Impact of acute renal failure on plasmatic levels of cleaved endocan.
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ABSTRACT:
SUBMITTER: Gaudet A
PROVIDER: S-EPMC6381621 | biostudies-literature | 2019 Feb
REPOSITORIES: biostudies-literature
Publications
Impact of acute renal failure on plasmatic levels of cleaved endocan.
Gaudet Alexandre A Parmentier Erika E De Freitas Caires Nathalie N Portier Lucie L Dubucquoi Sylvain S Poissy Julien J Duburcq Thibault T Hureau Maxence M Lassalle Philippe P Mathieu Daniel D
Critical care (London, England) 20190219 1
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Project description: Not available
| S-EPMC6625000 | biostudies-literature
Project description:BackgroundAcute respiratory distress syndrome (ARDS) is a life-threatening condition resulting from acute pulmonary inflammation. However, no specific treatment for ARDS has yet been developed. Previous findings suggest that lung injuries related to ARDS could be regulated by endocan (Esm-1). The aim of this study was to evaluate the potential efficiency of endocan in the treatment of ARDS.MethodsWe first compared the features of acute pulmonary inflammation and the severity of hypoxemia in a tracheal LPS-induced acute lung injury (ALI) model performed in knockout (Esm1-/-) and wild type (WT) littermate C57Bl/6 mice. Next, we assessed the effects of a continuous infusion of glycosylated murine endocan in our ALI model in Esm1-/- mice.ResultsIn our ALI model, we report higher alveolar leukocytes (p < 0.001), neutrophils (p < 0.001), and MPO (p < 0.001), and lower blood oxygenation (p < 0.001) in Esm1-/- mice compared to WT mice. Continuous delivery of glycosylated murine endocan after LPS-induced ALI resulted in decreased alveolar leukocytes (p = 0.012) and neutrophils (p = 0.012), higher blood oxygenation levels (p < 0.001), and reduced histological lung injury (p = 0.04), compared to mice treated with PBS.ConclusionsEndocan appears to be an effective treatment in an ARDS-like model in C57Bl/6 mice.
| S-EPMC9857156 | biostudies-literature
Project description:Background & aimsAcute-on-chronic liver failure is a syndrome characterized by organ failure and high short-term mortality. The lack of reliable biomarkers for the early detection of acute-on-chronic liver failure is a significant challenge. Endothelial dysfunction plays a key role in the development of organ failure. Serum endocan is a potential new biomarker for endothelial dysfunction. Therefore, this study aimed to assess the association between endocan and organ failure and 28-day mortality in patients with cirrhosis.MethodsHospitalized patients with cirrhosis with and without organ failure were prospectively enrolled according to the criteria of the European Association for the Study of Liver-Chronic Liver Failure consortium. The comparative performances of serum endocan, procalcitonin, and interleukin-6 for diagnosing organ failure and predicting mortality were studied.ResultsThe study included 116 hospitalized patients with cirrhosis, 55 of whom had organ failure on admission. Patients with organ failure had significantly higher endocan, procalcitonin, and interleukin-6 levels than those without it. At a cut-off value of 15.8 ng/mL, endocan showed a sensitivity of 63.6% and specificity of 67.2% for the diagnosis of organ failure, with an area under the receiver operating characteristic curve of 0.65, which is comparable to procalcitonin and interleukin-6. Multivariate analysis identified serum endocan, creatinine, and total bilirubin as independent factors for organ failure in hospitalized patients with cirrhosis. Patients who died within 28 days had significantly higher baseline biomarker levels than those who survived. Liver failure, hospital-acquired infection, mechanical ventilator use, and interleukin-6 ≥37 pg/mL were independent predictors of 28-day mortality.ConclusionSerum endocan is associated with organ failure and is an independent risk factor of organ failure in hospitalized patients with cirrhosis.
| S-EPMC11671009 | biostudies-literature
Project description:A prospective study of 120 patients of acute renal failure was done at CH (EC) Calcutta to document the changing trends in the incidence and etiology of acute renal failure and to assess the prognostic factors. Mean age of patients was 33.7 ± 20.2 years. 75% had a medical risk factor. The etiological factors were volume depletion (13.3%), septicaemia (25.6%), falciparum malaria (16.6%), a transplant related renal failure (5.7%) and drugs (16.7%). Renal histology showed acute tubular necrosis to be the most common lesion (53.3%). In 13.3% patients who died with acute renal failure, associated infection and multisystem involvement was more common.
