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흉부 X-선상 활동성 미정으로 판독된 경증 폐결핵 환자에서 활동성 판정에 대한 67Ga 평면영상과 SPECT의 비교분석
안민 ( An Min ),장원규 ( Jang Won Gyu ),김경곤 ( Kim Gyeong Gon ),김성민 ( Kim Seong Min ),김윤권 ( Kim Yun Gwon ),김소연 ( Kim So Yeon ),김영중 ( Kim Yeong Jung ),박병익 ( Park Byeong Ig ),조민구 ( Jo Min Gu ),이권전 ( Lee Gwon 대한결핵 및 호흡기학회 2000 Tuberculosis and Respiratory Diseases Vol.48 No.6
백운희 ( Baeg Un Hui ),김영욱 ( Kim Yeong Ug ),홍순창 ( Hong Sun Chang ),박상준 ( Park Sang Jun ),김윤권 ( Kim Yun Gwon ),김소연 ( Kim So Yeon ),김영중 ( Kim Yeong Jung ),조민구 ( Jo Min Gu ),이권전 ( Lee Gwon Jeon ) 대한신장학회 2003 Kidney Research and Clinical Practice Vol.22 No.4
Liddle`s syndrome is a rare inferited disease with characteristic clinical manifestations of hytertension an hypokalemic metabolic alkalosis. Markedly suppressed serum aldosterone and renin levels are important laboratory findings to differentiate this disorder from primary hyperaldosterionism. When Liddle et al. reported the disorder in 1963, they proposed aggressive Na+ absorption and increased excretion of K+ as the pathogenesis of the syndrome. Since then, specific mutaion in the epithelial Na+ channel located in the collecting duct of the kidney has been dlucidated as a disease mechanism. Liddle`s syndrome is inherited by an autosomal dominant trait and generally the onset of the syndrome is before the age of 20 with increased risk of premature death due to stroke or heart failure. Recently, however, a few cases of late onset and genetically proven non-familial cases with de novo mutation of β or γ Na+ channel have been reported. We report a case of seventy-one year old woman who had hypertension with hypokalemic metabolic alkalosis and was diagnosed as Liddle`s syndrome. Further evaluation revealed low renin and aldosterone levels. Primary aldosteronism, Cushing`s syndrome, glucocorticoid remediable aldosteronism and deficiency of 11 β-OHase and 17α-OHase were ruled out based on her laboratory data and history. Her hypertension and hypokalemia responded to amiloride treatment but not to spironolactone. (Korean J Nephrol 2003;22(4):464-468)
횡문근융해증으로 인한 급성신부전증의 핍뇨기에서 발생한 중증 고칼슘혈증
임수진 ( Im Su Jin ),이승희 ( Lee Seung Hui ),문창기 ( Mun Chang Gi ),정준오 ( Jeong Jun O ),박상준 ( Park Sang Jun ),김윤권 ( Kim Yun Gwon ),김소연 ( Kim So Yeon ),김영중 ( Kim Yeong Jung ),조민구 ( Jo Min Gu ),이권전 ( Lee Gwon 대한신장학회 2003 Kidney Research and Clinical Practice Vol.22 No.6
Hypercalcemia rarely develops in patients with acute renal failure associated with rhabdomyolysis. If hypercalcemia occurs, it happens mostly in diuretic phase and rarely in oliguric phase. Secondary hyperparathyroidism, abnormal metabolism of Vitamin D, immobilization of patient, and release of calcium from injured muscle are considered as possible pathogenetic mechanisms of hypercalcemia in acute renal failure associated with rhabdomyolysis. Among them, dissoultion of calcium from injured muscle into extracellular fluid is accepted as the major mechanism of pathogenesis of hypercalcemia. A twenty year old male patient, combat policeman, developed syncope in the course of regular physical training. He was diagnosed of acute renal failure associated with rhabdomyolysis at the hospital he initially visited. After being subjected to three sessions of acute hemodialysis, he was transferred to our hospital. During the treatment, laboratory test was performed upon his continuous complaints of lower extremity weakness. It showed severe hypercalcemia with plasma calcium level of 17.3 mg/dL. He was in oliguric phase at the time of this severe hypercalcemia. Patient`s lower extremity weakness was gradually improved by hemodialysis using low calcium dialysate. He was discharged after his renal function became normal. He has been followed on regular basis. (Korean J Nephrol 2003;22(6):731-735)