• Title/Summary/Keyword: Glomerular injury

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Pathology of C3 Glomerulopathy

  • Shin, Su-Jin;Seong, Yoonje;Lim, Beom Jin
    • Childhood Kidney Diseases
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    • v.23 no.2
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    • pp.93-99
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    • 2019
  • C3 glomerulopathy is a renal disorder involving dysregulation of alternative pathway complement activation. In most instances, a membranoproliferative pattern of glomerular injury with a prevalence of C3 deposition is observed by immunofluorescence microscopy. Dense deposit disease (DDD) and C3 glomerulonephritis (C3GN) are subclasses of C3 glomerulopathy that are distinguishable by electron microscopy. Highly electron-dense transformation of glomerular basement membrane is characteristic of DDD. C3GN should be differentiated from post-infectious glomerulonephritis and other immune complex-mediated glomerulonephritides showing C3 deposits.

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.

Pseudo-renal Failure Caused by Urinary Bladder Rupture in Multiple Trauma Patient

  • Jang, Jihoon;Lim, Kyoung Hoon
    • Journal of Trauma and Injury
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    • v.29 no.4
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    • pp.191-194
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    • 2016
  • Pseudo-renal failure presents with renal failure characteristics, such as hypercreatininemia and hyperkalemia without a change in glomerular filtration rate or structure of the kidney. Pseudo-renal failure due to trauma is difficult to diagnose, because symptoms are non-specific and other factors may cause hypercreatininemia and hyperkalemia. In a trauma patient, especially one with pelvic injury, the abrupt elevation of potassium, blood urea nitrogen, and creatinine levels without previous medical history is a key feature in the diagnosis of urinary ascites. We report a case of pseudo-renal failure caused by intraperitoneal bladder rupture in a multiple trauma patient.

Association Rules of Comorbidities in Dementia by Using Korea National Hospital Discharge In-depth Injury Survey Data

  • Kim, Mijung
    • International journal of advanced smart convergence
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    • v.11 no.1
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    • pp.127-133
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    • 2022
  • This study aims to find out the associative relationship between dementia and comorbidities. To conduct this study, we used KNHDIS(Korea National Hospital Discharge In-depth Injury Survey) data from 2009 to 2018 provided by the KDCA(Korean Disease Control and Prevention Agency) annually. We used MySQL for data preprocessing and R for data analysis. As a result of applying the Apriori algorithm criteria of support(≥0.01), confidence(≥ 0.6), and lift(>1), seventeen rules related to dementia were discovered. The diseases associated with dementia were diabetes mellitus, hypertension, disorders of lipoprotein metabolism, glomerular disorders in diabetes mellitus, renal diseases, cardiovascular disease, cerebrovascular disease, and other urinary system disorders. This study can be utilized as primary data for the care of patients with dementia and provides implications for improving effective dementia prevention policies.

Pathology and Classification of Focal Segmental Glomerulosclerosis (초점성 분절성 사구체 경화증의 병리와 분류)

  • Kim, Yong-Jin
    • Childhood Kidney Diseases
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    • v.16 no.1
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    • pp.21-31
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    • 2012
  • Focal segmental glomerulosclerosis (FSGS) is the name of the primary glomerular disease as well as the terminology to describe the secondary phenomena of any other glomerular diseases. It is characterized by sclerosis, hyalinosis, foam cell infiltration, vacuolar change of podocytes, and halo formation in the glomerulus. Throughout the interstitium, lymphocytes infiltration, tubular atrophy and vascular changes are accompanied. Occasionally, IgM and/or C3 depositions are noted in the sclerotic areas. Electron microscopically, diffuse effacement of foot processes are seen in non-sclerotic area like minimal change disease. Podocyte injury patterns including vacuolar changes are frequently examined. Recently, Columbia group has suggested morphologic classification of FSGS and they demonstrated very good prognosis of tip lesion and poor prognosis of both collapsing and cellular types. However, the pathogenetic classification has been suggested by others; hyperfilteration, podocyte injury, genetic lesions etc. Further studies are necessary to understand and treat this disease.

