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투석막에 따른 염증성 싸이토카인의 생성 및 응고기전 활성화에 관한 연구
한금현(Kum Hyun Han),이지은(Ji Eun Lee),서지아(Ji A Seo),성수아(Su Ah Sung),이소영(So Young Lee),조상경(Sang Kyung Jo),조원용(Won Yong Cho),김형규(Hyung Kyu Kim) 대한신장학회 2002 Kidney Research and Clinical Practice Vol.21 No.5
배 경 : 혈액투석 중 혈액-투석막간의 상호작용에 의해 혈액 옹고계, 섬유소성 용해계 및 혈구성분의 활성화가 일어나는지 알아보고, 생체적합도가 다르다고 알려진 hemophan 투석막과 polysulfone 투석막에서의 차이가 있는지 알아보았다. 방 법 : 유지혈액투석을 받는 25명의 말기 신부전 환자를 hemophan 투석막 (n=13), polysulfone 투석막 (n=12)의 두 군으로 나누어 2주간 혈액투석을 시행한 뒤, 투석 전후의 혈액을 채취하여 혈청 Thrombin-antithrombin complex (TAT), D-dimer, tissue plasminogen activator (tPA), plasminogen activator inhibitor-1 (PAI-1), fibrinogen, aPTT를 측정하고, 이들의 혈액투석 전후의 변화와 투석막에 따른 변화율의 차이를 비교하였다. 단핵구 활성시 생성되는 염증성 싸이토카인인 TNF-α 단백의 혈청 농도로 단핵구의 활성을 평가하였다. 결 과 : 혈액투석 후 혈청 TNF-α 단백 농도의 변화가 없었으며, Hemophan군과 polysulfone군 사이에도 차이가 없었다. 혈액투석 후 PAI-1를 제외한 aPTT, fibrinogen, TAT, D-dimer, tPA의 농도는 모두 의미있게 증가되었다. Hemophan굴과 polysulfone군 사이의 aPTT, fibrinogen, D-dimer, PAI-1, tPA의 투석 친후 변화량 (Δ)은 차이가 없었으나, TAT의 변화량 (Δ)은 polysulfone군에서 의미있게 적었다. 결 론 : 혈액-투석막간의 상호작용은 혈액 응고계 뿐 아니라 섬유소성 용해계도 활성화시키며, 혈액 응고계의 활성을 적게 일으킨다는 점에서 polysulfone의 생체적합도가 hemophan에 비해 우수하다. 혈액-투석막간의 상호작용이 혈청 TNF-α 단백 농도에 변화를 주지 못했는데, 향후 연구가 필요하리라 생각된다. Background : Blood-dialyzer membrane interaction in hemodialysis has the potential to activate blood coagulation and fibrinolysis, and it might elicit production of inflammatory cytokine such as TNF-α by monocytes activation. The aim of the present study was to; ⅰ) assess changes in coagulation status, fibrinolytic activity and plasma level of TNF-α during hemodialysis; ⅱ) determine whether the extent of activation is dependent on the dialyzer material used. Methods : Twenty-five end-stage renal failure patients who had undergone maintenance hemodialysis were included in the study. Patients were randomly divided into two groups; one using hemophan dialyzer membrane (n=13) and the other using polysulfone dialyzer membrane (n=12). On sixth dialysis session, blood samples were obtained before and at the end of hemodialysis. Thrombin-antithrombin complex (TAT) and D-dimer, each reflecting in vivo thrombin generation and fibrin degradation product respectively, were measured for coagulatory and fibrinolytic activity. Tissue plasminogen activator (tPA), plasminogen activator inhibitor-1 (PAI-1), and fibrinogen were measured. Activated partial thromboplastin time (aPTT) was measured for efficancy of anticoagulant. Plasma level of TNF- a was also measured. Results : During hemodialysis, plasma level of TNF-α did not change. Between hemophan dialysis and polysulfone dialysis group, the change in plasma level of TNF-α (Δ TNF-α) was not different. Significant changes were observed in aPTT, fibrinogen, TAT, D-dimer, tPA during hemodialysis (p<0.05) except in PAI-1 (p=0.71). Between two groups, changes in aPTT, fibrinogen, D-dimer, PAI-1 and tPA (ΔaPTT, Δfibrinogen, ΔD-dimer, ΔPAI-1, ΔtPA) were not different (p>0.05). However, the change in TAT (ΔTAT) was significantly lower in polysulfone dialysis group (p=0.049). Conclusion : Hemodialysis enhances coagulatory activity despite the use of anticoagulant and also enhances fibrinolytic activity, which is likely the result of tPA release. In activation of coagulatory system, biocompatibility of polysulfone membrane is superior to that of hemophan membrane. Plasma level of TNF-α did not change during hemodialysis, further study should be considered.
