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이슬비(Lee, Seul Bi),김용국(Kim, Yong Gug) 한국전시산업융합연구원 2015 한국과학예술융합학회 Vol.19 No.-
급성 신손상(acute kidney injury, AKI)은 신기능의 급격한 저하로 더 이상 체액, 전해질 등의 평형을 유지할 수 없고 단백 대사산물의 배설의 지장을 초래하는 상태이다. 최근 급성 신손상은 주로 중환자실에 입원하는 환자에서 패혈증 등으로 야기된 다장기 부전(multiple organ dysfunction syndrome)의 형태로 나타나며 이들 환자의 사망률은 동물모델을 이용한 급성 신손상의 병태생리기전에 대한 이해, 지속적 신대체 요법 등 지지적 치료법의 기술적 발달에도 불구하고 50%이상으로 매우 높은 실정이다. 본 연구의 제한점은, 우선 NGAL검사를 시행하기 시작한 달로부터 6개월간 연구를 한 결과, 2012년12월 - 2013년6월까지의 샘플수가 적어 AKI진단 받은 환자 40명에 한정되었으며, 한정적인 부분만을 다루었다는 점을 한계점으로 들 수 있다. 향후 대규모 연구를 통한다면 보다 흥미로운 결과로서 도출될 수 도 있을 것이다. Acute renal failure was a called , acute renal injury in a sudden drop of the longer renal fluid and electrolyte balance can not be maintained, such as protein excretion of metabolites that cause the trouble condition. Mortality of acute renal injury supportive therapy, despite the technical development of a very high 50% Korea. As such an appropriate biomarker of acute renal injury there is a demand. In NGAL as a biomarker to be emerging. NGAL is a 25kDa protein found in neutrophils as they become acute renal injury is a biological marker of rapidly increasing. Part of this study, 40 patients with AKI and NGAL intended to check the relevance of each of the variables and reports, indicators of the severity of acute renal injury Stage3 evaluated on the basis of the relevant study. Creatinine and the relevance of NGAL compared with the saw, you know, there was significant correlation, but, NGAL and Severity was not unlike relevance. If a large-scale study of the future through even more interesting will be derived as a result. NGAL and Severity was not unlike relevance. If a large-scale study of the future through even more interesting will be derived as a result.
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급성 신손상의 내과적 치료: 예방이 가능한 질환 중심으로
오동진 ( Dong Jin Oh ) 대한내과학회 2012 대한내과학회지 Vol.82 No.1
Acute kidney injury (AKI) severity predicts adverse outcomes, such as requirement for renal replacement therapy, Length of hospital stay, and mortality. In addition, the widespread use of the RIFLE (risk, injury, failure, Loss of kidney function, end-stage kidney disease) and AKI classification systems has shown that even small changes in glomerular filtration rate are associated with increased mortality. Furthermore, AKI contributes to dysfunction of other organs, such as heart, Lung, brain, and Liver. Consequently, primary/secondary prevention and early diagnosis of AKI are of central clinical importance. Herein, I briefly reviewed the established medical management of AKI, mainly focused on preventable diseases. (Korean J Med 2012;82:11-16)
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조상경 ( Sang Kyung Jo ),조원용 ( Won Yong Cho ) 대한내과학회 2012 대한내과학회지 Vol.82 No.1
Incidence of acute kidney injury (AKI) is increasing and despite advances in supportive care, mortality from AKI in critically ill patients still exceeds 50%. Major causes of AKI can be classified into prerenal, renal and postrenal AKI and many of prerenal or ischemic acute tubular necrosis (ATN) are caused by decreased renal blood flow. In addition, exposure to nephrotoxicant or diverse drugs can lead to AKI and diseases that affect larger renal vessels, glomeruli, or renal microvasculature are also other causes of AKI. Because type of renal injury or initiation of proper therapy in setting of AKI is important in determining patient prognosis, differential diagnosis utilizing patients history, physical examination, and Laboratory data including urinalysis, urine diagnostic indices, radiologic examination is important. Lack of sensitive biomarkers for early detection of AKI, which resembles troponin in acute myocardial infarction is one critical factor that has hampered the successful translation of various therapeutic strategies that were effective in animal research. However, over the Last decade, efforts to identify and validate novel urine or plasma biomarkers in AKI led to identification of several promising biomarkers including neutrophil gelatinase associated Lipocalin (NGAL), interleukin-18 (IL-18), cystatin-C and Liver type fatty acid binding protein (L-FABP). Although far from replacing serum creatinine in clinical practice yet, data from Large clinical studies are promising and here I briefly reviewed the characteristics of them and possible clinical utility in AKI. (Korean J Med 2012;82:5-10)
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김범석 ( Beom Seok Kim ) 대한내과학회 2012 대한내과학회지 Vol.82 No.1
Acute kidney injury (AKI) is characterized as acute decline of renal function. AKI is frequently combined in hospitalized patients and worsen the outcome of the affected patients. Recently new criteria named RIFLE and AKIN were made to define AKI more uniformly. Recent studies with RIFLE/AKIN showed that even Less severe forms of AKI are associated with reduced survival and worse outcome. In this review, we will discuss on the definition, Incidence, Etiology and outcome of AKI. (Korean J Med 2012;82:1-4)
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급성 신장 손상 ; 급성 신손상의 정의와 평가: 임상 진료 지침
김동기 ( Dong Ki Kim ),주권욱 ( Kwon Wook Joo ) 대한내과학회 2015 대한내과학회지 Vol.88 No.4
Acute kidney injury (AKI) is a common clinical syndrome that carries a poor prognosis even in cases with seemingly mild or reversible renal dysfunction. Although this potentially devastating disease is associated with increased mortality, early detection and timely intervention may improve clinical outcomes. In this regard, a standardized definition and classification of AKI, reflecting prognosis on the basis of evidence, may allow early recognition and stage-based management of the disease. Nevertheless, there has been considerable variability and inconsistency in the definition and classification of AKI, resulting in failure to bridge the gap between research and clinical practice. The definition of AKI has evolved, with the introduction of the “Risk, Injury, Failure, Loss, and End-stage renal disease” (RIFLE), and “AKI Network” (AKIN) criteria. The recent “Kidney Disease Improving Global Outcomes” (KDIGO) guidelines proposed a uniform definition of AKI, essentially merging the RIFLE and AKIN criteria. This review will focus on the definition and classification of AKI, as proposed by KDIGO in 2012, and their use in clinical practice for clinicians.
