN in rats.

Results

Conclusion
Together, increased SRF activity promotes EMT and dysfunction of TECs in HN. Targeting SRF by small molecule inhibitor may be an attractive therapeutic strategy for HN.
SO022EVALUATION OF GLOMERULAR HEMODYNAMIC CHANGES BY SGLT2 INHIBITION IN TYPE 2 DIABETIC RATS USING IN VIVO IMAGING TECHNIQUES
Authors: Wada Yoshihisa , KIDOKORO KENGO , Tokuyama Atsuyuki , Kondo Megumi , Kadoya Hiroyuki , Nagasu Hajime , Sasaki Tamaki , Kashihara Naoki 
Published: June 2020

Abstract

Background and Aims
In recent clinical trials, the SGLT2 inhibitor (SGLT2i) slowed the progression of kidney disease compared with the placebo in patients with type 2 diabetes. Improvement of glomerular hyperfiltration via tubuloglomerular feedback (TGF) is considered to be one of the possible pathways for renal protection with SGLT2 inhibition (SGLT2i) in diabetic kidney disease (DKD). We have successfully developed the novel method to measure single-nephron GFR (SNGFR) in mice using multiphoton laser microscopy and demonstrated that the adenosine/adenosine A1 receptor (A1aR) pathway plays a pivotal role in the TGF mechanism in the type 1 diabetic model, Akita mice (Kengo Kidokoro, David Z. I. Cherney et al. Circulation. 2019). It has been suggested that the mechanism of improvement effects in glomerular hyperfiltration by SGLT2i is different in type 1 diabetes and type 2 diabetes. However, the detailed regulatory mechanism of GFR by SGLT2i is not fully understood in type 2 diabetes. This study aims to clarify the effects of SGLT2i on glomerular hemodynamics in type 2 diabetic rats.

Method
Zucker lean (ZL) rats and Zucker diabetic fatty (ZDF) rats were used. In the first experiment, SNGFR and diameters of glomerular afferent/efferent arterioles were measured in both groups. Next, we examined the change of SNGFR and diameters of glomerular afferent/efferent arterioles, as well as urinary excretions of glucose and sodium in ZDF after a single-dose administration of SGLT2i (luseogliflozin; 10mg/kg, gavage) for 120 minutes, which generated the following three groups: SGLT2i group, SGLT2i + adenosine A1 receptor (A1aR) antagonist (8-cyclopentyl-1,3-dipropylxanthine, 1mg/kg) group, and insulin group.

Results
SNGFR in the ZDF group was significantly higher than in the ZL group. The diameter of the afferent arteriole and efferent arteriole was also wider in ZDF rats than in ZL rats. The SNGFR and diameter of the afferent arteriole were significantly decreased after a single-dose administration of SGLT2i in ZDF. However, there was no significant diameter change in the efferent arteriole. Moreover, a decrease of SNGFR was not observed in the A1aR antagonist group after SGLT2i administration. Urinary excretions of glucose and sodium showed a similar pattern in the SGLT2i and SGLT2i+ A1aR antagonist groups.

Conclusion
The adenosine/A1aR pathway plays an important role in the regulation of the tonus of the afferent arteriole and is involved in the suppression of glomerular hyperfiltration by SGLT2 inhibition in type 2 diabetes.
SO024THE GPR120 AGONIST TUG-891 AMELIORATES KIDNEY FIBROSIS AND INFLAMMATION IN DIABETIC NEPHROPATHY
Authors: Wei Tiantian , Ma Liang , Fu Ping 
Published: June 2020

Abstract

Background and Aims
ω3-Fatty acids (ω3FAs) attenuated inflammation, glomerulosclerosis and albuminuria in most experimental studies of diabetic nephropathy (DN). GPR120 has been identified as a first receptor for ω3FAs. Compared to ω3FAs, TUG-891 is a highly potent and selective agonist for GPR120. In this study, we examined the protective effects of GPR120 agonist TUG-891 in DN and investigated the possible mechanisms.

Method
Expression of GPR120 was detected in human renal biopsy tissue obtained from patients with early or advanced DN and in normal renal tissues. Effects of TUG-891 on the development of DN were investigated in male C57BLKS/J db/db mice and murine podocytes (MPC5). Expression of collagen IV, fibronectin, αSMA, TGF-β/smad2/3, IL-6, GPR120/β-arrestin2/TAK1 binding protein-1 and downstream pathways were measured.

Results
The expression of GPR120 was negatively correlated with the progression of DN. IF stainings showed that GPR120 was mainly expressed in podocytes of the glomerulus by co-localization of a special marker nephrin. In db/db mice, oral administration of TUG-891 significantly reduced urinary albumin excretion, improved podocyte injury and reduced collagen deposition in glomerulus. Meanwhile, TUG-891 inhibited the expression of fibronectin, collagen IV, α-SMA, TGF-β1 and IL-6, as well as down-regulated phosphorylation of Smad3 and STAT3 to alleviate the glomerulosclerosis. Mechanistically, TUG-891 effectively up-regulated the GPR120 expression in kidneys of db/db mice and HG-stimulated podocytes. TUG-891 also suppressed TAB1 expression and the phosphorylation of TAK1, IKKβ, NF-κB, JNK and p38 MAPK signals.

