• Title, Summary, Keyword: Acute injury

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Brain consequences of acute kidney injury: Focusing on the hippocampus

  • Malek, Maryam
    • Kidney Research and Clinical Practice
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    • v.37 no.4
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    • pp.315-322
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    • 2018
  • The high mortality rates associated with acute kidney injury are mainly due to extra-renal complications that occur following distant-organ involvement. Damage to these organs, which is commonly referred to as multiple organ dysfunction syndrome, has more severe and persistent effects. The brain and its sub-structures, such as the hippocampus, are vulnerable organs that can be adversely affected. Acute kidney injury may be associated with numerous brain and hippocampal complications, as it may alter the permeability of the blood-brain barrier. Although the pathogenesis of acute uremic encephalopathy is poorly understood, some of the underlying mechanisms that may contribute to hippocampal involvement include the release of multiple inflammatory mediators that coincide with hippocampus inflammation and cytotoxicity, neurotransmitter derangement, transcriptional dysregulation, and changes in the expression of apoptotic genes. Impairment of brain function, especially of a structure that has vital activity in learning and memory and is very sensitive to renal ischemic injury, can ultimately lead to cognitive and functional complications in patients with acute kidney injury. The objective of this review was to assess these complications in the brain following acute kidney injury, with a focus on the hippocampus as a critical region for learning and memory.

Definition and Diagnostic Criteria of Acute Kidney Injury (급성 신손상의 정의와 진단 기준)

  • NamGoong, Mee-Kyung
    • Childhood Kidney Diseases
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    • v.15 no.2
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    • pp.101-106
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    • 2011
  • Acute renal failure means that the word does not contain a mild kidney injury. In addition, the criteria for acute renal failure per researcher are different, and it is difficult in interpreting the results of research on acute renal failure. Therefore, rather than acute renal failure, a new term "acute kidney injury" meaning to include all the levels of injury is introduced. In 2002, to diagnose by means of serum creatinine, glomerular filtration rate and urine output, a detailed classification of acute kidney injury, the RIFLE criteria has been proposed. In 2007, the RIFLE criteria by transforming, AKIN criteria has been proposed. The pediatric RIFLE criteria for children has also been proposed. The author reviews here these criteria by comparing them.

The Effect of Acute Coagulopathy in Profoundly Traumatic Patients on Acute and Early Deaths (고도 중증외상 환자에서 급성 혈액응고장애가 초기 및 조기 사망에 미치는 영향)

  • Noh, Minsu;Yang, Song-Soo;Kyoung, Kyu-Hyouck
    • Journal of Trauma and Injury
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    • v.27 no.4
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    • pp.158-164
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    • 2014
  • Purpose: Numerous studies have investigated the pattern of traumatic death with a focus on the injury mechanism, the severity of the injury and the presence of hemorrhage. Acute coagulopathy has been treated as only one of many complications. The purpose of this study was to investigate the influence of acute coagulopathy on acute and early death due to trauma. Methods: A retrospective analysis of trauma patients with injury severity score (ISS)${\geq}25$ who had been treated between January 2011 and December 2012 was conducted. Based on the time of injury, traumatic death was categorized into acute (within 48 hours) and early (from 3 to 7 days). The correlations between various parameters within 24 hours after injury and time of death were analyzed. Results: A total of 124 patients were enrolled. Of them, 8.1% (n=10) of the patients experienced acute mortality. For those patients, significant differences in initial systolic blood pressure, coagulopathy score, amount of transfusion, abbreviated injury scale of the head and neck, the abdomen and the extremities were noted. Early mortality was experienced by 7.0% (n=8) of the patients, only coagulopathy score was found to be a significant independent risk factor for acute (odds ratio: 3.127; 95% confidence interval: 1.185-8.252; p=0.021) and early mortality (odds ratio: 2.470; 95% confidence interval: 1.029-5.929; p=0.043). Conclusion: Acute traumatic coagulopathy has an important role in the mortality, even after the acute phase. Early management and prevention of acute coagulopathy may improve survival of trauma patients.