| S-EPMC5529769 | biostudies-other
Project description:Acute respiratory distress syndrome (ARDS) and hospital-acquired pneumonia (HAP) are major problems of public health in intensive care units (ICUs), occurring in 15% of critically ill patients. Among the factors explaining ARDS development, sepsis is known as a frequent cause. Sepsis, ARDS, and HAP increase morbidity, mortality, length of stay in the ICU, and the overall costs of healthcare. The major challenge remains to identify accurately among critically ill patients those at risk of poor outcomes who could benefit from novel therapies. Endocan is released by the pulmonary endothelium in response to local or systemic injury. It inhibits mainly leukocyte diapedesis rather than leukocyte rolling or adhesion to the endothelial cells both in vitro and in vivo. Endocan was evaluated in 25 clinical reports, including 2454 critically ill patients and 452 healthy controls. The diagnostic value of endocan for sepsis or sepsis severity was equal to procalcitonin but its prognostic value was better. A predictive value for postoperative pneumonia was evidenced in two studies, and a predictive value for ARDS in four studies from three independent centers. This review presents an overview of the structure, expression, and functions of endocan. We also hereby summarize the potential applications of endocan in the prediction and prognosis of ARDS and HAP, as well as in the prognosis of sepsis.
| S-EPMC6204032 | biostudies-literature
Project description:Background:Endothelial cell specific molecule-1, also called as endocan, is a dermatan sulfate proteoglycan, which is expressed by endothelial cells in alveolar walls of the lung and kidney. High endocan levels are found associated with endothelial dysfunction and inflammation. We hypothesize that endocan level is also high in COPD due to systemic inflammation and endothelial dysfunction. We aimed to investigate the expression of endocan in patients with stable COPD. Material and methods:The study included patients with COPD and control subjects. COPD patients were classified according to the Global Initiative for Chronic Obstructive Lung Disease (GOLD) 2017 criteria. Demographics, body mass index, smoking history, and comorbidities were recorded. Endocan levels of COPD patients and controls were compared. Results:Totally, 88 subjects (47 stable COPD patients, 41 controls) were evaluated. Endocan levels were significantly higher in COPD patients than control group (860.1±259.8 vs 647.3±316.9 pg/mL, P=0.001). There was no relationship between GOLD COPD categories and endocan levels. Also endocan levels were similar between COPD patients with or without hypoxemia. Conclusion:Serum endocan level was significantly higher in patients with stable COPD. Further studies should be performed to better understand the relationship between endocan and COPD.
| S-EPMC6197208 | biostudies-other
Project description:Endocan is a soluble dermatan sulfate proteoglycan expressed by endothelial cells and detected in serum/plasma. Its expression is increased in tumors/tumor vessels in several human malignancies, and high expression (high serum/plasma levels or tumor levels) has an adverse prognostic impact in several malignancies. The p14 endocan degradation product can also be detected in serum/plasma, but previous clinical studies as well as previously unpublished results presented in this review suggest that endocan and p14 endocan fragment levels reflect different biological characteristics, and the endocan levels seem to reflect the disease heterogeneity in acute leukemia better than the p14 fragment levels. Furthermore, decreased systemic endocan levels in previously immunocompetent sepsis patients are associated with later severe respiratory complications, but it is not known whether this is true also for immunocompromised acute leukemia patients. Finally, endocan is associated with increased early nonrelapse mortality in (acute leukemia) patients receiving allogeneic stem cell transplantation, and this adverse prognostic impact seems to be independent of the adverse impact of excessive fluid overload. Systemic endocan levels may also become important to predict cytokine release syndrome after immunotherapy/haploidentical transplantation, and in the long-term follow-up of acute leukemia survivors with regard to cardiovascular risk. Therapeutic targeting of endocan is now possible, and the possible role of endocan in acute leukemia should be further investigated to clarify whether the therapeutic strategy should also be considered.
