• 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.

• Advances in Traditional Medicine
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• v.9 no.4
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• pp.292-302
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• 2009

Ischemia/reperfusion injury, which is commonly seen in the field of renal surgery or transplantation, is a major cause of acute renal failure. Previous studies showed that antioxidant treatments attenuated renal ischemia/reperfusion injury. The objective of this study was to examine the role of hesperidin in modulating reactive oxygen species induced inflammation and apoptosis after renal ischemia/reperfusion injury. Rats were subjected to right nephrectomy, 15 days later 45 min of renal ischemia and 24 h reperfusion with or without treatment with hesperidin. Renal function, inflammation and apoptosis were compared at 24 h after reperfusion injury. Hesperidin improved the renal dysfunction and reduced inflammation and apoptosis after ischemia/reperfusion injury. In conclusion, hesperidin shows potent anti-apoptotic and antiinflammatory properties due to antioxidant property. These findings may have major implications in the treatment of human ischemic acute renal failure.

• Neonatal Medicine
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• v.17 no.2
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• pp.161-167
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• 2010

Acute kidney injury (AKI), formerly referred to as acute renal failure (ARF) is defined as the sudden impairment of kidney function (estimated from the glomerular filtration rate [GFR]) that results in the lack of excretion of waste products. More than 30 definitions of AKI exist in the literature, most of which are based on serum creatinine. Lack of a uniform and multidimensional AKI definition has led to failure to recognize significant renal injury, delays in treatment, and inability to generalize single-study results. The RIFLE criteria were developed to standardize the diagnosis of ARF and in the process the term AKI has been proposed to encompass the entire spectrum of the syndrome from minor changes in renal function to requirement for renal replacement therapy. Large prospective studies are needed to test definitions and to better understand risk factors, incidence, independent outcomes, and mechanisms that lead to poor short- and long-term outcomes. Early biomarkers of AKI need to be explored in critically ill neonates.

• 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.

• Childhood Kidney Diseases
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• v.19 no.2
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• pp.71-78
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• 2015

The incidence of acute kidney injury (AKI) in critically ill pediatric patients has been reported as increasing to 25 %, depending on population characteristics. The etiology of AKI has changed over the last 10-20 years from primary renal disease to the renal conditions associated with systemic illness. The AKI in pediatric population is associated with increased mortality and morbidity, and prevention is needed to reduce the consequence of AKI. It is known that the most important risk factors for AKI in critically ill pediatric patients are clinical conditions to be associated with decreased renal blood flow, direct renal injury, and illness severity. Renal hypoperfusion leads to neurohormonal activation including renin-angiotensin-aldosterone system, sympathetic nervous system, antidiuretic hormone, and prostaglandins. Prolonged renal hypoperfusion can result in acute tubular necrosis. The direct renal injury can be predisposed under the condition of renal hypoperfusion, and appropriate treatment of volume depletion is important to prevent AKI. The preventable causes of AKI include contrast-induced nephropathy, hemodynamic instability, inappropriate mediation use, and multiple nephrotoxic insults. Given the evidence of preventable factors for AKI, several actions such as the use of protocol for prevention of contrast-induced nephropathy, appropriate treatment of volume depletion, vigorous treatment of sepsis, avoidance of combinations of nephrotoxic medications, and monitoring of levels of drugs should be recommended.

• Korean Journal of Oriental Medicine
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• v.7 no.1
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• pp.135-144
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• 2001

Objectives : This study was carried out to research the protective effects of Sagunja-Tang(SA) through in vivo experiments, and tried to investigate the relation between oxidation of renal tissues and deficiency of Qi. Methods : Acute renal injury which initiated from free radical induced by $HgCl_2$, were applied to mice and metabolic data were obtained. In order to measure the degree of renal injury, serum level of creatinine, blood urea nitrogen(BUN), total protein(TP) and glucose were measured. Besides, serum level of alanine aminotransferase(AST), aspartate aminotransferase(ALT) were measure too. Lipid peroxidation of renal cortex was examined by measuring malondialdehyde(MDA), a product of lipid peroxidation. Results : SA had protective effects on acute renal injury caused by decrease of glomerular filtration which was initiated by subcutaneous injection of $HgCl_2$. SA protected acute liver injury too. Conclusions : Through this study, we found that SA have healing effects on renal injury of $HgCl_2$ induced oxidative stress that is similar to deficiency of Qi. And further studies have to be followed to certify the mechanisms.

