• Childhood Kidney Diseases
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• 제14권1호
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• pp.51-61
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• 2010

목 적 : 최근 Chemokine (C-C motif) ligand-2 (CCL-2; also known as MCP-1)와 CCL-5 (also known as RANTES)가 다양한 염증성 및 비염증성 신질환과 연관성을 보인다는 연구결과들이 보고되고 있다. 이에 본 저자들은 CCL-2 및 CCL-5 유전자의 단일염기다형성(single nucleotide polymorphism; SNP)가 소아 IgA 신병증의 발생 및 임상양상과 어떠한 연관성을 보이는지 알아보기 위하여 본 연구를 시행하였다. 방 법 : 경희의료원 소아청소년과에서 학교 검뇨상 이상소견을 보여 전원된 환아 중 신생검을 통해 IgA 신병증으로 확진된 196명의 소아환아와 285명의 건강한 대조군을 대상으로 geneotyping을 통해 6 개의 SNP 대립 유전자 빈도를 조사하여 분석하였다. 또한, 단백뇨(>4 mg/$m^2$/hour), 병리 소견 상 족세포의 족돌기 융합과 병리학적 진행성 병변의 유무에 따라 환자군을 다시 세 개의 하위그룹으로 세분화하여 비교하였다. 결 과 : IgA 신병증 환아 및 대조군의 SNP 대립 유전자 빈도를 분석하였을 때, CCL-2 및 CCL-5 유전자 모두에서 질환의 발생과 연관성을 보이는 SNP는 발견되지 않았다. 두 개의 linkage disequilibrium block이 형성되었으나 하플로타입 분석에서는 유의한 하플로타입을 찾을 수 없었다. 또한, 환자의 하위그룹을 비교하였을 때에도 단백뇨, 병리 소견 상 족세포의 족돌기 융합과 병리학적 진행성 병변과 연관성을 보이는 SNP는 발견되지 않았다. 결 론 : 한국 소아 환자를 대상으로 시행한 본 연구에서 CCL-2 및 CCL-5유전자 다형성과 IgA 신병증의 임상병리 양상 간에 유의한 연관성은 없었다.

• 대한한의학방제학회지
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• 제29권1호
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• pp.33-44
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• 2021

Renal ischemia-reperfusion injury(IRI), an important cause of acute renal failure (ARF), cause increased renal tubular injury. Jesaeng-sinkihwan (JSH) was recorded in a traditional Chines medical book named "Bangyakhappyeon (方藥合編)". JSH has been used for treatment of diabetes and glomerulonephritis with patients. Here we investigate the effects of Jesaeng-sinkihwan (JSH) in a mouse model of ischemic acute kidney injury. The animals model were divided into four groups at the age of 8 weeks; sham group: C57BL6 male mice (n=9), I/R group: C57BL6 male mice with I/R surgery (n=9), JSH Low group: C57BL6 male mice with surgery + JSH 100 mg/kg/day (n=9) and JSH High group: C57BL6 male mice with surgery + JSH 300 mg/kg/day (n=9). Ischemia was induced by clamping the both renal arteries during 25 min, and reperfusion was followed. Mouse were orally given with JSH (100 and 300 mg/kg/day during 3 days after surgery. Treatment with JSH significantly ameliorates creatinine clearance(Ccr), Creatinine (Cr) and blood urea nitrogen(BUN) in obtained plasma. . Treatment with JSH reduced kidney inflammation markers such as Neutrophil Gelatinase Associated Lipocalin (NGAL) and kidney injury molecule-1 (KIM-1). JSH also reduced the periodic acid schiff (PAS) staining intensity and picro sirius red staining intensity in kidney of I/R group. These findings suggest that JSH ameliorates tubular injury including renal dysfunction in I/R induced ARF mouse.