A Case of Secondary FSGS due to Chronic Chloride Diarrhea

  • Kim, Byung Kwan;Lee, Hyun Soon;Yim, Hyung Eun;Cheong, Hae Il;Yoo, Kee Hwan
    • Childhood Kidney Diseases
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    • v.20 no.2
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    • pp.83-87
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    • 2016
  • Congenital chloride diarrhea (CLD) is a rare autosomal recessive disease that is difficult to diagnose. CLD requires early treatment to correct electrolyte imbalance and alkalosis and to prevent severe dehydration. Renal injury is clearly associated with defective electrolyte balance induced by CLD, particularly during the first months or years of life. A 7-year-old boy was diagnosed with CLD following detection of a homozygous mutation (c.2063-1G>T) in SLC26A3 at 6 months of age. During treatment with electrolyte supplements, mild proteinuria was detected at 8 months of age, and is still present. Renal biopsy showed the presence of focal renal dysplasia, with metaplastic cartilage and mononuclear cell infiltration, calcification, and fibrosis in the interstitium. Up to two-thirds of the glomeruli exhibited global obsolescence, mostly aggregated in the dysplastic area. In nondysplastic areas, the glomeruli were markedly increased in size and severely hypercellular, with increased mesangial matrix, and displayed segmental sclerosis. The marked glomerular hypertrophy with focal segmental glomerulosclerosis suggested a compensatory reaction to the severe nephron loss or glomerular obsolescence associated with renal dysplasia, with superimposed by CLD aggravating the tubulointerstitial damage.

Antioxidant Effects of Sagunja-Tang (Sijunzi-Tang) (사군자탕(四君子湯)의 항산화(抗酸化) 효과(效果))

  • Lee Yong-Tae;Cho Su-In;Kim Young-Kyun
    • Journal of Society of Preventive Korean Medicine
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    • v.4 no.2
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    • pp.170-192
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    • 2000
  • Objectives : This study was carried out to research antioxidant effects of Sagunja-Tang(SA) through in vitro and vivo experiments, and tried to investigate the relation between oxidation of tissues and deficiency of Qi. Methods and results : HPLC analysis of glycyrrhizine - known to be the main compound of Radix Glycyrrhizae - was done to certify the quality of SA. Chemiluminescence was initiated by adding tort-butyl hydroperoxide (t-BHP) to rabbit polymorphonuclear leukocytes (neutrophils), and generated reactive oxygen species (superoxide anion) decreased significantly by SA as dose dependent manner. Cell injury during 60 minutes tissue incubation was initiated by adding t-BHP, a hydrophobic hydroperoxide and $H_2O_2$, an water soluble oxidant to rat renal cortical and liver slices. Percentage cell death and lipid peroxidation were estimated by measuring lactate dehydrogenase (LDH) and malondialdehyde (MDA), a product of lipid peroxidation. t-BHP induced % cell death of renal cortical slices and lipid peroxidation of renal cortical and liver slices were decreased significantly by SA. SA decreased significantly % cell death and lipid peroxidation of renal cortical and liver slices induced by $H_2O_2$, too. Acute renal and liver injury induced by $HgCl_2\;and\;CCl_4$, which initiated from free radical, were applied to mice and metabolic data were obtained. Data showed protective effects of SA on acute renal injury caused by decrease of glomerular filtration. SA protected acute liver injury too. Conclusions Through this study, we found that SA have antioxidant effects and tissue oxidation was similar to deficiency of Qi. And further studies have to be followed to certify the mechanisms.

