• Kidney Research and Clinical Practice
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• 제37권4호
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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.

• Journal of Yeungnam Medical Science
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• 제41권2호
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• pp.61-73
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• 2024

Acute kidney ischemia-reperfusion (IR) injury is a life-threatening condition that predisposes individuals to chronic kidney disease. Since the kidney is one of the most energy-demanding organs in the human body and mitochondria are the powerhouse of cells, mitochondrial dysfunction plays a central role in the pathogenesis of IR-induced acute kidney injury. Mitochondrial dysfunction causes a reduction in adenosine triphosphate production, loss of mitochondrial dynamics (represented by persistent fragmentation), and impaired mitophagy. Furthermore, the pathological accumulation of succinate resulting from fumarate reduction under oxygen deprivation (ischemia) in the reverse flux of the Krebs cycle can eventually lead to a burst of reactive oxygen species driven by reverse electron transfer during the reperfusion phase. Accumulating evidence indicates that improving mitochondrial function, biogenesis, and dynamics, and normalizing metabolic reprogramming within the mitochondria have the potential to preserve kidney function during IR injury and prevent progression to chronic kidney disease. In this review, we summarize recent advances in understanding the detrimental role of metabolic reprogramming and mitochondrial dysfunction in IR injury and explore potential therapeutic strategies for treating kidney IR injury.

• Childhood Kidney Diseases
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• 제19권2호
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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.

• Childhood Kidney Diseases
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• 제15권2호
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• pp.101-106
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• 2011

급성신부전은 그 단어 의미에 약한 신장 손상을 포함하지 못한다. 또한 급성신부전에 대한 기준이 연구자마다 달라서 연구결과 해석상에 어려움을 주었다. 따라서 급성신부전보다는, 급성신손상이란 용어가, 신손상의 모든 정도를 포함하는 의미로 사용될 수 있다. 2002년에, 급성신손상을 자세히 분류하고 진단하기위해, 혈청크레아티닌, 사구체 여과율과 요량을 기준으로 하여, RIFLE 기준이 제안되었다. 2007년에는, RIFLE 기준을 변형하여, AKIN 기준이 제안되었다. 소아를 위해 소아-RIFLE 기준도 제안되었다. 저자는 여기서 이들 기준과 각각에 대한 비교를 기술하였다.

• Childhood Kidney Diseases
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• 제15권2호
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• pp.116-124
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• 2011

Acute kidney injury (AKI) can result in mortality or progress to chronic kidney disease in hospitalized patients. Although serum creatinine has long been used as the best biomarker for diagnosis of AKI, it has some clinical limitations, especially in children. New biomarkers are needed for early diagnosis, differential diagnosis, and reliable prediction of prognosis in AKI. Up to the present, candidate AKI biomarkers include neutrophil gelatinase-associated lipocalin (NGAL), kidney injury molecule-1 (KIM-1), interleukin-18 (IL-18), livertype fatty acid-binding protein (L-FABP), matrix metalloproteinase-9 (MMP-9), and Nacetyl-$\ss$-D-glucosaminidase (NAG). However, whether these are superior to serum creatinine in the confirmation of diagnosis and prediction of prognosis in AKI is unclear. Further studies are needed for clinical application of these new biomarkers in AKI.

• Childhood Kidney Diseases
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• 제21권1호
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• pp.31-34
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• 2017

Tumor lysis syndrome is a serious complication of malignancy, resulting from the massive and rapid release of cellular components into the blood. Generally, it occurs after initiation of chemotherapy. The onset of spontaneous tumor lysis syndrome (STLS) before anti-cancer treatment is rare and occurs mostly in Burkitt lymphoma and non-Hodgkin's lymphoma. There are only a few case reports in children. Here, we report a case of STLS secondary to T-cell acute lymphoblastic leukemia (ALL), which presented with urinary stone and subsequent acute kidney injury with severe hyperuricemia. Occult malignancy should be considered in case of unexplained acute kidney injury with extreme hyperuricemia.