• Childhood Kidney Diseases
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• 제6권2호
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• pp.142-154
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• 2002

목적 : 사이클로스포린(cyclosporine)은 효과적인 면역 억제제로서 현재에는 장기 이식 후 뿐 아니라 다양한 자가면역성 질병에서 그 사용 범위를 넓히고 있다. 신독성은 사이클로스포린의 대표적인 부작용으로서 그 특징적인 조직학적 소견은 간질의 섬유화와 세 동맥의 초자양 변화이다. 간질 섬유화에는 전통적으로 $TGF-{\beta}$가 관여하는 것으로 알려져 있으며 최근에 osteopontin이라는 단백도 관여한다는 사실이 동물 실험을 통해 알려지고 있다. 사이클로스포린에 의한 간질 섬유화에 osteopontin이 관여한다는 사실이 여러 동물실험을 통하여 알려져 있으나 사람에서는 아직까지 분명한 결론을 얻지 못하고 있다. 동일 환자에서 사이클로스포린 치료 전과 후에 두 번 생검을 시행한 신장 조직에서 osteopontin과 $TGF-{\beta}$의 발현을 조사하여 사이클로스포린과 이들의 관계를 밝히는 것이 본 연구의 목적이다. 대상 및 방법 : 연세의대 세브란스 병원 소아과에서 신장 생검으로 미세변화 신증후군으로 진단 받은 19예를 대상으로 하여 사이클로스포린 치료 전 조직 검사 검체를 대조군으로 하고, 치료 후 조직 검사 검체를 비교군으로 하였다. 사구체 메산지움과 세뇨관에서의 osteopontin 발현과 간질에서의 $TGF-{\beta}$ 발현을 면역조직화학염색으로 측정하였다. 결과 : 사이클로스포린 치료 후 사구체 메산지움과 세뇨관에서 osteopontin의 발현이 의의 있게 증가하였지만 간질에서 $TGF-{\beta}$의 증가는 뚜렷하지 않았다. 또한 세뇨관의 osteopontin과 간질의 $TGF-{\beta}$의 변화는 광학현미경으로 관찰되는 간질 섬유화와는 상관관계가 없었다. 따라서 사이클로스포린 사용시 osteopontin의 발현의 증가와 간질 섬유화 간에는 직접적인 연관이 없는 것으로 사료된다. 결론 : 본 연구의 결과 실험 동물에서와는 달리 사람의 신장에서 osteopontin은 간질 섬유화에 직접 관여하기 보다는 신장 손상에 대한 표지자로서의 의미가 있다고 추정된다.

• International Journal of Industrial Entomology and Biomaterials
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• 제5권2호
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• pp.201-204
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• 2002

This study was undertaken to find effects of ethanol extracts from Bombyx mori on the hyperglycemia induced by streptozotocin in rats. Blood glucose level of rats increased depending on experimental days after streptozotocin treatment. But there was no difference in blood glucose level between the rats injected with ethanol extracts of B. mori and normal rats. There was no significant difference in the kidney fibrosis between the rats injected with ethanol extrscts of B. mori and normal rats at all ages examined. The transforming growth factor-$\beta$l ($TGF-{\beta}1$) protein was detected in the glomerulay endothelial cells and tubular epithelial cells of streptozotocin rats at 14 days of age. In the rats injected with ethanol extracts of B. mori to the kidneys, the $TGF-{\beta}1$ protein was detected very faintly. The $TGF-{\beta}1$ mRNA of streptozotocin rats increased at 14 days of age, and this was higher than the rats injected with ethanol extrscts of B. mori. Taken these together, the results suggest that the ethanol extracts of B. mori ameliorate hyperglycemia of the rats induced by streptozotocin.

• Fisheries and Aquatic Sciences
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• 제18권3호
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• pp.333-339
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• 2015

Red lip mullet Chelon haematocheilus (body weight = $468{\pm}91g$) which became sick during an outbreak of disease at mariculture facilities at Cheonsu Bay, Korea, during July-August 2013, were examined to identify the cause of the disease. Diseased mullets displayed green liver syndrome, and Lactococcus garvieae were isolated from their internal organs. Argulus sp., Trichodina sp., and/or Vibrio spp. were also discovered in some infected fish. Histopathological examination revealed that fatty liver syndrome with hepatocyte degeneration, reflected in heterokaryons, inflammatory lesions, and melanomacrophage centers ($MMC_S$), had caused fibrosis around the kidney, spleen, and blood vessels. After the outbreak, visceral fat and green liver syndrome in the mullets were consistently observed throughout the year in the same mariculture facilities, indicating that the cultured mullets suffered a chronic metabolic disorder. Although Vibrio spp. were also isolated from some individuals, L. garvieae, which is known to be a causative agent of red lip mullet mortality, was isolated from all diseased individuals. This is the first report of L. garvieae infection in cultured red lip mullet.