당뇨병성 신증쥐에서 retinoid와 PPAR-γ 촉진제 병합투여에 관한 연구
한상엽 ( Sang Youb Han ),김시현 ( Cy Hyun Kim ),한금현 ( Kum Hyun Han ),차대룡 ( Dae Ryong Cha ),김한성 ( Han Seong Kim ) 대한신장학회 2007 Kidney Research and Clinical Practice Vol.26 No.5
Purpose : An inflammatory mechanism has been suggested to contribute to the progression of diabetic nophropathy. Both retinoid and PPAR-7 agonist, known anti-inflammatory agents, have been reported to be beneficial in diabetic nephropathy. Because they form heterodimer for transcription within the nucleus, we investigated the effect of a combination treatment with them in streptozotocin (STZ)-induced diabetic rats. Methods: STZ-induced diabetic rats were treated with retinoid and PPAR- r agonist. The effects were determined by measuring urinary monocyte chemoattractant peptide (MCP)-i, proteinuria, and intrarenal ED-1 expression. Results Blood glucose concentration was higher in diabetic rats than in control rats. Retinoid and PPAR- r agonist did not affect blood glucose concentration. Urinary protein excretion (8.6 I 0.69 vs. 22.1 mg/mgCr, p<0.0l) and urinary MCP-1 (19.8z3.4 vs. 61.5±6.1 pg/mgCr, p`cO.Ol) were significantly higher in diabetic rats at four weeks after the induction of diabetes compared with controls. Proteinuria in the group with retinoic acid (16.9 1.4, mg/mgCr, pcz0.05) and PPAR-7 agonist (14.6 `1.5 mg/mgCr, pc0.05) were decreased. Retinoic acid (42.2±2.7 pglmgCr, p<O.05) and PPAR- agonist (40.5 `4.2pg/mgCr, pc0.05) significantly suppressed MCP-1 level in diabetic rats. However, combination treatment ment was not effective to proteinuria and urinary MCP-1 concentration. Urinary protein excretion was significantly correlated with MCP-1 (r0.9, p`c0.0i). Immunohistochemistry revealed a significant increase in staining for ED-i protein in the diabetic kidneys. Both retinoid and PPAR-γagonist significantly suppressed intrarenal ED-i synthesis. However combination treatment didnt show any additional beneficial effects. Conclusion: Both retinoic acid and PPAR-γagonist suppressed preteinuria and inflammatory changes in diabetic rats. However, there were no additional effects of the combination treatment present. Further ressrch is needed to determine the effect of the combination treatment on diabetic nephropathy.
이혁 ( Hyuk Lee ),한금현 ( Kum Hyun Han ),전준성 ( Joon Seong Jeon ),서정욱 ( Jung Wook Seo ),한상엽 ( Sang Youb Han ) 대한신장학회 2009 Kidney Research and Clinical Practice Vol.28 No.5
The main feature of acute renal failure is a decline in the glomerular filtration rate. However, urine leakage into the peritoneal cavity due to bladder rupture may cause pseudo-renal failure. This is a situation in which renal function is normal, along with the presence of elevated serum creatinine. A 47-year-old woman presented with abdominal distension and pretibial pitting edema on both lower extremities. She had no traumatic history. She did not complain of abdominal pain, and exhibit neither oliguria nor anuria. Her blood urea nitrogen (BUN) and serum creatinine was 105 and 11.2 mg/dL. Ascites showed that urea nitrogen and creatinine were 160 and 29 mg/dL, respectively. We confirmed bladder rupture by an abdominal CT scan and retrograde cystography. She underwent an emergency laparotomy to repair the ruptured bladder. Azotemia was normalized 2 days after the operation. Here we present a rare case of uremia due to bladder rupture.
