bluuebunny/crossref_metadata_2025_split huggingface dataset:
#1478 Effect of low vs standard dialysate sodium on 48-h ambulatory blood pressure in patients with intradialytic hypertension: a randomized crossover study
Authors: Iatridi Fotini , Ekart Robert , Efstathios Xagas , Revela Ioanna , Karpetas Antonios , Theodorakopoulou Marieta P , Karagiannidis Artemios , Georgiou Areti , Malandris Konstantinos , Tsouchnikas Ioannis , Sarafidis Pantelis 
Published: May 2024

Abstract

Background and Aims
Intradialytic hypertension (IDH) is associated with increased risk for cardiovascular events and mortality. Patients with IDH exhibit higher 48-h blood pressure (BP) levels than patients without this condition. Volume and sodium excess are considered a major factor contributing in the development of this phenomenon. This study evaluated the effect of low (137 mEq/L) compared to standard (140 mEq/L) dialysate sodium concentration on 48-h BP in patients with IDH.

Method
In this randomized, single-blind, crossover study, 29 patients with IDH underwent 4 hemodialysis sessions with low (137 mEq/L) followed by 4 sessions with standard (140 mEq/L) dialysate sodium or vice-versa. Mean 48-h BP, pre-/post-dialysis and intradialytic BP, pre-dialysis weight, interdialytic weight gain (IDWG) and lung ultrasound B-lines were assessed.

Results
Mean 48-h SBP/DBP were significantly lower with low compared to standard dialysate sodium concentration (137.6 ± 17.0/81.4 ± 13.7 mmHg with low vs 142.9 ± 14.5/84.0 ± 13.9 mmHg with standard dialysate sodium, p = 0.005/p = 0.007 respectively); SBP/DBP levels were also significantly lower during the 44-h and different 24-h periods. Low dialysate sodium significantly reduced post-dialysis (SBP/DBP: 150.3 ± 22.3/91.2 ± 15.1 mmHg with low vs 166.6 ± 17.3/94.5 ± 14.9 mmHg with standard dialysate sodium, p &lt; 0.001/p = 0.134 respectively) and intradialytic (141.4 ± 18.0/85.0 ± 13.4 mmHg with low vs 147.5 ± 13.6/88.1 ± 12.5 mmHg with standard dialysate sodium, p = 0.034/p = 0.013, respectively) BP compared with standard dialysate sodium. Pre-dialysis weight, IDWG and pre-dialysis B-lines were also significantly decreased with low dialysate sodium.

Conclusion
Low dialysate sodium concentration significantly reduced 48-h ambulatory BP compared with standard dialysate sodium in patients with IDH. These findings support low dialysate sodium as a major non-pharmacologic approach for BP management in patients with IDH.
Registered at ClinicalTrials.gov with study number NCT05430438.
#1485 Hypertension management of CKD patients referred to Hypertension Excellence centres in 27 countries: on behalf of the ESH Hypertension and Kidney WG
Authors: Halimi Jean Michel , Sarafidis Pantelis , Persu Alexandre , Kreutz Reinhold , Vogt Liffert 
Published: May 2024

Abstract

Background and Aims
Real-life management of hypertensive patients with chronic kidney disease (CKD) is unclear and may vary across countries. Our aim was to identify unmet needs and heterogeneity of management in this population of patients in Europe and the Middle-East through our network of European Society of Hypertension (ESH) Excellence Centers.

Method
A survey was conducted in 2023 by the ESH to assess management of CKD patients referred to ESH-Hypertension Excellence Centres (ESH-ECs) at first referral visit. The questionnaire contained 64 questions with which ESH-ECs representatives were asked to estimate pre-existing CKD management quality and data for their management are reported here.