• Journal of Nutrition and Health
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• 제33권2호
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• pp.134-140
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• 2000

This study was performed to investigate the effects of n-3 fatty acids on renal function in male Sprague-Dawley rats of different ages 5-, 15- and 19-months old. The rats were fed a 20%(w/w) lipid diet containing 10% fish oil, compared with control animals fed a 20% lipid diet without fish oil for 4 weeks. The results were as follows: kidney weights were significantly higher in fish oil-fed rats compared to control rats. Plasma levels of total lipid, total cholesterol, and triglyceride markedly increased, with aging and LDL-cholesterol showing a significantly lower level in fish oil-fed rats than control rats. The urinary protein and glomerular filtration rate (GFR) increased with aging. GFR was higher in fish oil-fed rats. However, urinary protein was the same in the two groups. Renal medulla thromboxane B$_2$(TXB$_2$)tended to be lower in fish oil-fed 19-month-old rats. Urinary TXB$_2$and PGE$_2$were found to be higher proteinuria. Light microscopic examination showed interstitial inflammation, tubular atrophy, interstitial fibrosis and glomerular mesangium increase. Although glomerular sclerosis increased with aging, fish oil in the diet had no effect on histological changes. In conclusion, plasma lipid, urinary protein excretion and renal histological change showed a significant increase with aging. The reduction of TXB$_2$in the medulla and increase of GFR caused by fish oil indicated n-3 fatty acid could affect renal function in line with the hypolipidemic effect.

• Childhood Kidney Diseases
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• 제1권2호
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• pp.183-188
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• 1997

Familial juvenile hyperuricemic nephropathy is an autosomal dominant disease characterized by progressive renal disease and hyperuricemia or gout, affecting young people of either sex equally. There are two biochemical markers of this disorder. The first is hyperuricemia disproportionate to the degree of renal dysfunction; the second is a grossly reduced clearance of uric acid relative to creatinine, dispropotionate to age, sex and degree of renal failure. We experienced 2 family members with hyperuricemia. One family member, a 13-year-old girl who had suffered from tophaceous gout and chronic renal failure. Her younger brother also had hyperuricemia and moderately reduced renal function. Their urinary excretion fractions of uric acid($FE_{uric\;acid}$) were reduced and renal biopsy specimens showed interstitial fibrosis with tubular atrophy and interstitial urate crystal deposition. We have treated these two patients with allopurinol but we have done renal transplantation because she progressed to end stage renal disease at 16 year old age.

• Kidney Research and Clinical Practice
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• 제35권2호
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• pp.69-77
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• 2016

Diabetic nephropathy (DN) is the leading cause of end-stage renal disease, and its pathogenesis is complex and has not yet been fully elucidated. Abnormal glucose and lipid metabolism is key to understanding the pathogenesis of DN, which can develop in both type 1 and type 2 diabetes. A hallmark of this disease is the accumulation of glucose and lipids in renal cells, resulting in oxidative and endoplasmic reticulum stress, intracellular hypoxia, and inflammation, eventually leading to glomerulosclerosis and interstitial fibrosis. There is a growing body of evidence demonstrating that dysregulation of 50 adenosine monophosphate-activated protein kinase (AMPK), an enzyme that plays a principal role in cell growth and cellular energy homeostasis, in relevant tissues is a key component of the development of metabolic syndrome and type 2 diabetes mellitus; thus, targeting this enzyme may ameliorate some pathologic features of this disease. AMPK regulates the coordination of anabolic processes, with its activation proven to improve glucose and lipid homeostasis in insulin-resistant animal models, as well as demonstrating mitochondrial biogenesis and antitumor activity. In this review, we discuss new findings regarding the role of AMPK in the pathogenesis of DN and offer suggestions for feasible clinical use and future studies of the role of AMPK activators in this disorder.