| S-EPMC9027427 | biostudies-literature
Project description:Hyperammonemia has been associated with intracranial hypertension and mortality in patients with acute liver failure (ALF). We evaluated the effect of renal replacement therapy (RRT) on serum ammonia level and outcomes in ALF. This was a multicenter cohort study of consecutive ALF patients from the United States ALF Study Group registry between January 1998 and December 2016. First, we studied the association of ammonia with hepatic encephalopathy (HE) and 21-day transplant-free survival (TFS; n = 1,186). Second, we studied the effect of RRT on ammonia for the first 3 days post study admission (n = 340) and on 21-day TFS (n = 1,186). Higher admission (n = 1,186) median ammonia level was associated with grade 3-4 HE (116 vs. 83 μmol/L) and mortality at day 21 attributed to neurological (181 vs. 90 μmol/L) and all causes (114 vs. 83 μmol/L; P < 0.001 for all). Among 340 patients with serial ammonia levels, 61 (18%) were on continuous RRT (CRRT), 59 (17%) were on intermittent RRT (IRRT), and 220 (65%) received no RRT for the first 2 days. From days 1 to 3, median ammonia decreased by 38%, 23%, and 19% with CRRT, IRRT, and no RRT, respectively. Comparing to no RRT use, whereas ammonia reduction with CRRT was significant (P = 0.007), with IRRT it was not (P = 0.75). After adjusting for year of enrollment, age, etiology, and disease severity, whereas CRRT (odds ratio [OR], 0.47 [95% confidence interval {CI}, 0.26-0.82]) was associated with reduction in 21-day transplant-free all-cause mortality, IRRT (OR, 1.68 [95% CI, 1.04-2.72]) was associated with an increase. Conclusion: In a large cohort of ALF patients, hyperammonemia was associated with high-grade HE and worse 21-day TFS. CRRT was associated with a reduction in serum ammonia level and improvement of 21-day TFS. (Hepatology 2018;67:711-720).
| S-EPMC5832542 | biostudies-literature
Project description:Metastatic calcification, a known complication of prolonged end-stage renal disease, is herein described for the first time in a 10-month-old boy with acute renal failure, manifesting as a painful and swollen arm. Imaging revealed diffuse calcification and technetium-99 methylene diphosphonate (99Tc-MDP) uptake around the humerus and axilla. Calcium and vitamin D restriction, followed by intravenous administration of sodium thiosulfate caused a full symptomatic, radio- and scintigraphic improvement.
| S-EPMC1805049 | biostudies-other
Project description:Aims: Inflammation-driven endothelitis seems to be a hallmark of acute heart failure (AHF) and cardiogenic shock (CS). Endocan, a soluble proteoglycan secreted by the activated endothelium, contributes to inflammation and endothelial dysfunction, but has been scarcely explored in human AHF. We aimed to evaluate serum (S-Endocan) and urinary endocan (U-Endocan) profiles in AHF and CS patients and to correlate them with biomarkers/parameters of inflammation, endothelial activation, cardiovascular dysfunction and prognosis. Methods: Blood and spot urine were collected from patients with AHF (n = 23) or CS (n = 25) at days 1-2 (admission), 3-4 and 5-8 and from controls (blood donors, n = 22) at a single time point. S-Endocan, U-Endocan, serum IL-1β, IL-6, tumour necrosis factor-α (S-TNF-α), intercellular adhesion molecule-1 (S-ICAM-1), vascular cell adhesion molecule-1 (S-VCAM-1) and E-selectin were determined by ELISA or multiplex immunoassays. Serum C-reactive protein (S-CRP), plasma B-type natriuretic peptide (P-BNP) and high-sensitivity troponin I (P-hs-trop I), lactate, urea, creatinine and urinary proteins, as well as prognostic scores (APACHE II, SAPS II) and echocardiographic left ventricular ejection fraction (LVEF) were also evaluated. Results: Admission S-Endocan was higher in both patient groups, with CS presenting greater values than AHF (AHF and CS vs. Controls, p < 0.001; CS vs. AHF, p < 0.01). Admission U-Endocan was only higher in CS patients (p < 0.01 vs. Controls). At admission, S-VCAM-1, S-IL-6 and S-TNF-α were also higher in both patient groups but there were no differences in S-E-selectin and S-IL-1β among the groups, nor in P-BNP, S-CRP or renal function between AHF and CS. Neither endocan nor other endothelial and inflammatory markers were reduced during hospitalization (p > 0.05). S-Endocan positively correlated with S-VCAM-1, S-IL-6, S-CRP, APACHE II and SAPS II scores and was positively associated with P-BNP in multivariate analyses. Admission S-Endocan raised in line with LVEF impairment (p = 0.008 for linear trend). Conclusion: Admission endocan significantly increases across AHF spectrum. The lack of reduction in endothelial and inflammatory markers throughout hospitalization suggests a perpetuation of endothelial dysfunction and inflammation. S-Endocan appears to be a biomarker of endothelitis and a putative therapeutic target in AHF and CS, given its association with LVEF impairment and P-BNP and its positive correlation with prognostic scores.
| S-EPMC9407685 | biostudies-literature