흰 쥐에서 양측 요관 폐쇄 해제 후 신장의 Aquaporin-2와 Na-K-2Cl Cotransporter의 발현 변화 및 항이뇨호르몬 치료의 효과
신진호 ( Jin Ho Shin ),성수아 ( Su Ah Sung ),서지아 ( Ji A Seo ),한금현 ( Kum Hyun Han ),조원용 ( Won Yong Cho ),표희정 ( Heui Jung Pyo ),유기환 ( Kee Hwan Yoo ),원남희 ( Nam Hee Won ) 대한신장학회 2003 Kidney Research and Clinical Practice Vol.22 No.1
목적 : 혈액 용적 감소에 관련된 신장의 aquaporin-2 (AQP2) 수분 통로 발현 변화를 용적 감소 수 경과 시간에 따라 조사하였다. 방법 : Sprague-Dawley 숫쥐에서 몸무게의 약 2%에 이르는 급성 출혈을 일으키고 1시간 및 3시간 뒤에 신장 조직의 AQP2 mPNA 및 단백 발현을 각각 역전사 중합효소 연쇄반응법과 Western blot 분석법으로 조사하였다. 결과 : 출혈 후 1시간에 신장의 내수질에서 AQP2 mPNA 발혈은 유의하게 증가되었으나 AQP2 단백 이동 및 발현은 별화가 없?B다. 출혈 후 3시간에 AQP2 mRNA 발현 뿐 아니라 AQP2 단백 이동 및 발현이 모두 유의하게 증가하였다. 결론 : 혈액 종적 감소에 기인하여 신장에서 AQP2 수분 통로 발현이 증가되며 이는 체액용적 확보를 위한 보상 기전의 하나로서 작용하리라 추측되었다. Background : The present study was aimed to examine the regulation of aquaporin (AQP)-2 water channels in the kidney following blood volume depletion. Methods : Male Sprague-Dawley rats were acutely blood volume0depleted by withdrawal of arterial blood up to 2% of body weight. The expression of transcription - polymerase chain reaction and Westem blot analysis, respectively, in the inner medulla of the kidney 1 and 3 hours after the hemorrhage. Results : The mRNA expression if AQP2 was significantly increased 1 hour after thd bleeding However, neither the shuttling nor the total abundance of QQP2 proteins was significantly altered. On the contrary, 3 hours after the bleeding, the expression of AQP2 proteins as well as that of AQP2 mRNA was significantly incresaed. The shuttling of AQP2 proteins was also increased. Conclusion : These results sugest that an increased expression of AQP2 channels in the kidney may confer one of compensatory mechanisms restoring the circulation volume in an acute hypovolemic state.
이차 부갑상샘기능항진증이 있는 혈액투석 환자에게서 발생한 종양성 석회증
류우선 ( Woo Sun Rou ),이효근 ( Hyo Keun Lee ),한금현 ( Kum Hyun Han ),김덕원 ( Deok Weon Kim ),김용훈 ( Yong Hoon Kim ),주미 ( Mee Joo ),한상엽 ( Sang Youb Han ) 대한신장학회 2010 Kidney Research and Clinical Practice Vol.29 No.3
Tumoral calcinosis is a periarticular calcific lesion and rare complication in patients with maintenance hemodialysis. The pathogenesis of tumoral calcinosis is poorly understood but may be due to elevated serum phosphorus, a high calcium phosphorus (Ca×P) product or secondary hyperparathyroidism in hemodialysis patients. A 30-year-old man presented with pain and palpable mass of left shoulder. He had been on maintenance hemodialysis with high flux dialyzer for 10 years. Laboratory finding showed hyperphosphatemia and elevated intact PTH concentration. A shoulder X-ray and CT scan demonstrated a massive calcification. Following partial resection, pain was relieved. Here we report a case of tumoral calcinosis of shoulder in a hemodialysis patient with untreated hyperphosphatemia and secondary hyperparathyroidism.