• 대한한의학회지
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• 제44권4호
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• pp.163-169
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• 2023

Methods: This study presents a comprehensive case study of an elderly male diagnosed with acute kidney injury (AKI) resulting from severe dehydration, supported by an extended follow-up with laboratory findings. Results: An 83-year-old male patient experienced severe diarrhea overnight, leading to hospitalization due to symptoms of dehydration and hypotension. His laboratory results displayed a typical AKI pattern, including a significant increase in creatinine levels (5.19 mg/dL) and the presence of hyperkalemia and hyponatremia. Following general treatments, including the administration of an herbal drug (Bulhwangeumjeonggi-san), the estimated glomerular filtration rate (eGFR) improved from 10 ml/min (Stage 5) to 34 ml/min (Stage 3) within five days when he was discharged. Although subsequent eGFR tests, conducted one and two months later as an outpatient, revealed an improvement of 42 ml/min, the patient still experienced mild chronic dysfunction as a consequence. Conclusion: This study presents a noteworthy case of acute kidney injury attributed to severe dehydration, emphasizing the importance of medical awareness regarding diarrhea-induced kidney function impairment, especially in the elderly population.

• BMB Reports
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• 제43권9호
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• pp.629-634
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• 2010

Endotoxin including lipopolysaccharide (LPS) confers organ tolerance against subsequent challenge by ischemia and reperfusion (I/R) insult. The mechanisms underlying this powerful adaptive defense remain to be defined. Therefore, in this study we attempted to determine whether nitric oxide (NO) and its associated enzymes, inducible NOS (iNOS) and endothelial NOS (eNOS, a constitutive NOS), are associated with LPS-induced renal tolerance against I/R injury, using iNOS (iNOS knock-out) or eNOS (eNOS knock-out) gene-deleted mice. A systemic low dose of LPS pretreatment protected kidney against I/R injury. LPS treatment increased the activity and expression of iNOS, but not eNOS, in kidney tissue. LPS pretreatment in iNOS, but not eNOS, knock-out mice did not protect kidney against I/R injury. In conclusion, the kidney tolerance to I/R injury conferred by pretreatment with LPS is mediated by increased expression and activation of iNOS.

• Natural Product Sciences
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• 제28권4호
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• pp.194-200
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• 2022

Albizia julibrissin Durazz. (AJ; family Minosaceae) is widely distributed worldwide, and its stem bark has been used as a traditional herbal medicine. Acute kidney injury (AKI) is a clinical syndrome that results in sudden loss of renal function. This study aimed to investigate the effects of AJ against cisplatin-induced AKI using a human kidney proximal tubule epithelial cell line (HK-2) and cisplatin-treated mice. In vitro, cisplatin treatment increased apoptosis in HK-2 cells. However, AJ treatment decreased apoptosis of cisplatin-treated HK-2 cells. In vivo, cisplatin treatment accelerated renal injury by increasing the levels of renal injury markers, such as blood urea nitrogen, creatinine, kidney injury molecule 1, and neutrophil gelatinase-associated lipocalin, which were reversed by AJ treatment. Histopathologically, AJ treatment resulted in decreased renal damage with less tubular necrosis and brush border desquamation compared with the AKI group. Additionally, cisplatin treatment upregulated mitochondrial fission, a pathological characteristic of AKI, which was downregulated by AJ treatment. Along with increased mitochondrial fission, AJ treatment also reduced cisplatin-induced apoptosis. These results suggest that AJ may be a potential therapeutic agent for cisplatin-induced AKI.

• Journal of Medicine and Life Science
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• 제15권2호
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• pp.37-41
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• 2018

Mitochondrial injury in renal tubule has been recognized as a major contributor in acute kidney injury (AKI) pathogenesis. Ischemic insult, nephrotoxin, endotoxin and contrast medium destroy mitochondrial structure and function as well as their biogenesis and dynamics, especially in renal proximal tubule, to elicit ATP depletion. Mitochondrial fatty acid ${\beta}$-oxidation (FAO) is the preferred source of ATP in the kidney, and its impairment is a critical factor in AKI pathogenesis. This review explores current knowledge of mitochondrial dysfunction and energy depletion in AKI and prospective views on developing therapeutic strategies targeting mitochondrial dysfunction in AKI.