Results
Overall, 88 ESH-ECs from 27 countries participated (fully completed surveys: 66/88 (75.0%)). ESH-ECs reported that 28% (median, interquartile range: 15-50%) had pre-existing CKD, of whom 10% (5- 30%) were previously referred to a nephrologist, while 30% (15-40%) had resistant hypertension. The reported rate of previous recent (&lt;6 months) estimated glomerular filtration rate (eGFR) and urine Albumin- Creatinine Ratio (UACR) testing were 80% (50-95%) and 30% (15-50%), respectively. The reported use of renin-angiotensin system blockers was 80% (70-90%). When a nephrologist was part of the ESH-EC teams the reported rates for SGLT2 inhibitors (27.5% (20-40%) vs 15% (10-25), p = 0.003), GLP1-RA (10% (10-20%) vs 5% (5-10%), p = 0.003) and mineralocorticoid receptor antagonists (20% (10-30%) vs 15% (10-20%), p = 0.05) use were greater as compared to ESH-ECs without nephrologist participation. The rate of reported resistant hypertension, recent eGFR and UACR results and management of CKD patients prior to referral varied widely across centres in Europe countries and in the Middle East.

Conclusion
Our results indicate deficits regarding CKD screening, use of nephroprotective drugs and referral to nephrologists before referral to ESH-ECs but results varied widely across centres. This information can be used to build specific programs to improve care in hypertensives with CKD.
#1047 Duration of dual antiplatelet therapy after stent placement in renal artery stenosis
Authors: Nanwani Avinash Chandu , Herrera Aidana Maria Barrera , Suarez German Perez , Galvez Ana Cristina Rodenas , Granados Saulo Jesús Fernández , Prieto Daniel Cubillo , Taboada Alexis Bravo De Laguna , Tejedor Yeray Aguilar , Cacabelos Enrique Buceta , Canton Cesar García 
Published: May 2024

Abstract

Background and Aims
Renovascular hypertension (RVH) is currently considered one of the most prevalent and important causes of secondary hypertension and renal organ damage. The prevalence of RVH in hypertensive patients increases more than 40% in elderly, comorbid and atherosclerotic patients. Although controlled trials in patients with Atherosclerotic Renovascular Disease (ARVD) have not been conclusive about the superiority of Percutaneous Revascularization (PR) over optimal medical treatments, this procedure is still indicated in selected patients, however the optimal duration of dual antiplatelet therapy after PR to avoid stent restenosis has not been well described.

Method
Retrospective study including 51 patients (median age 66.8 years IR: 48.7-87.6; male 35.3%) with resistant hypertension. All patients were diagnosed of Atherosclerotic renovascular hypertension (ARVH) through angioTC and renal arteriography (≥50% stenosis). All of them underwent PR by angioplasty plus stent placement. Patients were stratified into two groups according to dual antiplatelet therapy duration (with Aspirin 100 mg and Clopidrogrel 75 mg). Group I: Dual antiplatelet therapy for 3 months (n = 14) and Group II: Dual antiplatelet therapy for 6 months (n = 37). All patients continued with single antiplatelet therapy at the end of the dual antiplatelet period and were followed during a mean of 4.5 ± 3.8 years. Clinical, analytical and demographic data were collected, as well as cardiovascular risk factors and number of antihypertensive drugs. Besides, blood pressure and kidney function were measured before and after the procedure.

Results
During the follow up, stent restenosis occurred in thirteen patients (25.5%), (group I: 6 (46.2%), group II: 7 (53.8%), p = 0.080).
No differences in blood pressure between two groups were observed (SBP/DBP before and after PR (group I: 175.3/94.7 mmHg and 122.5/71.9 mmHg and group II: 181.1/94.5 mmHg and 125.0/75.5 mmHg, p = N/S)). The number of antihypertensive drugs was similar between two groups before and after the procedure (Group I: 4.6 ± 2.2 and 3.4 ± 1.3; Group II 4.8 ± 1.4 and 3.5 ± 1.7, p = N/S).
There was an improvement in blood pressure control in both groups after PR (SBP/DBP 179.5/94.5 mmHg to 124.9/74.9 mmHg, p = 0.000) and this reduction persisted one year after treatment SBP/DBP 139.2/78.0 mmHg, (p = 0.001). In addition, a reduction in antihypertensive drugs were observed in both groups (4.8 vs 3.5 p = 0.000). Stable renal function was observed previously and two years after treatment.
In multivariate analysis, risk factors associated to stent restenosis were LDL (1.0 CI: 1.0- 1. 05; p = 0.034) and triglycerides (1.0 CI 1.0- 1.1; p 0.038) at 6 month post-stent placement.

