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혈액투석 중인 만성 신부전 환자에서 발생한 Reversible Posterior Leukoencephalopathy Syndrome
구영선(Young Sun Koo),김도희(Do Hee Kim),장윤경(Yoon Kyung Chang),양종오(Jong Oh Yang),강민규(Min Gyu Kang),황평주(Pyeong Joo Hwang),송창준(Chang June Song),이강욱(Kang Wook Lee),신영태(Young Tai Shin) 대한신장학회 2001 Kidney Research and Clinical Practice Vol.20 No.1
A Reversible Posterior Leukoencephalopathy Syndrome(RPLS) consists of neurologic symptoms and signs - headache, consciousness change, seizure, visual impairment - and brain imaging finding showing brain(espicially white matter) edema usually involving the posteior parietal-temporal-occipital areas. The causes are thought to be hypertensive encephalopathy, preeclampsia or eclampsia, renal failure with fluid overload and immunosuppressive agents such as cyclosporin A or FK506. RPLS may usually reversible if treated early by decreasing blood pressure and discontinuing offending drugs. A 23-year- old man had been hemodialyzed with chronic renal failure for two years. His blood pressure elevated to 240/150mmHg 3 days before admission and he complained of severe headache, vomiting, and total visual loss at the day of admission. Brain T2-weighted MRI imaging showed increased signal intensity involving the both parietal, posterior temporal, and occipital lobes. After antihypertensive and dexamethason treatment, a follow-up brain MRI performed on 7 days after admission showed nearly normalized findings and all symptoms including visual loss were recovered completely in one week.
일측 신장의 허혈-재관류 모델에서 신조직내 TGF-β, TNF-α, 및 Endothelin-1 유전자 발현에 관한 연구
신영태(Young Tai Shin),김종학(Jong Hak Kim),황평주(Pyeung Joo Hwang),이강욱(Kang Wook Lee),서광선(Kwang Sun Suh),구영선(Young Sun Koo),강민규(Min Kyu Kang) 대한신장학회 2000 Kidney Research and Clinical Practice Vol.19 No.1
N/A Although the exact pathogenetic mechanisms of the renal ischemia-reperfusion injury(I-R injury) have not been clearly elucidated yet, the reactive oxygen spe-cies(ROS) and mononuclear cell infiltration have been suggested to contribute to this renal injury process. The cytokines and growth factors produced by infiltrated leukocytes and renal parenchymal cells could accelerate the process of tissue damage by inducing cellular proliferation, fibrosis, and further recruitment of other inflammatory cells. The renin-angiotensin sys- tem(RAS) also has been suggested to be one of the most important mediators in the renal injury process of many animal models and human renal diseases. In order to evaluate the change of the levels of TNF-α, endothelin-l, and TGF-βgene expression in unilateral I-R injured renal cortical tissue, competitive RT-PCR was performed for the above mRNAs in Sprague-Dawley rats(60 minutes of ischemic time by non-traumatic vessel clamp and 24 hours of reperfusion). Also the plasma renin activity(PRA) and an-giotensin II(AII) level were measured at the time of sacrifice by radioimmunoassay. On the light miscroscopic examination, I-R injured renal cortical tissue showed typical findings of acute tubular necrosis, such as mononuclear ceU infiltration, necrosis, swelling and denudation of proximal tubular cells. Compared to control sham operated group, I-R injured group tissues showed significantiy increased level of TGF-β(p<0.05), endothelin-l(p<0.05) and TNF-α(p<0.05) gene expression in 24 hours after I-R renal injury. The levels of PRA and AIl were also significantly elevated compared to sham group(p< 0.05, p<0.05, respectively). In conclusion, we speculate that the early activation of RAS and elevated gene expression of TNF-α, endothelin and TGF-β of renal cortieal tissue may contribute to the early pathogenetic mechanism of I-R renal injury process.