• Journal of Veterinary Clinics
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• v.28 no.1
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• pp.52-56
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• 2011

Acute renal injury induced by ischemia is a major cause of high morbidity and mortality in hospitalized patients and a common complication in hospitalized patients. Thus, the work with acute renal failure and renal ischemia has been studied for many years. Although serum creatinine concentration that is widely used as an index of renal function performs fairly well for estimating kidney function in patients with stable chronic kidney disease, it performs poorly in the setting of acute disease. Thus, an ideal biomarker for acute kidney injury would help clinicians and scientists diagnose the most common form of acute kidney injury in hospitalized patients, acute tubular necrosis, early and accurately, and may aid to risk-stratify patients with acute kidney injury by predicting the need for renal replacement therapy, the duration of acute kidney injury, the length of stay and mortality. In this study, renal ischemia and reperfusion were performed by clapming and un-clamping right renal artery in miniature pigs. Plasma blood urea nitrogen (BUN) and creatinine were examined at pre- clamping, after-clamping at 0, 1 and 3 hours. And we searched initial indicators in these samples. Also, renal tissue was collected and searched the initial indicator by PCR and western blotting. As a result, hypoxia inducible factor $1{\alpha}$ ($HIF1{\alpha}$), nuclear factor kappa-B ($NF{\kappa}B$), $I{\kappa}B$, erythropoietin (EPO), erythropoietin receptor (EPOR), angiopoietin-1 and vascular endothelial growth factor (VEGF) were showed significant changes among the renal protein. $HIF1{\alpha}$, EPO, and EPOR were showed significant changes among the renal gene. Thus, these markers will be used as initial diagnosis of acute renal failure.

• 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.

• Clinical and Experimental Pediatrics
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• v.61 no.11
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• pp.339-347
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• 2018

Acute kidney injury (AKI) is characterized by abrupt deterioration of renal function, and its diagnosis relies on creatinine measurements and urine output. AKI is associated with higher morbidity and mortality, and is a risk factor for development of chronic kidney disease. There is no proven medication for AKI. Therefore, prevention and early detection are important. Physicians should be aware of the risk factors for AKI and should monitor renal function in high-risk patients. Management of AKI includes optimization of volume status and renal perfusion, avoidance of nephrotoxic agents, and sufficient nutritional support. Continuous renal replacement therapy is widely available for critically ill children, and this review provides basic information regarding this therapy. Long-term follow-up of patients with AKI for renal function, blood pressure, and proteinuria is recommended.

• Childhood Kidney Diseases
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• v.23 no.1
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• pp.48-52
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• 2019

The ketogenic diet (KD) has been used as an effective antiepileptic therapy for intractable childhood epilepsy. However, various adverse effects have been reported with use of the KD. We report a case of a child who developed acute tubular necrosis subsequent to therapy with KD. A 5-year-old girl had myoclonic epilepsy with developmental delay. She was under the treatment with antiepileptic drugs since the age of 3 months and on the KD during the past 18 months. Proteinuria persisted intermittently with the initiation of the KD and subsequently increased in the past 2 months. She was admitted with intermittent mild fever, vomiting, and lethargy for the past 3-4 weeks. At the time of admission, she presented with hypertriglyceridemia, heavy proteinuria, renal Fanconi syndrome, and acute kidney injury. Renal sonography showed a marked increase in the size and parenchymal echogenicity of both kidneys. A renal biopsy revealed acute tubular necrosis accompanied by early interstitial fibrosis. After the withdrawal of the KD and supportive therapy, without changing other anticonvulsants and their dosages, improvement of renal function was observed. Proteinuria had disappeared after 1 month and kidney size returned to normal after 8 months. It is hypothesized that the KD can induce and/or aggravate the renal tubulointerstitial injury in some patients who are under the treatment with anticonvulsants.