The Change of Secretory Activity of the Alveolar Type ll Cell During Acute Alveolar Injury Induced by N-Nitroso-N-Methylurethane

  • Lee, Young-Man;Bang, In-Sook;Lee, Suck-Kang
    • The Korean journal of physiology & pharmacology
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    • v.28 no.1
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    • pp.71-77
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    • 1994
  • In the animal model of acute respiratory distress syndrome (ARDS) induced by N-nitroso-N-methylurethane (NNNMU) the secretory activity of alveolar type H cells during acute alveolar injury was investigated by determining phospholipid and pulmonary surfactant associated proteins in crude surfactant. The mechanism of the secretory change was studied by determination of DNA and RNA levels in the lung tissue. After induction of acute alveolar injury with NNNMU, pulmonary hemorrhage, atelectasis and gross hypertrophy were observed. Seven days after NNNMU treatment the level of total DNA in lung homogenate was increased markedly indicating that a hypertrophy was induced by cellular proliferation. Although the total DNA level increased, the RNA/DNA ratio was gradually decreased after NNNMU treatment. Seven days after NNNMU treatment the RNA/DNA ratio returned to the normal control level. During the acute alveolar injury, phospholipid and surfactant associated proteins were reduced significantly as compared with the control, implying that the secretory activity of alveolar type II cells was altered during acute alveolar injury induced by NNNMU. The protein content in crude surfactant during peak injury(7 days after NNNMU) was decreased significantly but phospholipid/protein ratios were identical in both control and NNNMU treatment groups. SDS-PAGE of proteins in crude pulmonary surfactant showed a decrease in major surfactant associated protein(M.W. 38,000) during acute alveolar injury. The present study may suggest that while alveolar type H cells proliferate markedly, transcription of alveolar type ll cell gene was inhibited by an unknown mechanism such as DNA methylation induced by NNNMU. Such an inhibition of transcriptional activity is thought to be associated with the decreased secretory activity of alveolar type ll cells, which may lead to pulmonary atelectasis and edema during the acute alveolar injury.

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Clinical Outcomes of Diffuse Axonal Injury According to Radiological Grade

  • Lee, Hak-Jae;Sun, Hyun-Woo;Lee, Jae-Seok;Choi, Nak-Joon;Jung, Yoon-Joong;Hong, Suk-Kyung
    • Journal of Trauma and Injury
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    • v.31 no.2
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    • pp.51-57
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    • 2018
  • Purpose: Patients with diffuse axonal injury experience various disabilities and have a high cost of treatment. Recent researches have revealed the underlying mechanism and pathogenesis of diffuse axonal injury. This study aimed to investigate the correlation between the radiological grading of diffuse axonal injury and the clinical outcomes of patients. Methods: From January 2011 to December 2016, among 294 patients with traumatic brain injury, 44 patients underwent magnetic resonance imaging (MRI). A total of 18 patients were enrolled in this study except for other cerebral injuries, such as cerebral hemorrhage or hypoxic brain damage. Demographic data, clinical data, and radiological findings were retrospectively reviewed. The grading of diffuse axonal injury was analyzed based on patient's MRI findings. Results: For the most severe diffuse axonal injury patients, prolonged intensive care unit (ICU) stay (p=0.035), hospital stay (p=0.012), and prolonged mechanical ventilation (p=0.030) were observed. However, there was no significant difference in healthcare-associated infection rates between MRI grading (p=0.123). Massive transfusion, initial hemoglobin and lactate levels, and MRI gradings were found to be highly significant in predicting the duration of unconsciousness. Conclusions: This study showed that patients with high grade diffuse axonal injury have prolonged ICU stays and significantly longer hospital stays. Deteriorated mental patients with high energy injuries should be evaluated to identify diffuse axonal injuries by using an appropriate imaging tool, such as MRI. It will be important to predict the duration of consciousness recovery using MRI scans.