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급성 신장 손상 ; 급성 신손상: 만성 콩팥병의 원인인가?
이소영 ( So Young Lee ) 대한내과학회 2015 대한내과학회지 Vol.88 No.4
Although it was thought that survivors from an acute kidney injury (AKI) recovered kidney function completely, cumulative observational data have shown that AKI can cause end-stage renal disease directly, increase the risk of developing incident chronic kidney disease (CKD), and worsen an underlying CKD. These data have confirmed an association between AKI and an increased risk of permanent kidney damage, with subsequent development of CKD. However, many studies have focused on early injury following ischemic insult; the mechanisms of long-term injury remain poorly understood. Established and new data suggest that endothelial injury, loss of peritubular capillary volume, and chronic hypoxia affect structural changes after an ischemic insult. The repair process after acute kidney injury can be both adaptive and maladaptive. A maladaptive response includes persistent upregulation of proinflammatory and profibrotic signals and maladaptive cellular regeneration; this is thought to be one of the mechanisms leading to progressive renal injury and, ultimately, end-stage renal disease. The purpose of this brief review was to focus on recent advances related to the mechanisms of the progression from AKI to CKD. This review suggests that a new approach is required to manage AKI patients to prevent and/or arrest CKD progression.
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장혜련 대한이식학회 2017 Korean Journal of Transplantation Vol.31 No.3
Acute kidney injury (AKI) is classified into three types according to its pathophysiology: prerenal, intrinsic renal, and post-renal AKI. Experimental models of AKI can be divided into two categories: in vivo and in vitro. Models can be further subdivided according to how AKI is simulated. The pathophysiology of intrinsic renal and post-renal AKI has been investigated using animal models. Most studies have been conducted in murine models using male mice or rats, while large mammals like sheep, pigs, and monkeys have been used in a limited number of studies. The intrinsic renal AKI model is divided into septic vs. aseptic AKI. Aseptic AKI is subdivided into ischemic vs. nephrotoxic AKI. Lipopolysaccharides (LPS) injection or cecal ligation and puncture (CLP) have been used to simulate the septic AKI model in rodents. Ischemic AKI is the most extensively investigated field to date because ischemic AKI is the most common and serious cause of AKI in both native kidneys and renal allografts. Ischemia-reperfusion injury (IRI) surgery has been used to induce ischemic AKI. There are two different methods of IRI surgery: laparotomy vs. flank approach. Warm temperature and male sex are critical to induction of sufficient grade of renal injury in this model. Many nephrotoxicants pertinent to human disease have been used to reproduce nephrotoxic AKI in rodent models. Cisplatin, a common chemotherapeutic agent, has many pathophysiologic features that overlap with IRI. Other nephrotoxicants such as gentamicin or glycerol were studied in the past, whereas much more attention has recently been devoted to environmental nephrotoxicants such as cadmium. However, variant susceptibility to different doses of nephrotoxicants is a big hurdle to set up a reproducible and consistent model of nephrotoxic AKI. Post-renal AKI is simulated with ureteral obstruction surgery, whereas the unilateral ureteral obstruction (UUO) model has frequently been used. Although some novel findings have been reported through numerous studies using murine AKI models, AKI still remains a challenging condition that lacks specific diagnostic or therapeutic tools because of species barriers or experimental settings. Animal AKI models using mammals genetically closer to human like monkeys would be valuable to simulate human AKI more appropriately.
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이식 ( Sik Lee ) 대한내과학회 2015 대한내과학회지 Vol.88 No.4
Acute kidney injury (AKI) has various triggers, such as ischemia, nephrotoxins, radiocontrast, and bacterial endotoxins. It occurs in about one-third of patients treated in the intensive care unit. There is a higher mortality in patients with AKI compared with their non-AKI counterparts. The diagnosis of AKI usually depends on serum creatinine (SCr) measurements. However, SCr is a delayed and unreliable indicator of AKI. The lack of early biomarkers has limited the ability to manage AKI. Fortunately, understanding the early stress response of the kidney to injury has resulted in the identification and validation of several potential novel urine and blood biomarkers. Recently, new biomarkers of AKI with more favorable characteristics than SCr have been identified and studied in various experimental and clinical settings. This article reviews the most well-established biomarkers of AKI.
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