ArticleSpringerPlus2014
Association of inflammatory and endothelial cell activation biomarkers with acute kidney injury after sepsis.
Article in SpringerPlus, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.
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Who cites it
18 citing papers in PubMed, 35 citations in OpenAlex.
- Article
- Modified furosemide responsiveness index and biomarkers for AKI progression and prognosis: a prospective observational study.Annals of intensive care · 2024Article
- MicroRNA-192-5p downregulates Fat Mass and Obesity-associated Protein to aggravate renal ischemia/reperfusion injury.Renal failure · 2023Article
- Online Hemodiafiltration Compared to Conventional Hemodialysis in Critically Ill Patients.Kidney international reports · 2022Article
- Article
- Using best subset regression to identify clinical characteristics and biomarkers associated with sepsis-associated acute kidney injury.American journal of physiology. Renal physiology · 2020Article
- Observational
- Acute kidney injury in hospitalized patients who underwent percutaneous kidney biopsy for histological diagnosis of their renal disease.BMC nephrology · 2019Article
- Biomarkers of AKI Progression after Pediatric Cardiac Surgery.Journal of the American Society of Nephrology : JASN · 2018Article
- Predicting acute kidney injury: current status and future challenges.Journal of nephrology · 2018Review
- Interleukin-8 and Tumor Necrosis Factor Predict Acute Kidney Injury After Pediatric Cardiac Surgery.The Annals of thoracic surgery · 2017Article
- Markers of acute kidney injury in patients with sepsis: the role of soluble thrombomodulin.Critical care (London, England) · 2017Observational
- Association of markers of endothelial dysregulation Ang1 and Ang2 with acute kidney injury in critically ill patients.Critical care (London, England) · 2016Article
- Acute kidney injury induced by thrombotic microangiopathy in a patient with hemophagocytic lymphohistiocytosis.BMC nephrology · 2016Article
- Cystatin C and long term risk of community-acquired sepsis: a population-based cohort study.BMC nephrology · 2015Article
- Sepsis-associated acute kidney injury.Seminars in nephrology · 2015Review
- Mitochondrial ROS Induces Cardiac Inflammation via a Pathway through mtDNA Damage in a Pneumonia-Related Sepsis Model.PloS one · 2015Article
- Low-Dose vasopressin and renal perfusion in pediatric cardiac surgery.Annals of cardiac anaesthesiaArticle
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Authors and funding
6 authors at 3 institutions in 1 country.
Funding
Abstract
objectiveAcute kidney injury (AKI) is a sequela of sepsis associated with increased morbidity and mortality. We sought to determine if individuals with elevated baseline levels of inflammation and endothelial cell activation are at increased risk for future AKI after sepsis.
methodsWe conducted an analysis of individuals developing sepsis in the national 30,239 subject REGARDS cohort. Biomarkers measured at the beginning of an 8-year observation period included high-sensitivity C-reactive protein (hsCRP), interleukin-6 (IL-6), tumor necrosis factor (TNF-α), E-selectin, inter-cellular adhesion molecule-1 (ICAM-1), vascular cell adhesion molecule-1 (VCAM-1), and urinary Albumin-to-creatinine ratio (ACR). We defined subsequent sepsis as hospitalization for a serious infection with ≥2 Systemic Inflammatory Response Syndrome (SIRS) criteria. We excluded patients with prior dialysis or kidney transplantation, or those receiving less than two serum creatinine (sCr) measurements during hospitalization. We defined AKI as an increase in sCr ≥0.3 mg/dL from the initial sCr measurement, or the initiation of hemodialysis. Using logistic regression, we evaluated the associations between AKI and biomarker quartiles, adjusting for comorbidities.
resultsWe identified 212 sepsis cases encompassing 41 (19.3%) AKI. Elapsed time from biomarker measurement to sepsis episode was 3.1 years (IQR 1.6-4.5). Compared with non-AKI, AKI individuals exhibited higher TNF-α (9.4 vs. 6.2 pg/mL, p = 0.003) and ACR (504.82 vs 61.81 mg/g, p < 0.001). hsCRP, IL-6, E-selectin, ICAM-1 and VCAM-1 were similar between AKI and non-AKI. After adjustment for confounders, AKI after sepsis was more likely in those with higher E-selectin (adjusted ORs 2.91 (0.95-8.93), 1.99 (0.61-6.47), 4.01 (1.30-12.35), test of linear trend p = 0.04), and higher ACR (adjusted ORs 2.29 (0.99-5.30), 10.67 (3.46-32.90), test of linear trend p < 0.001). Baseline hsCRP, TNF-α, IL-6, VCAM-1 and ICAM-1 were not associated with AKI after sepsis.
conclusionElevated baseline levels of E-selectin and ACR are associated with future AKI in the setting of sepsis. Baseline inflammatory and endothelial activation biomarkers may be useful for predicting future risk of AKI in sepsis.
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