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慢性肾衰竭及肾移植后血浆内皮素水平:对高血压及环孢素A相关肾毒性的影响

Plasma levels of endothelin in chronic renal failure and after renal transplantation: impact on hypertension and cyclosporin A-associated nephrotoxicity.

作者信息

Stockenhuber F, Gottsauner-Wolf M, Marosi L, Liebisch B, Kurz R W, Balcke P

机构信息

Department of Renal Disease and Dialysis, University of Vienna, Austria.

出版信息

Clin Sci (Lond). 1992 Mar;82(3):255-8. doi: 10.1042/cs0820255.

Abstract
  1. Plasma levels of endothelin were measured in 30 patients with chronic renal failure, 32 patients on chronic haemodialysis treatment and 25 renal graft recipients with stable renal graft function. 2. In patients with chronic renal failure as well as in patients on regular haemodialysis treatment, mean plasma levels of endothelin were significantly increased (4.59 +/- 2.09 pg/ml, 10.08 +/- 3.12 pg/ml, respectively) when compared with normal subjects (1.88 +/- 0.6 pg/ml, P less than 0.01, P less than 0.001, respectively). 3. In the group with chronic renal failure a positive correlation between the plasma level of endothelin and the plasma concentration of creatinine was observed (P less than 0.003). 4. Renal graft recipients on cyclosporin A with stable renal graft function had a normal plasma level of endothelin suggesting that cyclosporin A nephrotoxicity is not mediated by endothelin. 5. Hypertensive patients with chronic renal failure or on regular haemodialysis and hypertensive renal graft recipients did not differ from the corresponding normotensive population with regard to the plasma level of endothelin, demonstrating that an increased plasma level of endothelin does not play a major role in the pathogenesis of renal hypertension.
摘要
  1. 对30例慢性肾衰竭患者、32例接受慢性血液透析治疗的患者以及25例肾移植功能稳定的肾移植受者测定了血浆内皮素水平。2. 与正常受试者(分别为1.88±0.6 pg/ml)相比,慢性肾衰竭患者以及定期接受血液透析治疗的患者血浆内皮素平均水平显著升高(分别为4.59±2.09 pg/ml、10.08±3.12 pg/ml,P<0.01,P<0.001)。3. 在慢性肾衰竭组中,观察到内皮素血浆水平与肌酐血浆浓度之间呈正相关(P<0.003)。4. 肾移植功能稳定且服用环孢素A的肾移植受者内皮素血浆水平正常,提示环孢素A肾毒性并非由内皮素介导。5. 慢性肾衰竭或定期接受血液透析的高血压患者以及高血压肾移植受者在内皮素血浆水平方面与相应的血压正常人群无差异,表明血浆内皮素水平升高在肾性高血压发病机制中不起主要作用。

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