• 한국수산과학회지
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• 제54권5호
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• pp.676-684
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• 2021

Euryhaline teleost have extraordinary ability to deal with a wide range of salinity changes. To study the seawater adaptability of rainbow trout Oncorhynchus mykiss (body weight 638±54 g, length 38.6±2 cm) to salinity increase fish were transferred from freshwater to 7, 14, 21, 28 and 32 psu and checked for mortality over 5 days. No mortality was observed in 0-32 psu. In fish transferred to 0-32 psu, blood osmolality was maintained within physiological range. The changes of serum enzyme activities (aspartate transaminase, AST and alanine transaminase, ALT) showed no significant level during experimental period. To explore the underlying molecular physiology of gill and kidney responsible for body fluid regulation, we measured mRNA expression of five genes, Na⁺/K⁺/2Cl^- cotransporter1 (NKCC1), aquaporin3 (AQP3), cystic fibrosis transmembrane conductance regulator (CFTR), glucocorticoid receptor (GR) and growth hormone receptor (GHR) in response to salt stress. Based on our result, rainbow trout could tolerate gradual transfer up to 32 psu for 5 days without mortality under physiological stress. This study suggests to alleviate osmotic stress to fish, a gradually acclimation to increasing salinity is recommended.

• Childhood Kidney Diseases
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• 제6권1호
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• pp.75-84
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• 2002

목 적 :성장기 신장에서의 급성신우신염은 신반흔으로 진행된다. 신반흔의 형성에는 세균자체보다도 숙주의 염증반응과 면역반응의 산물인 TGF-${\beta}1$이 세포 고사를 증가시키고 세포증식을 억제함으로서 섬유화를 촉진한다고 하였다. 이에 저자는 항염증제인 methyl-prednisolone (MP)이 실험적으로 급성신우신염을 일으킨 이유기 백서에서 신반흔 형성에 미치는 영향을 관찰하고자 하였다. 대상 및 방법 : 생후 3주(체중 50-60g)된 이유기 Sprague-Dawley 백서의 방광에 삽입된 16 guage의 실리콘 도관내로 107/mL 농도의 E coli (ATCC No. 25922, pili형)를 5 mL씩 주입하여 급성신우신염을 유발하였다. 실험군은 1군 (ceftriaxone 단독투여, n=31)과 2군 (MP와 ceftriaxone투여, n=28)으로 나누었고 대조군 (n=43)에는 약제를 투여하지 않았다. 실험 1주와 3주에 실험동물을 희생하여 병리 조직학적 소견상 염증점수, 세포고사 지수와 TGF-${\beta}1$ 발현점수 및 섬유화 점수를 관찰하였다. 결 과 : 사망률은 II군이 $21.4\%$였으나 대조군 $41.9\%$, I군 $32.3\%$와 유의한 차이는 없었다. 염증 점수는 실험 1주에 II군에서 $0.8{\pm}0.87$로 대조군의 $2.3{\pm}0.87$, I군의 $1.7{\pm}0.79$에 비하여 유의하게 낮았다 (P<0.05. 세포고사 지수는 실험 1주에 II군에서 $2.9{\pm}2.15$로 대조군의 $10.0{\pm}1.95$, I군의 $8.3{\pm}2.53$에 비하여 유의 하게 낮았다 (P<0.05). TGF-${\beta}1$발현도 실험 1주에 II군에서 $0.8{\pm}0.72$로 대조군의 $1.90{\pm}67$, I군의 $1.8{\pm}0.60$에 비하여 유의하게 낮았다 (P<0.05). 섬유화 지수는 실험 3주에 II군에서 $0.8{\pm}0.63$로 대조군의 $1.8{\pm}0.83$에 비하여 유의하게 낮았다 (P<0.05) 결 론 : 성장기 백서의 실험적 급성 신우신염에서 MP는 ceftriaxone단독 투여에 비하여 염증 반응, 세포고사, TGF-${\beta}1$발현, 섬유화를 모두 감소 시켰다. 즉 항생제 외에 항염증제의 병용투여가 신반흔의 정도를 감소시킬 수 있으므로 치료지연등 신반흔의 위험인자가 있는 경우에 고려할 수 있을 것으로 생각된다.