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去甲金霉素对低钠血症肝硬化患者肾功能、尿前列腺素E2和激肽释放酶的影响。

Effect of demeclocycline on renal function and urinary prostaglandin E2 and kallikrein in hyponatremic cirrhotics.

作者信息

Pérez-Ayuso R M, Arroyo V, Camps J, Jiménez W, Rodamilans M, Rimola A, Gaya J, Rivera F, Rodés J

出版信息

Nephron. 1984;36(1):30-7. doi: 10.1159/000183112.

DOI:10.1159/000183112
PMID:6419136
Abstract

8 cirrhotics with hyponatremia were given demeclocycline (DMC) 900 mg/day to investigate its effect on renal function, plasma renin activity, aldosterone and urinary excretion of prostaglandin E2 and kallikrein. In 7 patients DMC induced an increase of free water clearance (from -0.36 +/- 0.06 to 0.13 +/- 0.06 ml/min) and serum sodium concentration (from 125.4 +/- 0.09 to 131.1 +/- 1.0 mEq/l, mmol/l). In 5 of these patients DMC also induced a marked reduction of glomerular filtration rate (from 72.2 +/- 6.2 to 31,2 +/- 4.7 ml/min) and renal plasma flow (from 468 +/- 98 to 195 +/- 55 ml/min) which could not be explained on the basis of hypovolemia. In each case this renal impairment was not associated with changes in urinary concentration of beta 2-microglobulin, urinary casts excretion, fresh urine sediment or urine protein content and disappeared after discontinuation of the drug. DMC induced a marked increase in the urinary excretion of prostaglandin E2 (from 0.82 +/- 0.27 to 6.16 +/- 1.91 ng/min) in 6 out of the 7 patients who responded to DMC and a marked reduction in urinary kallikrein (from 16.1 +/- 4.4 to 4.2 +/- 1.6 pkat/min) in the 5 patients who developed renal insufficiency. The serum DMC concentration was greater than 5 micrograms/ml in all patients who responded to DMC, greater than 8 micrograms/ml in all cases who developed renal insufficiency and of 3 micrograms/ml in the case not responding to DMC. (ABSTRACT TRUNCATED AT 250 WORDS)

摘要

8例伴有低钠血症的肝硬化患者接受了每天900毫克地美环素(DMC)治疗,以研究其对肾功能、血浆肾素活性、醛固酮以及前列腺素E2和激肽释放酶尿排泄的影响。7例患者中,DMC使自由水清除率增加(从-0.36±0.06增至0.13±0.06毫升/分钟),血清钠浓度升高(从125.4±0.09增至131.1±1.0毫当量/升,毫摩尔/升)。其中5例患者中,DMC还使肾小球滤过率显著降低(从72.2±6.2降至31.2±4.7毫升/分钟),肾血浆流量减少(从468±98降至195±55毫升/分钟),这无法用血容量不足来解释。在每种情况下,这种肾功能损害均与β2-微球蛋白尿浓度、尿沉渣排泄、新鲜尿沉渣或尿蛋白含量的变化无关,停药后消失。7例对DMC有反应的患者中有6例DMC使前列腺素E2尿排泄显著增加(从0.82±0.27增至6.16±1.91纳克/分钟),5例出现肾功能不全的患者尿激肽释放酶显著降低(从16.1±4.4降至4.2±1.6皮卡特/分钟)。所有对DMC有反应的患者血清DMC浓度均大于5微克/毫升,所有出现肾功能不全的病例中血清DMC浓度均大于8微克/毫升,无反应的病例中血清DMC浓度为3微克/毫升。(摘要截于250字)

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Guidelines on the management of ascites in cirrhosis.肝硬化腹水管理指南
Gut. 2006 Oct;55 Suppl 6(Suppl 6):vi1-12. doi: 10.1136/gut.2006.099580.
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Sustained aquaretic effect of the V2-AVP receptor antagonist, RWJ-351647, in cirrhotic rats with ascites and water retention.
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Br J Pharmacol. 2005 Nov;146(5):654-61. doi: 10.1038/sj.bjp.0706375.
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Use of urea for treatment of water retention in hyponatraemic cirrhosis with ascites resistant to diuretics.使用尿素治疗对利尿剂耐药的低钠血症肝硬化腹水患者的水潴留。
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Gut. 1990 Feb;31(2):204-7. doi: 10.1136/gut.31.2.204.
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