Inhibition of Phospholipase $A_2$ Diminishes the Acute Alveolar Injury Induced by $Interleukin-1{\alpha}$

  • Lee, Young-Man
    • The Korean Journal of Physiology and Pharmacology
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    • v.1 no.1
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    • pp.71-78
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    • 1997
  • In an attempt to investigate the role of phospholipase $A_2$($PLA_2$) in interleukin-l (IL-l) induced acute lung injury, mepacrine was tried to inhibit $PLA_2$ in IL-l induced ARDS rats. For confirmation of acute lung injury by IL-l, and to know the role of neutrophils in this injury, lung leak index, lung myeloperoxidase(MPO), number of neutrophils and protein content in the bronchoalveolar lavage (BAL) and wet lung weight were measured. At the same time lung $PLA_2$ was measured to know the effect of IL-l on $PLA_2$ activity. Pulmonary surfactant was also measured for an investigation of type II alveolar cell function. Neutrophil adhesion assay was performed to know the effect of $PLA_2$ inhibition in vitro with human umbilical vein endothelial cells (HUVEC). For precise location of injury by IL-l, morpholgical study was performed by electron microscopy. Five hours after instillation of IL-l (50 ng/rat), lung leak index, protein content, number of neutrophils, lung MPO and wet lung weight were increased significantly. Five hours after IL-l instillation lung $PLA_2$ activity was increased significantly, and increased surfactant release was observed in IL-l induced ARDS rats' BAL. In contrast, in rats given mepacrine and IL-l, there was decrease of acute lung injury i.e. decrease of lung leak index, wet lung weight, protein content, number of neutrophils in BAL and decreased lung MPO activity. Mepacrine decreased surfactant release also. Interestingly, inhibition of $PLA_2$ decreased adhesion of human neutrophils to HUVEC in vitro. Morphologically, IL-l caused diffuse necrosis of endothelial cells, type I and II epithelial cells and increased the infiltration of neutrophils in the interstitium of the lung but after mepacrine treatment these pathological findings were lessened. On the basis of these experimental results it is suggested that $PLA_2$ has a major role in the pathogenesis of acute lung injury mediated by neutrophil dependent manner in IL-l induced acute lung injury.

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Neutrophil Gelatinase-Associated Lipocalin and Kidney Diseases

  • Yim, Hyung Eun
    • Childhood Kidney Diseases
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    • v.19 no.2
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    • pp.79-88
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    • 2015
  • Neutrophil gelatinase-associated lipocalin (NGAL) has emerged as one of the most promising biomarkers of renal epithelial injury. Numerous studies have presented the diagnostic and prognostic utility of urinary and plasma NGAL in patients with acute kidney injury, chronic kidney disease, renal injury after kidney transplantation, and other renal diseases. NGAL is a member of the lipocalin family that is abundantly expressed in neutrophils and monocytes/macrophages and is a mediator of the innate immune response. The biological significance of NGAL to hamper bacterial growth by sequestering iron-binding siderophores has been studied in a knock-out mouse model. Besides neutrophils, NGAL is detectable in most tissues normally encountered by microorganisms, and its expression is upregulated in epithelial cells during inflammation. A growing number of studies have supported the clinical utility of NAGL for detecting invasive bacterial infections. Several investigators including our group have reported that measuring NGAL can be used to help predict and manage urinary tract infections and acute pyelonephritis. This article summarizes the biology and pathophysiology of NGAL and reviews studies on the implications of NGAL in various renal diseases from acute kidney injury to acute pyelonephritis.

A Study on the Defence Effect of Banhasasim-tang for White Rat's Acute Duodenal Injury (흰쥐의 급성 십이지장 손상에 대한 반하사심탕의 방어효과에 관한 연구)

