Background: We aimed to diagnose possible acute kidney injury (AKI) with new early biochemical markers in patients who were admitted to the emergency department frequently with mild and moderate brain trauma, and to prevent possible complications, shorten the duration of treatment and hospital stay. With this purpose, we decided to reach our scientific target using the experimental rat model.
Methods: Wistar albino rats were included our experiment. Fifteen rats were randomly separated into three groups: Sham control (n=1: Underwent craniotomy alone), control (n=7: Without craniotomy), and trauma group (n=7: Underwent craniotomy followed by brain injury).
Results: There were no significant differences groups creatinine levels within 0 and 24 h (0.35±0.02 and 0.33±0.03, respectively, p>0.05). Plasma NGAL and KIM1 concentrations were statistically significant different in both control and trauma groups (Friedman p<0.05) and significant differences at both NGAL and KIM-1 concentrations at dual comparisons by means of all sampling time (0-2 h, 0-24 h, and 2-24 h) (Wilcoxon p<0.001, after Bonferroni correction).
Conclusion: The presence of AKI in patients with mild-to-moderate brain trauma increases the risk of mortality. Early diagnosis of AKI reduces the hospitalization period and requiring of dialysis. Diagnosis of AKI within 24 h with early biomarkers and starting therapy is crucial issues.
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http://dx.doi.org/10.14744/tjtes.2020.29015 | DOI Listing |
Transl Psychiatry
January 2025
Department of Neurosurgery, General Hospital of Northern Theater Command, Postgraduate Training Base of General Hospital of Northern Theater Command of Jinzhou Medical University, Shenyang, Liaoning, China.
Traumatic brain injury (TBI) is identified as a risk factor for Parkinson's disease (PD), which is a neurodegenerative disease characterized by the loss of dopaminergic neurons in the substantia nigra (SN). However, the precise mechanism by which chronic TBI initiates PD pathogenesis is not yet fully understood. In our present study, we assessed the chronic progression and pathogenesis of PD-like behavior at different intervals in TBI mice.
View Article and Find Full Text PDFLancet Neurol
February 2025
Department of Neurology AB51, University of Groningen, University Medical Center Groningen, Groningen, Netherlands.
The age-specific incidence of traumatic brain injury in older adults is rising in high-income countries, mainly due to an increase in the incidence of falls. The severity of traumatic brain injury in older adults can be underestimated because of a delay in the development of mass effect and symptoms of intracranial haemorrhage. Management and rehabilitation in older adults must consider comorbidities and frailty, the treatment of pre-existing disorders, the reduced potential for recovery, the likelihood of cognitive decline, and the avoidance of future falls.
View Article and Find Full Text PDFJ Cereb Blood Flow Metab
January 2025
KG Jebsen Centre for Brain Fluid Research, University of Oslo, Oslo, Norway.
A potential two-way passage of cells and substances between the brain and skull bone marrow may open for new insights into neurological disease. The arachnoid membrane was traditionally considered to restrict cells and larger molecules in CSF from entering the dura and bone marrow directly. However, new data on exchange between brain and skull bone marrow have recently emerged.
View Article and Find Full Text PDFJ Cereb Blood Flow Metab
January 2025
Departments of Neurology and Radiology, Massachusetts General Hospital and Harvard Medical School, Boston, USA.
Therapeutic drug development for central nervous system injuries, such as traumatic brain injury (TBI), presents significant challenges. TBI results in primary mechanical damage followed by secondary injury, leading to cognitive dysfunction and memory loss. Our recent study demonstrated the potential of carbon monoxide-releasing molecules (CORMs) to improve TBI recovery by enhancing neurogenesis.
View Article and Find Full Text PDFJ Integr Neurosci
January 2025
Department of Hepatology, Federal University of Health Sciences of Porto Alegre (UFCSPA), 90050-170 Porto Alegre, Rio Grande do Sul (RS), Brazil.
Mitochondria are organelles of eukaryotic cells delimited by two membranes and cristae that consume oxygen to produce adenosine triphosphate (ATP), and are involved in the synthesis of vital metabolites, calcium homeostasis, and cell death mechanisms. Strikingly, normal mitochondria function as an integration center between multiple conditions that determine neural cell homeostasis, whereas lesions that lead to mitochondrial dysfunction can desynchronize cellular functions, thus contributing to the pathophysiology of traumatic brain injury (TBI). In addition, TBI leads to impaired coupling of the mitochondrial electron transport system with oxidative phosphorylation that provides most of the energy needed to maintain vital functions, ionic homeostasis, and membrane potentials.
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