Conclusion
#651 Diagnostiс criteria of the functional state of the kidneys in patients with type 2 diabetes mellitus
Authors: Muminova Sitora , Daminova Lola , Adylova Durdona 
Published: May 2024

Abstract

Background and Aims
The constant increase in the number of patients with type 2 diabetes is clearly explained by the incidence of microvascular complications, including diabetic nephropathy (DN). According to statistics, CKD develops initially in 15% of individuals in the general population. To assess the functional state of the kidneys in patients with type 2 diabetes mellitus.

Method
The study included 120 patients with T2DM and were divided into 2 groups. Gr1: 60 patients with DN C1,A1, gr2 with DN C2,A2 whose average age was 60.1 ± 7.6 years. The average DM experience was 7 ± 3.16 years, HbA1C 9 ± 1.82%, BMI 28.05 ± 3.45. Average GFR cr. was 92.6 ± 11.81 ml/min/1.73 m2, albuminuria—13.19 ± 3.1 mg/g.

Results
In the first group, the decrease in eGFRcr was 7.1%, although the average value was within the reference values. At the same time, the level of serum cystacin C and the calculated eGFRcys in this group were significantly different from the control. The serum concentration of cystacin C was significantly higher (0.64 ± 0.09 mg/ml versus 1.07 ± 0.08 mg, p &lt; 0.05), and the eGFRcys indicator was significantly lower (81.32 ± 6.31 ml /min versus 96.60 ± 5.22 ml/min, p &lt; 0.05) indicator for healthy individuals. In the second group of patients, there was a significant decrease in glomerular filtration rate for both markers compared to the control and the first group. Thus, in patients with DN C2, A2, compared with the control and the first group of patients, the eGFRcr indicator was reduced by 24.2% and 18.3%, respectively (p &lt; 0.01 and p &lt; 0.05), which indicates a pronounced decrease in renal function in this category of patients with type 2 diabetes.

Conclusion
Thus, the results obtained showed that in patients with subclinical diabetic nephropathy there is a decrease in glomerular filtration rate, determined by the level of cystacin C. Therefore, eGFRcys is a more accurate indicator of a hidden impairment of renal filtration function compared to eGFRcr.
#185 The role of angiotensin 2 type 1 receptor and type 2 receptor after postischemic acute kidney injury in spontaneously hypertensive rats
Authors: Ivanov Milan , Mihailovic-Stanojevic Nevena , Jovovic Djurdjica , Karanovic Danijela , Vajic Una-Jovana , Zivotic Maja , Miloradovic Zoran 
Published: May 2024

Abstract

Background and Aims
Renal ischemia/reperfusion injury is a common cause of acute kidney injury (AKI), and hypertension might contribute to the increased incidence of AKI. AKI has a multifactorial causality, but the mechanism of pathogenesis and the development of this disease are still incompletely defined. The purpose of this study was to compare the effects of AT1R blockade and AT2R simulation on AKI development in spontaneously hypertensive rats (SHR).

Method
We used male 24 weeks old SHR. Animals were divided into following experimental groups: sham operated rats (SHAM); rats with induced postischemic AKI (AKI); a group which received AT1R antagonist Losartan (10 mg/kg b.w.)(AKI+LOS) and group which received AT2R agonist novokinin (0.3 mg/kg b.w.)(AKI+NOVO) in the moment of kidney reperfusion. AKI was induced by surgical removal of right kidney followed by atraumatic clamp occlusion of the left renal artery for 40 minutes. Hemodynamic and biochemical measurements were done 24 hours after reperfusion.

