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증례 : 신장 ; 판코니 증후군을 동반한 간질성 신염 포도막염 증후군 1예
김미연 ( Miyeon Kim ),김현우 ( Hyun Woo Kim ),김지영 ( Ji Young Kim ),정진호 ( Jinho Jeong ),박은정 ( Eun Jung Park ),김진석 ( Jinseok Kim ),김소미 ( So Mi Kim ) 대한내과학회 2015 대한내과학회지 Vol.88 No.6
본 증례에서는 간질성 신염으로 진단되어 스테로이드 치료 후 호전된 중년여성에서 판코니 증후군 양상의 세뇨관장애 및 포도막염이 발생하여 간질성 신염 포도막염 증후군으로 재진단하고, 스테로이드로 치료한 1예를 경험하여 문헌고찰과 함께 보고하는 바이다. Tubulointerstitial nephritis and uveitis (TINU) syndrome is a rare disease that comprises 4.7% of acute interstitial nephritis. With reno-ocular manifestations, TINU syndrome is accompanied by symptoms such as fever, fatigue, malaise, anorexia, vomiting, and arthralgia. TINU syndrome is reported mainly in children or adolescent girls, and it is rare in adults. Although TINU syndrome can present with multiple renal tubular defects, Fanconi syndrome characterized by generalized impairment of proximal tubular function, leading to renal glucosuria, hyperuricosuria, hyperphosphaturia, proximal renal tubular acidosis, and kaliuresis leading to hypokalemia, has rarely been described. We report a case of TINU syndrome with Fanconi syndrome in a 46-year-old HLA B27-positive Korean woman. (Korean J Med 2015;88:711-714)
전통목조건축에서 도리와 직접 결구되는 보 방향 긴결재에 관한 연구
김소미(Kim, So-Mi),전봉희(Jeon, Bong-Hee) 대한건축학회 2023 대한건축학회 학술발표대회 논문집 Vol.43 No.1
The purpose of this study is to classify the terminology used in Purlin-form tie which includes Chogong, Chobang, and Gyeryang. The Purlin-form tie is a member that connects two or more purlin columns, improving structural stability. In this paper, the Purlin-form tie is sorted by its function, position, and form properties then subdivided into support or connecting member, bracket or non-bracket member, and straight or curved member. As a result, the Chobang, Gyeryang, and Umiryang is reclassified based on the comparative analysis using preceding classification.
김소미 ( So Mi Kim ),유한욱 ( Han Wook Yoo ),김현우 ( Hyun Woo Kim ) 대한내과학회 2013 대한내과학회지 Vol.85 No.2
본 증례는 판코니-비켈 증후군으로 유전자 검사를 통해 진단되었으나 전형적인 임상양상과는 다른 경한 경과를 보여 유전자 돌연변이를 포함하여 문헌고찰과 함께 보고하는 바이다. Fanconi-Bickel syndrome is a rare autosomal recessive disorder caused by a mutation in the facilitative glucose transporter 2 gene (GLUT2 or SLC2A2 gene) that codes for the glucose transporter protein 2 expressed in hepatocytes, pancreatic beta-cells, enterocytes, and renal tubular cells. Mutation of this gene leads to defective carbohydrate metabolism, hepatomegaly, glucose intolerance, proximal renal tubular dysfunction, and hypophosphatemic rickets. We report a case of Fanconi Bickel syndrome in an 18-year-old man who presented due to renal glycosuria; a mutation was identified in the GLUT2 gene (c.482C > A + c.1556G > A). To the best of our knowledge, unlike previous reports of Fanconi-Bickel syndrome, this case was relatively unusual in that it caused only mild clinical signs. (Korean J Med 2013;85:210-213)
문맥압 항진증을 동반한 간경변증 환자에서의 급성 신손상
김소미 ( So Mi Kim ),송일한 ( Il Han Song ) 대한소화기학회 2016 대한소화기학회지 Vol.68 No.5
Acute kidney injury (AKI) is one of the most common manifestations encountered in clinical practice. It is associated with high morbidity and mortality in cirrhotic pre- and post-transplantation patients. Hepatorenal syndrome (HRS), a special form of AKI in cirrhotic patients, was recognized as a consequence of renal vasoconstriction from systemic/renal hemodynamic alterations developed in advanced cirrhosis with portal hypertension. Recently, multiple factors-such as infection/inflammation, underlying glomerulonephritis, bile cast, or increased abdominal pressure-have been considered to contribute to renal dysfunction in cirrhotic patients, which were presumed to induce HRS. Moreover, in addition to changing the definition of AKI in the nephrologic guidelines, the new AKI definition for early diagnosis and intervention based on characteristics of liver cirrhosis has been proposed in an international meeting. This article provides a comprehensive and recent review of AKI definition, laying out the topics in accordance with the pathophysiologic mechanisms and therapeutic interventions of AKI in cirrhotic patients with portal hypertension. (Korean J Gastroenterol 2016;68:237-244)