Incidence and Burden of Acute Kidney Injury among Traumatic Brain-Injury Patients

Wang, Ruoran; Zhang, Jing; Xu, Jing; He, Min; Xu, Jianguo

doi:10.2147/rmhp.s335150

Cited by 10 publications

(6 citation statements)

References 31 publications

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“…Osmotic therapy during ICU stay appears to affect the mortality due to AKI[ 29 ]. A recent study suggested that the AKI stage was associated with mortality in patients with TBI, but not AKI duration or AKI burden; in addition, most deaths occurred during the first 3 d of ICU stay[ 30 ]. The use of renoprotective measures affects the mortality due to AKI in patients with TBI[ 31 ].…”

Section: Discussionmentioning

confidence: 99%

Acute kidney injury in traumatic brain injury intensive care unit patients

Huang¹,

Liu²,

Huang³

et al. 2022

WJCC

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BACKGROUND The exact definition of Acute kidney injury (AKI) for patients with traumatic brain injury (TBI) is unknown. AIM To compare the power of the “Risk, Injury, Failure, Loss of kidney function, and End-stage kidney disease” (RIFLE), Acute Kidney Injury Network (AKIN), Creatinine kinetics (CK), and Kidney Disease Improving Global Outcomes (KDIGO) to determine AKI incidence/stage and their association with the in-hospital mortality rate of patients with TBI. METHODS This retrospective study collected the data of patients admitted to the intensive care unit for neurotrauma from 2001 to 2012, and 1648 patients were included. The subjects in this study were assessed for the presence and stage of AKI using RIFLE, AKIN, CK, and KDIGO. In addition, the propensity score matching method was used. RESULTS Among the 1648 patients, 291 (17.7%) had AKI, according to KDIGO. The highest incidence of AKI was found by KDIGO (17.7%), followed by AKIN (17.1%), RIFLE (12.7%), and CK (11.5%) ( P = 0.97). Concordance between KDIGO and RIFLE/AKIN/CK was 99.3%/99.1%/99.3% for stage 0, 36.0%/91.5%/44.5% for stage 1, 35.9%/90.6%/11.3% for stage 2, and 47.4%/89.5%/36.8% for stage 3. The in-hospital mortality rates increased with the AKI stage in all four definitions. The severity of AKI by all definitions and stages was not associated with in-hospital mortality in the multivariable analyses (all P > 0.05). CONCLUSION Differences are seen in AKI diagnosis and in-hospital mortality among the four AKI definitions or stages. This study revealed that KDIGO is the best method to define AKI in patients with TBI.

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Section: Discussionmentioning

confidence: 99%

Acute kidney injury in traumatic brain injury intensive care unit patients

Huang¹,

Liu²,

Huang³

et al. 2022

WJCC

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“…Post-TBI liver and kidney injury has been shown to prolong hospital and intensive care unit length of stay (6,66,67). Currently, relatively few studies link the mechanisms of TBI to either kidney or liver injury.…”

Section: Kidney and Livermentioning

confidence: 99%

“…Severe TBI has been linked to an early systemic inflammatory response syndrome (SIRS). The TBI-induced SIRS has been postulated as a mechanism resulting in multiorgan dysfunction (MOD), which can manifest as coagulopathy, hemodynamic and cardiovascular dysfunction, shock liver, acute kidney injury, and acute lung injury (2,(4)(5)(6)(7).…”

Section: Introductionmentioning

confidence: 99%

The neuro-endothelial axis in traumatic brain injury: mechanisms of multi-organ dysfunction, novel therapies, and future directions

