RESUMO
Traumatic brain injury (TBI) stands as a significant contributor to traumatic death and disability worldwide. In recent years, researchers have identified biomarkers to gauge useful outcomes in TBI patients. However, the enigma of timely sample collection to measure the biomarkers remains a controversial point in the case of TBI, unlike other degenerative diseases like Alzheimer's disease and Parkinson's disease, where we can collect the sample at any point in time. The purpose of this study is to evaluate the sensitivity of biomarkers in TBI concerning time of injury by analyzing recent available data on biomarkers in the medical literature. A total of 2,256 studies were initially retrieved from the search engine. After an initial screening, only 1,750 unique articles remained. After excluding review articles, animal studies, meta-analysis, and studies with children (screened by title and abstract), 30 kinds of literature were found relevant to search the required variables. Further 16 studies were excluded due to the nonavailability of complete variables or data. Finally, 14 studies remained and were included in the analysis. This study has analyzed the four most commonly described biomarkers for TBI in the literature: glial fibrillary acidic protein (GFAP), S100 calcium-binding protein B, ubiquitin carboxy-terminal hydrolase L1, and Tau. According to this statistical analysis, all biomarkers included in the study have shown their serum levels after trauma. So, all these biomarkers can be used for further study in the outcome prediction and diagnosis of TBI patients. The meta-analysis suggests that the best biomarker for TBI is Tau in cases where sample collection is done within 24 hours, while GFAP is the best biomarker to be studied for TBI if sample collection is done 24 hours after trauma.
RESUMO
Objective: Loss of Wilms tumor-1 (WT1) protein, a podocytopathy marker, through urine exosome (uE), could be an early indication of kidney injury. We examined WT1 in uE (uE-WT1), along with other urine markers of glomerular and kidney tubule injury, in individuals without chronic kidney disease (CKD). Methodology: The cross-sectional study included individuals who reported having no evidence of chronic kidney disease (CKD). Albumin-to-creatinine ratio (ACR) and estimated glomerular filtration rate (eGFR) were used to assess kidney function. eGFR was calculated using the 2009 CKD-EPI (CKD-Epidemiological) equation. WT1 was analyzed in uE from humans and Wistar rats (before and after the 9th week of diabetes, n = 20). uE-WT1, urinary neutrophil gelatinase-associated lipocalin (NGAL), and kidney injury molecule-1 (KIM-1) were estimated using ELISA. The Kruskal-Wallis H test, Mann-Whitney U test, and stepwise multivariable linear regression were performed. Results: Urine NGAL and ACR increase with uE-WT1 quartiles (n = 146/quarter). Similarly, uE-WT1, KIM-1, and NGAL were positively associated with ACR. Furthermore, KIM-1, NGAL, and uE-WT1 correlated with ACR. uE-WT1 outperformed KMI-1 and NGAL to explain ACR variability (25% vs. 6% or 9%, respectively). Kidney injury in streptozotocin-induced diabetic rats was associated with a significant rise in uE-WT1. Moreover, the findings were confirmed by the histopathology of kidney tissues from rats. Conclusion: uE-WT1 was strongly associated with kidney function in rats. In individuals without CKD, uE-WT1 outperformed NGAL as a determinant of differences in ACR.