  • 한이수;최준혁;임성우
    • The Journal of Korean Medicine
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    • v.23 no.3
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    • pp.188-199
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    • 2002
  • Objectives : Banhasasim-tang has been clinically used to treat upper gastric intestinal discomfort. The object of this study is to examine the defense effect of Banhasasim-tang for acute duodenal injury of the mouse. Methods and Materials : Twenty-one rats were divided into 3 groups and treated as follows: the control group was untreated mice. The ADE group was acute duodenal-damage-elicited mice. The BST group was Banhasasim-tang treated mice before acute duodenal damage elicitation. The groups were examined with common morphology, paneth cells in intestinal crypt, absorptive cells and goblet cells in epithelium, cell division in mucose, COX-l as mucosal protector, COX-2 (which appears to play an important role in inflammation), IL-2R-inducing cellular immuno-chainreaction, and the distribution of apoptotic cells. Results : 1. Common morphology: the ADE group was observed with duodenal injury - loss of villi, infiltration of cells concerned to inflammation (lymphocytes, granular leukocytes) to submucosal layer - by hemorrhagic erosions, while the BST group was seen the same as normal in proportion to increasing treatment time before injury. 2. Histochemical change: the ADE group was observed with noticeable decreased distribution of absorptive cells with microvilli, acid mucin secreted goblet cell, neutral mucin secreted goblet cell, paneth cells compared to the normal group. The BST group was seen to have distribution of epithelium cells resembling normal in proportion to increasing treatment time before injury. 3. Imnunohistochemical change: the ADE group showed a change of factors leading to duodenal injury as reduce of cytokinesis, COX-1, increase of COX-2, IL-2R-. In contrast, the BST group tended to reduction of cytokinesis, COX-1, increase of COX-2, IL-2R- in proportion to increasing taking time before injury. 4. Apoptosis change: the ADE group showed increasing apoptosis cells, in contrast to the BST group which was the same as normal in proportion to increasing treatment time before injury. Conclusions : According to the above results, by increasing the defense system of mucosal epithelium, Banhasasim-tang is thought to effectively protect tissue against ulcers resulting from acute duodenal injury.

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Effects of Lepidii Semen on Acute Edematous Lung Injury Induced by Skin Burn

  • Myoung-Je Cho;Hyun Gug Cho
    • Biomedical Science Letters
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    • v.9 no.1
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    • pp.37-42
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    • 2003
  • The present study was conducted to determine whether administration of heat extract of Lepidii Semen has an inhibitory effect on neutrophil-derived oxidative injury following dermal scald burn in rats. Acute lung injury was induced by scald burn (15% of TBSA) in rats. To identify acute edematous lung injury, protein concentrations and numbers of polymorphonuclear leukocytes were measured in bronchoalveolar lavage (BAL) at 5 h after skin burn. In addition, the level of lung KC (neutrophil chemoattractant cytokine) and activity of lung myeloperoxidase (MPO) were measured, and histopathological changes were observed as well. Lung weight and concentration of BAL protein, the index of lung injury, were clearly increased at 5 h postburn compared with those of sham-operated group. Administration of heat extract of Lepidii Semen after scald burn inhibited the production of KC in lung tissue and decreased the activity of lung MPO related to infiltration of neutrophils. In histopathological changes in lung tissue, infiltration of inflammatory cells and pulmonary edema induced by skin burn were decreased by administration of heat extract of Lepidii Semen after scald burn. These results suggest that Lepidii Semen may be an effective medical stuff for acute lung injury induced by skin burn.

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Morphological Study of Acute Lung Injury Induced by Interleukin-1$\alpha$ Intratracheally in Young and Old Rats (젊은 흰쥐와 늙은 흰쥐에서 인터루킨-1$\alpha$로 유도된 급성폐손상에 관한 형태학적 연구)

  • 조현국;이영만;박원학
    • Biomedical Science Letters
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    • v.3 no.2
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    • pp.139-150
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    • 1997
  • In order to investigate the effect of aging and the $H_2O$$_2$ localization in association with histological, ultrastructural, and cytochemical studies in lung tissue after interleukin-1$\alpha$(IL-1) induced lung injury, an acute lung injury was induced by instillation of IL-1 into the trachea. Both of 4- and 20-months-old male rats, protein contents in IL-1 treated branchoalveolar lavage increased significantly compared to each control rats. Acute lung injury occured by oxidative stress because neutrophils accumulated in vascular lumen and formed the adhesion with endothelial cells. As these cause, tissue proteins were exuded and leukocytes migrated into the alveolar lumen. Neverthless in these lung injury $H_2O$$_2$ localization of IL-1 treated 20 months rats was not different compared to IL-1 treated 4 months rats. After all aging was not a factor to accelate IL-1 induced lung injury. Based on these results, it is suggested that neutrophil infilteration might be an important cause in acute lung injury, and aging is not a factor to change the acute lung injury by oxidative stress.

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