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作 者:汪华林[1] 谭树芬[1] 刘长波[1] 谢辉[1] 郭颖[2] 俞小敏[1] 杨热电[1] 崔如健[1] 陈秀萌[1] 黄元寿[1]
机构地区:[1]广州医学院第一附属医院肾内科,广州510120 [2]广东省广州市珠江医院肾移植科,广州510282
出 处:《中国血液净化》2006年第8期426-429,436,共5页Chinese Journal of Blood Purification
基 金:广州市医药卫生科技项目(2005-YB-131)
摘 要:目的探讨慢性肾衰竭患者血浆及尿液中尾加压素Ⅱ(UrotensinⅡ,UⅡ)水平变化以及血液透析、腹膜透析及肾移植对其的影响。方法采用放射免疫方法,以正常人为对照,分别观察广州医学院第一附属医院肾内科和广东省广州市珠江医院肾移植科慢性肾衰竭未透析患者(ND组)、维持性血液透析患者(HD组)、持续性不卧床腹膜透析患者(CAPD组)、肾移植患者(KT组)血浆及尿液中的尾加压素Ⅱ水平变化。结果ND组、HD组、PD组和KT组患者的血浆UⅡ水平较正常人显著增高(P<0.0001),以HD组最高,ND组次之,PD组再次之,KT组最低;尿UⅡ排泄在ND组、HD组、PD组均显著减少(P<0.05),但在KT组显著增加(P<0.01);结论证实在非糖尿病的慢性肾衰竭患者血UⅡ水平显著增高,尿UⅡ排泄明显减少,血液透析患者和腹膜透析患者变化更为显著;肾移植患者血浆UⅡ水平增高减轻,而尿UⅡ水平显著增加;本研究提示UⅡ是慢性肾衰竭发展过程中一个重要的多肽。Objective To observe the levels of plasma and urinary urotensin Ⅱ (U Ⅱ) in the chronic renal failure patients (CRF) and the influence of hemodialysis, continuous ambulance peritoneal dialysis(CAPD) and allograft renal transplantation on U Ⅱ levels respectively. Methods Controlled with normal subjects, the plasma and urinary U Ⅱ levels were examined by radioimmunoassay method in a population of 72 CRF patients who received non-dialysis (ND group), maintenance hemodialysis (HD group), continuous ambulatory peritoneal dialysis (PD group) or allograft renal transplantation (KT group) respectively. Results The plasma UⅡ levels increased significantly in all patients (P 〈0.0001), Which in HD group was the highest, ND group the second, then PD group and KT group was the lowest. The urinary U Ⅱ excretion decreased in ND group, HD group, PD group obviously (P〈0.05), but increased singnificantly in KT group(P〈 0.01); Conclusions The investigation proved that a higher level of plasma urotensin Ⅱ and a lower urinary UⅡ excretion exist in the patients with chronic renal failure, and these changes become even more obvious in the patients who received hemodialysis or peritoneal dialysis. Allograft renal transplantation can reduce the increased levels of plasma U Ⅱ and can increase urinary UⅡ excretion in CRF patients. The research imply that U Ⅱ may be an important peptide which involved in the pathophysiology of chronic renal failure.
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