Results

Conclusion
Our results confirm the dominant role of AT1R on AKI development, but AT2R stimulation failed to buffer deleterious effects of AT1R hyperactivity on renal vasoconstriction and glomerular filtration. However, the role of AT2R during AKI development in hypertension will be in focus in our further studies.
#523 Continuous electronic urine output monitoring for the management of acute cardio-renal syndrome in patients with acute decompensated heart failure
Authors: Shacham Yacov , Banai Shmuel , Rozenfeld Anna 
Published: May 2024

Abstract

Background and aims
: Patients admitted for acute decompensated heart failure (ADHF) are at high risk for type I cardio-renal syndrome (CRS) related to venous congestion and diuretic resistance. Positive fluid balance has been associated with adverse outcomes including acute kidney injury (AKI) and mortality. In critically ill patients urine output (UO) is used both to assess deterioration of renal function as well as for management of fluid balance. We investigated the possible effect of real-time UO monitoring, fluid balance, renal outcomes and 30-day mortality of patients admitted to the cardiac intensive care unit (ICU) with ADHF.

Methods
We performed a case series of 50 patients admitted to the cardiac ICU from July 2021 and June 2023 with ADHF. Their standard foley catheter was connected to an electronic monitoring system (Clarity-RMS sensor kit) that continuously monitors UO in real-time. Its technology is described elsewhere (1). The UO monitoring system displays UO trends on the consoles that are updated in real-time. UO trends were utilized to guide an individualized approach for the pharmacologic management of each patient, based on blood pressure, hourly UO and total fluid balance. Daily and accumulated fluid balance was registered at up to 72 hours following admission. Patient outcomes included change in fluid balance, incidence of AKI and 30-day mortality. The case series group was than compared to a historical group of 50 matched controlled patients admitted between 2019-2020. Patients were matched according to cause of admission, age and glomerular filtration rate.

Results
In the study cohort the median age was 71 ± 12 years, and 36 (72%) were men. In the historical cohort the median age was 71 ± 13 years, and 36 (72%) were men. Patients in the electronic urinary monitoring cohort demonstrated significantly more negative daily and cumulative fluid balance as compared to the historical cohort, (P &lt; 0.001 for all, Fig. 1). Incidence of AKI and the combined endpoint of AKI and 30-day mortality was significantly lower in the electronic UO monitoring cohort (24% vs. 46%, p = 0.0197 and 40% vs 78%, P &lt; 0.0001 respectively). These changes were more prominent in the subgroup of patients with chronic kidney disease (Fig. 2).

Conclusion
We demonstrated that real time monitoring of UO was associated with better prevention of fluid overload and the management of type I CRS in patients with ADHF. Further studies on larger populations are required to validate the potential utility of UO trending in the management of critically ill patients with ADHF.
#668 Combined biomarker testing for the assessment of acute kidney injury among myocardial infarction patients
Authors: Shacham Yacov , Frydman Shir , Banai Shmuel 
Published: May 2024

Abstract

Background and aims
The utility of different biomarkers for the prediction of acute kidney injury following ST-elevation myocardial infarction (STEMI) has been evaluated in several studies however, very few data exist on the prognostic value of combining biomarkers. Among numerous biomarkers examined, C-reactive protein (CRP) and Neutrophil gelatinase associated Lipocalin (NGAL) stand high in their utility to assess AKI risk. The aim of this study was to assess the prognostic value of combined CRP and NGAL measurement for the assessment of the risk of AKI in reperfused STEMI patients

Methods
Blood samples for plasma NGAL and CRP were drawn 24 hours after admission. High NGAL and CRP were defined as values within the 4th quartile (&gt;75percentile). Patients were stratified into 4 study groups: Low NGAL/Low CRP, LOW NGAL/high CRO, High NGAL /low CRP and high NGAL/high CRP. Patients were assessed for the occurrence of in-AKI based on the KDIGO criteria.

