Observational studyScientific reports2019
Acute Tubular Injury is Associated With Severe Traumatic Brain Injury: in Vitro Study on Human Tubular Epithelial Cells.
Observational study in Scientific reports, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 papers, 1 of them a synthesis that pooled it.
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Who cites it
27 citing papers in PubMed, 1 synthesis or guideline pooled it.
- Incidence and risk factors of acute kidney injury following Stanford type A aortic dissection surgery: a systematic review and meta-analysis.Frontiers in cardiovascular medicine · 2026Pooled it
- Incidence and risk factors of acute kidney injury among neurocritical patients in high-altitude regions: a retrospective cohort study.Frontiers in medicine · 2026Article
- Advances in cellular and molecular mechanisms of trauma-induced organ inflammation and dysfunction.Burns & trauma · 2026Review
- Brain-derived extracellular vesicles circUsp32 polarized macrophages causing acute kidney injury after traumatic brain injury.Science advances · 2025Article
- Mass Spectrometry-Based Comparative Analysis ofACS chemical neuroscience · 2025Article
- Treatment with MG53 ameliorates traumatic brain injury-associated acute kidney injury.The journal of trauma and acute care surgery · 2025Article
- Kidneys on the Frontline: Nephrologists Tackling the Wilds of Acute Kidney Injury in Trauma Patients-From Pathophysiology to Early Biomarkers.Diagnostics (Basel, Switzerland) · 2025Review
- Protective effects of tasimelteon on kidney injury in a traumatic brain injury rat model: a histopathological and immunohistochemical study.European journal of trauma and emergency surgery : official publication of the European Trauma Society · 2025Article
- Association between traumatic brain injury and risk of developing infections in the central nervous system and periphery.Metabolic brain disease · 2025Review
- Acute Kidney Injury Secondary to Trauma Brain Injury (TBI) and the Role of Angiotensin-1-7.Advanced biomedical research · 2025Article
- Predictive value of triglyceride glucose index in acute kidney injury in patients with severe traumatic brain injury.Scientific reports · 2024Article
- Cascading renal injury after brain death: Unveiling glycocalyx alteration and the potential protective role of tacrolimus.Frontiers in cell and developmental biology · 2024Article
- Hyperchloremia, a necessary evil in neurocritical care.Critical care (London, England) · 2023Article
- Kidney Dysfunction After Traumatic Brain Injury: Pathophysiology and General Management.Neurocritical care · 2023Review
- The role of the microbiota-gut-brain axis in long-term neurodegenerative processes following traumatic brain injury.The European journal of neuroscience · 2023Review
- Subclinical Acute Kidney Injury in COVID-19: Possible Mechanisms and Future Perspectives.International journal of molecular sciences · 2022Review
- Acute Kidney Injury at the Neurocritical Care Unit.Neurocritical care · 2022Review
- Assessing the Global Impact on the Mouse Kidney After Traumatic Brain Injury: A Transcriptomic Study.Journal of inflammation research · 2022Article
- Prevalence and Mortality of Post-traumatic Acute Kidney Injury in Children; a Systematic Review and Meta-analysis.Archives of academic emergency medicine · 2022Review
- Continuous Renal Replacement Therapy in Acute Brain Injury.Frontiers in nephrology · 2022Review
Corrections and comments
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Authors and funding
10 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Acute kidney injury following traumatic brain injury is associated with poor outcome. We investigated in vitro the effects of plasma of brain injured patients with acute tubular kidney injury on kidney tubular epithelial cell function. we performed a prospective observational clinical study in ICU in a trauma centre of the University hospital in Italy including twenty-three ICU patients with traumatic brain injury consecutively enrolled. Demographic data were recorded on admission: age 39 ± 19, Glasgow Coma Score 5 (3-8). Neutrophil Gelatinase-Associated Lipocalin and inflammatory mediators were measured in plasma on admission and after 24, 48 and 72 hours; urine were collected for immunoelectrophoresis having healthy volunteers as controls. Human renal proximal tubular epithelial cells were stimulated with patients or controls plasma. Adhesion of freshly isolated human neutrophils and trans-epithelial electrical resistance were assessed; cell viability (XTT assay), apoptosis (TUNEL staining), Neutrophil Gelatinase-Associated Lipocalin and Megalin expression (quantitative real-time PCR) were measured. All patients with normal serum creatinine showed increased plasmatic Neutrophil Gelatinase-Associated Lipocalin and increased urinary Retinol Binding Protein and α1-microglobulin. Neutrophil Gelatinase-Associated Lipocalin was significantly correlated with both inflammatory mediators and markers of tubular damage. Patient' plasma incubated with tubular cells significantly increased adhesion of neutrophils, reduced trans-epithelial electrical resistance, exerted a cytotoxic effect and triggered apoptosis and down-regulated the endocytic receptor Megalin compared to control. Plasma of brain injured patients with increased markers of subclinical acute kidney induced a pro-inflammatory phenotype, cellular dysfunction and apoptotic death in tubular epithelial cells.
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