Ho,

Dawood,

Taylor

et al. 2024

Shock

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Severe traumatic brain injury (TBI) often initiates a systemic inflammatory response syndrome (SIRS), which can potentially culminate into multi-organ dysfunction (MOD). A central player in this cascade is endotheliopathy, caused by perturbations in homeostatic mechanisms governed by endothelial cells due to injury-induced coagulopathy, heightened sympathoadrenal response, complement activation, and pro-inflammatory cytokine release. Unique to TBI is the potential disruption of the blood-brain barrier (BBB), which may expose neuronal antigens to the peripheral immune system and permit neuroinflammatory mediators to enter systemic circulation, propagating endotheliopathy systemically. This review aims to provide comprehensive insights into the “neuro-endothelial axis” underlying endothelial dysfunction following TBI, identify potential diagnostic and prognostic biomarkers, and explore therapeutic strategies targeting these interactions, with the ultimate goal of improving patient outcomes following severe TBI.

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“…In particular, acute kidney injury (AKI) is thought to be potentially associated with TBI, and the concomitant occurrence of AKI is thought to be associated with causing unfavorable outcomes in TBI patients. [3][4][5][6][7] Studies have previously found that the incidence of AKI after TBI is approximately 10-20%. [5][6][7][8] Although elevated serum creatinine and decreased urine output are criteria for the diagnosis of AKI in TBI, patients who do not meet these criteria may be at risk of developing subclinical AKI due to acute tubular injury or other possible mechanisms.…”

Section: Introductionmentioning

confidence: 99%

“…[3][4][5][6][7] Studies have previously found that the incidence of AKI after TBI is approximately 10-20%. [5][6][7][8] Although elevated serum creatinine and decreased urine output are criteria for the diagnosis of AKI in TBI, patients who do not meet these criteria may be at risk of developing subclinical AKI due to acute tubular injury or other possible mechanisms. 3 In addition to using RIFLE, AKIN and KDIGO criteria for AKI diagnosis, biomarkers such as neutrophil gelatinase-associated lipocalin (NGAL), cystatin C, and serum lactate have been evaluated as screening tools for predicting AKI in critically ill patients including those with TBI.…”

Section: Introductionmentioning

confidence: 99%

Assessing the Global Impact on the Mouse Kidney After Traumatic Brain Injury: A Transcriptomic Study

Chan¹,

Hsu²,

Cheng³

et al. 2022

JIR

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In this study, we use animal models combined with bioinformatics strategies to investigate the potential changes in overall renal transcriptional expression after traumatic brain injury. Methods: Microarray analysis was performed after kidney acquisition using unilateral controlled cortical impact as the primary mouse TBI model. Multi-oriented gene set enrichment analysis was performed for differentially expressed genes. Results:The results showed that TBI affected the gene set associated with mitochondria function in kidney cells, and a negative enrichment of gene sets associated with immune cell migration and epidermal development was also observed. Analysis of the disease phenotype gene set revealed that differential expression of mitochondria-related genes was associated with lactate metabolism. Alternatively, activation and adhesion of immune cells associated with the complement system may promote autoinflammation in kidney tissue. The simulated immune cell infiltration analysis showed an increase in the proportion of activated memory CD4 T cells and a decrease in the proportion of resting memory CD4 T cells, suggesting that activated memory CD4 T cell infiltration may be involved in the inflammation of renal tissue and cause damage to renal cells, such as principal cells, mesangial cells and loops of Henle cells. Conclusion:This study is the first to reveal the effects of brain trauma on the kidney. TBI may affect the expression of mitochondria function-related gene sets in renal cells by increasing lactate. It may also affect renal mesangial cells by inducing increased infiltration of immune cells through mechanisms related to complement system activation or autoimmune antibodies.

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Incidence and Burden of Acute Kidney Injury among Traumatic Brain-Injury Patients

Cited by 10 publications

References 31 publications

Acute kidney injury in traumatic brain injury intensive care unit patients

Acute kidney injury in traumatic brain injury intensive care unit patients

The neuro-endothelial axis in traumatic brain injury: mechanisms of multi-organ dysfunction, novel therapies, and future directions

Assessing the Global Impact on the Mouse Kidney After Traumatic Brain Injury: A Transcriptomic Study

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