Results
A total of 311 patients were included (mean age 66 ± 14 years, 81% males).
According to the 4 study groups, there was a stepwise increase in the proportion of AKI (9% vs. 21% vs. 40% vs. 68%; p 0.001; Fig. 1). In a multivariate regression model, compared to patients having low NGAL/low CRP we observed a graded, independent increase in the risk for AKI for low NGAL/high CRP, high NGAL/low CRP and high NGAL/high CRP(OR 2.89, p = 0.02 vs. OR 3.29, p &lt; 0.001 vs. OR 17.6, p &lt; 0.001 respectively, Table 1). Peak concentrations showed significant areas under the curves (AUCs) for the prediction of AKI for both CRP AUC (0.692, 95% CI 0.62-0.76) and NGAL (AUC 0.778, 95% CI 0.72-0.84). The combination of NGAL and CRP yielded a significant increase in AUC to 0.822 (95% CI 0.77 to 0.88) (combined biomarkers vs CRP: p &lt; 0.001 and combined vs. NGAL: p = 0.02; Fig. 2).

Conclusions
In patients with reperfused STEMI, the combined assessment of NGAL and CRP provided incremental prognostic information for the prediction AKI when compared with single-biomarker measurement.
#984 Macrophage BRCC3 ameliorates sepsis-induced kidney injury by mediating renal NLRP3 inflammation
Authors: Wang Yao 
Published: May 2024

Abstract

Background and Aims
Sepsis-induced kidney injury (S-AKI) is an inflammatory disease characterized by high mortality rates. Macrophages are key inflammatory cells in the pathogenesis of S-AKI, and a rationale to target macrophage-endothelial cell interactions has been elucidated. Some study reported that BRCC3, a deubiquitylating enzyme, which is a critical regulator of NLRP3 activity in vitro experiments. However, the role of Macrophage BRCC3 role in S-AKI remains unclear.

Method
The S-AKI model was established by injecting lipopolysaccharide (LPS) into wild-type (WT) and macrophage-specific BRCC3 knockdown (KO-Mφ) mice. Transfecting RAW264.7 macrophages with siBRCC3 and establishing the co-culture system of RAW264.7 macrophages and murine tubular epithelial cells (mTECs) in Transwell.

Results
We found that macrophage BRCC3 deficiency ameliorates S-AKI. Compared with WT-S-AKI mice, the macrophage infiltration was decreased, the serum creatinine, BUN and the renal histologic injury scoring was decreased, as well as the expression of NLRP3 and Pro-Caspase-1 was clearly attenuated in KO-Mφ S-AKI mice. However, the serum IL-1β, IL-6, and TNF-α changes had on different between S-AKI groups. In vitro study, knockdown of BRCC3 in macrophages decreased NLRP3 inflammasome activation and cell apoptosis in mTECs. Mechanistically, BRCC3 knockdown promoted K63-linked ubiquitination of NLRP3 in macrophages. NLRP3 overexpression in mTEC abolished the renal protective effects of macrophages BRCC3 knockoff in S-AKI mice.

Conclusion
We showed that the macrophage BRCC3 as a key regulator in the activation of NLRP3 inflammasome by ubiquitination pathway in S-AKI. Our study unveils that macrophage BRCC3 has the potential to be the novel therapeutic target for S-AKI treatment.
#1385 Dipeptidyl-peptidase-4 inhibitor teneligliptin attenuates folic acid-induced tubular cell death via inhibiting ferroptosis
Authors: Yasuda Hideo , Ema Chiemi , Iwakura Takamasa 
Published: May 2024

Abstract

Background and Aims
Dipeptidyl peptidase-4 (DPP-4) inhibitors have been shown to attenuate several types of acute kidney injury (AKI) in animal models [1–3]. However, the mechanisms underlying their renoprotective effects remain to be clarified. Previous studies had identified ferroptosis as the primary cell death pathway for folic acid-induced AKI in mice [4]. Referring to that report, we previously reported that teneligliptin, a DPP-4 inhibitor, ameliorates folic acid-induced AKI. In the present study, we investigated whether teneligliptin attenuates folic acid-induced tubular cell death through its anti-ferroptotic properties.