Conclusion
In summary, our result highlighted that TUG-891 ameliorated kidney fibrosis and inflammation by activating the intracellular GPR120 signaling pathway.
SO035EFFECT OF DIETARY SALT REDUCTION ON BLOOD PRESSURE IN KIDNEY TRANSPLANT PATIENTS: A RANDOMISED CONTROLLED TRIAL
Authors: Ross Louise , Suckling Rebecca , He Fengjun , Dockrell Mark , Bailey Thomas , Swift Pauline 
Published: June 2020

Abstract

Background and Aims
Cardiovascular morbidity and mortality are increased in kidney transplant patients. High blood pressure (BP) contributes significantly to this risk and is associated with shortened allograft survival. Dietary salt reduction is widely recommended as a strategy to lower BP in the general population and in chronic kidney disease. Due to a lack of evidence there is currently no consensus on dietary salt restriction in kidney transplant patients. The primary aim of the study was to examine the impact of reduced dietary salt intake on BP in kidney transplant patients.

Method
Sixty stable kidney transplant patients, ≥ 6-months post-transplantation, with BP ≥120/80 mmHg, and sodium intake ≥80 mmol/24hrs, were randomised in this parallel-designed study to receive either a regular-salt diet (target 150 mmol/24hr) or a low-salt diet (target 80 mmol/24hr) for 8-weeks. The primary outcome measure was systolic and diastolic BP. Secondary outcome measures included 24-hour ambulatory BP (ABP) and proteinuria. Dietary salt intake was assessed by 48-hour urinary sodium excretion.

Results
At baseline, patients (72% men) were 56±11 years with estimated glomerular filtration rate (eGFR) 53±18 mL/min/1.73m2. Mean urinary sodium was 128±42 mmol/24hr, mean systolic BP was 132±12 mmHg, and mean diastolic BP was 77±10 mmHg. At the end of the intervention period sodium excretion was significantly lower in the low-salt group compared with the regular-salt group (90±37 vs. 132±51 mmol/24hr; adjusted mean difference, -36 [95% CI, -59 to -14] mmol/24hr; P=0.002). We found no difference in systolic BP (adjusted mean difference, -2 [95% CI, -12 to 9] mmHg; P=0.750), diastolic BP (adjusted mean difference, 0 [95% CI, -4 to 4] mmHg; P=0.887), 24-hour systolic ABP (adjusted mean difference, -3 [95% CI, -9 to 2] mmHg; P=0.213) or 24-hour diastolic ABP (adjusted mean difference, -2 [95% CI, -5 to 1] mmHg; P=0.267). There was no significant effect on proteinuria or eGFR.

Conclusion
In this study baseline urinary sodium was lower than expected and baseline BP was well controlled. Reducing dietary salt by 2g/day did not have a significant effect on office blood pressure readings.
SO039BETA3-ADRENORECEPTOR AS A NEW PLAYER IN SYMPATHETIC REGULATION OF THE ACID-BASE HOMEOSTASIS IN THE KIDNEY
Authors: Milano Serena , Gerbino Andrea , Carmosino Monica , Svelto Maria , Procino Giuseppe 
Published: June 2020

Abstract

Background and Aims
Sympathetic nervous system has a key role in the regulation of renal function. We previously showed that, in mouse, the β3-adrenoreceptor (β3-AR) localizes in most of the nephron segments and its selective agonism promotes a potent antidiuretic effect. Here, we evaluate the expression of β3-AR in kidney intercalated cells (ICs) which are associated with the regulation of acid-base homeostasis in distal segments of the kidney tubule. The aim of this study is to investigate whether the β3-AR might play a role in the acid-base homeostasis operated by the kidney.

Method
The β3-AR expression in mouse kidney ICs was investigated by confocal microscopy. Wild type (wt) and β3-AR knock-out (ko) mice were used to study the role of β3-AR in the renal acid-base homeostasis. Mouse urine were collected using metabolic cages and pH was measured. Immunofluorescence and Western blotting experiments were performed to evaluate the localization and the abundance of renal H+-ATPase in wt and β3-AR ko mice. Kidney cells expressing human β3-AR (M1-β3-AR) and endogenous H+-ATPase were used to investigate the possible effects of β3-AR stimulation on the activity/localization of H+-ATPase. Live imaging experiments using the pH-sensitive dye BCECF were carried out to determine intracellular pH and assess H+-ATPase activity. Immunofluorescence experiments were performed to reveal the effects of β3-AR activation on H+-ATPase localization.

Results
Co-localization study of β3-AR with either H+-ATPase or Cl−/HCO3− exchanger pendrin in mouse kidney showed that β3-AR is expressed in H+-secreting type A, in HCO3— secreting type B, and in non-A non-B ICs. The urine pH of β3-AR ko mice was significantly higher compared with wt mice. In line with these results, localization and expression analysis showed that renal H+-ATPase significantly decreased in β3-AR ko mice compared to wt mice, supporting the idea that H+ secretion is partially blunted in these animals. Of note, exposure of M1-β3-AR cells to a selective β3-AR agonist induced a 2.5 fold increase of H+-ATPase activity compared to resting cells and this effect was prevented by a selective β3-AR antagonist or by the H+-ATPase inhibitor bafilomycin. Moreover, β3-AR agonism enhanced H+-ATPase apical expression in M1-β3-AR cells. In addition, the PKA inhibitor H89 abolished the stimulatory effect of β3-AR agonism, demonstrating the involvement of the cAMP/PKA pathway.

Conclusion
The present data suggest that modulation of H+-ATPase activity in renal ICs by endogenous β3-AR agonists may play an addition physiological role in hormonal control of renal acid-base homeostasis.