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The Risk Factors and Outcomes of Acute Kidney Injury after Thoracic Endovascular Aortic Repair

  • Jeon, Yun-Ho;Bae, Chi-Hoon
    • Journal of Chest Surgery
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    • v.49 no.1
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    • pp.15-21
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    • 2016
  • Background: We aimed to evaluate the incidence, predictive factors, and impact of acute kidney injury (AKI) after thoracic endovascular aortic repair (TEVAR). Methods: A total of 53 patients who underwent 57 TEVAR operations between 2008 and 2015 were reviewed for the incidence of AKI as defined by the RIFLE (risk, injury, failure, loss, and end-stage kidney disease risk) consensus criteria. The estimated glomerular filtration rate was determined in the perioperative period. Comorbidities and postoperative outcomes were retrospectively reviewed. Results: Underlying aortic pathologies included 21 degenerative aortic aneurysms, 20 blunt traumatic aortic injuries, six type B aortic dissections, five type B intramural hematomas, three endoleaks and two miscellaneous diseases. The mean age of the patients was $61.2{\pm}17.5years$ (range, 15 to 85 years). AKI was identified in 13 (22.8%) of 57 patients. There was an association of preoperative stroke and postoperative paraparesis and paraplegia with AKI. The average intensive care unit (ICU) stay in patients with AKI was significantly longer than in patients without AKI (5.3 vs. 12.7 days, p=0.017). The 30-day mortality rate in patients with AKI was significantly higher than patients without AKI (23.1% vs. 4.5%, p=0.038); however, AKI did not impact long-term survival. Conclusion: Preoperative stroke and postoperative paraparesis and paraplegia were identified as predictors for AKI. Patients with AKI experienced longer average ICU stays and greater 30-day mortality than those without AKI. Perioperative identification of high-risk patients, as well as nephroprotective strategies to reduce the incidence of AKI, should be considered as important aspects of a successful TEVAR procedure.

Nephrin phosphorylation regulates podocyte adhesion through the PINCH-1-ILK-α-parvin complex

  • Zha, Dongqing;Chen, Cheng;Liang, Wei;Chen, Xinghua;Ma, Tean;Yang, Hongxia;van Goor, Harry;Ding, Guohua
    • BMB Reports
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    • v.46 no.4
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    • pp.230-235
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    • 2013
  • Nephrin, a structural molecule, is also a signaling molecule after phosphorylation. Inhibition of nephrin phosphorylation is correlated with podocyte injury. The PINCH-1-ILK-${\alpha}$-parvin (PIP) complex plays a crucial role in cell adhesion and cytoskeleton formation. We hypothesized that nephrin phosphorylation influenced cytoskeleton and cell adhesion in podocytes by regulating the PIP complex. The nephrin phosphorylation, PIP complex formation, and F-actin in Wistar rats intraperitoneally injected with puromycin aminonucleoside were gradually decreased but increased with time, coinciding with the recovery from glomerular/podocyte injury and proteinuria. In cultured podocytes, PIP complex knockdown resulted in cytoskeleton reorganization and decreased cell adhesion and spreading. Nephrin and its phosphorylation were unaffected after PIP complex knockdown. Furthermore, inhibition of nephrin phosphorylation suppressed PIP complex expression, disorganized podocyte cytoskeleton, and decreased cell adhesion and spreading. These findings indicate that alterations in nephrin phosphorylation disorganize podocyte cytoskeleton and decrease cell adhesion through a PIP complex-dependent mechanism.

Upstream Regulators and Downstream Effectors of NADPH Oxidases as Novel Therapeutic Targets for Diabetic Kidney Disease

  • Gorin, Yves;Wauquier, Fabien
    • Molecules and Cells
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    • v.38 no.4
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    • pp.285-296
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    • 2015
  • Oxidative stress has been linked to the pathogenesis of diabetic nephropathy, the complication of diabetes in the kidney. NADPH oxidases of the Nox family, and in particular the homologue Nox4, are a major source of reactive oxygen species in the diabetic kidney and are critical mediators of redox signaling in glomerular and tubulointerstitial cells exposed to the diabetic milieu. Here, we present an overview of the current knowledge related to the understanding of the role of Nox enzymes in the processes that control mesangial cell, podocyte and tubulointerstitial cell injury induced by hyperglycemia and other predominant factors enhanced in the diabetic milieu, including the renin-angiotensin system and transforming growth factor-${\beta}$. The nature of the upstream modulators of Nox enzymes as well as the downstream targets of the Nox NADPH oxidases implicated in the propagation of the redox processes that alter renal biology in diabetes will be highlighted.