Method
In in vitro experiments, we used HK-2 cells, human proximal tubular epithelial cells. HK-2 cells were co-cultured with folic acid and z-VAD-FMK (zVAD), an apoptosis inhibitor; Necrostatin-1s (Nec-1s), a necroptosis inhibitor; Ferrostatin-1 (Fer-1), a ferroptosis inhibitor; or teneligliptin. Co-incubation of erastin, a ferroptosis inducer, and teneligliptin was also performed. The 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT) assay was conducted on HK-2 cells to assess cell viability.

Results
Fer-1, but not z-VAD or Nec-1s, inhibited folic acid-induced cell death (Fig. 1A-C), indicating that ferroptosis contributes to folic acid-induced tubular cell death, rather than apoptosis or necroptosis. Teneligliptin also inhibited folic acid- and erastin-induced tubular cell death (Fig. 1D,E), suggesting that the DPP-4 inhibitor inhibits folic acid-induced tubular cell death via its anti-ferroptotic properties.

Conclusion
DPP-4 inhibitor prevents folic acid-induced tubular cell death by inhibiting ferroptosis in vitro, which may contribute to the attenuation of AKI in vivo.
#594 Long-term risk of incident/progressive chronic kidney disease, or end-stage kidney disease post-acute kidney injury: systematic review, meta-analysis
Authors: Veltkamp Denise Mj , Porras Cindy P , Kok Maarten B , Verhaar Marianne , van Solinge Wouter W , Haitjema Saskia , Vernooij Robin Wm 
Published: May 2024

Abstract

Background and Aims
Little is known about which patients to follow-up after an episode of acute kidney injury (AKI) for future risks. The aim of this review is to assess the association between AKI and the incidence or progression of chronic kidney disease (CKD) or end-stage kidney disease (ESKD), stratified by subcategories of AKI-stages, -durations, and clinical settings.

Method
A systematic search of the literature in PubMed and Embase was performed by two reviewers to identify studies that examined CKD incidence (development of CKD stage ≥3), CKD progression (worsening of kidney function in patients with CKD stage ≥3), or ESKD, in patients with AKI versus patients without AKI. The risk of bias was assessed using the Newcastle-Ottawa Scale. Relative effect estimates (odds and hazard ratios) were pooled using a random effects model.

Results
In total, 48 retrospective and 13 prospective studies, encompassing 140.985 patients with AKI, were included in this review. All the studies were of moderate or high quality. The pooled effect ratio was 3.36 (95% confidence interval (CI) 2.68-4.03) for CKD incidence (n = 31 studies). This remained 3.40 (95% CI 1.79-5.00) in a sub analysis including patients with a recovered kidney function post-AKI, and 1.49 (95% CI 1.44-1.55) in a sub analysis including patients with an AKI lasting less than 3 days (Fig. 1). Overall, the effect ratio for CKD progression (n = 11 studies) was 1.70 (95% CI 1.38-2.01) and 3.81 (95% CI 2.58-5.04) for ESKD (n = 24 studies). The increased risk of these two outcomes were not seen in the sub analyses only including patients with AKI lasting less than 3 days. Overall, there is an observable higher risk for CKD incidence, CKD progression, and ESKD with increased AKI staging, although not always statistically significant. Minimal variations were observed across clinical settings.

Conclusion
In our review, including over 60 studies, we found that AKI was associated with an increased risk of CKD incidence, CKD progression, and ESKD. Patients with higher AKI-stages had even larger risks. Notably, even brief episodes of AKI (lasting less than 3 days) were associated with a higher risk of CKD incidence compared to patients without AKI. In contrary, the risk for ESKD is not enlarged in a sub analysis including patients with recovered kidney function compared to patients without AKI. These result warrant close monitoring of the kidney function post-AKI, specifically in patients with AKI lasting 3 days or longer. Future research should focus more on the risk of CKD progression in order to tailor follow-up care in these more vulnerable patients.