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[肾病综合征患儿的心房利钠肽]

[Atrial natriuretic peptide in children with nephrotic syndrome].

作者信息

Jovanovitsh O, Popovitsh-Rolovitsh M, Radoshevitsh P, Stankovitsh R, Dujitsh A, Gajitsh M, Peco-Antitsh A, Krushchitsh D, Kostitsh M

机构信息

University Children's Hospital, Belgrade.

出版信息

Srp Arh Celok Lek. 1995 Nov-Dec;123(11-12):291-4.

PMID:16296241
Abstract

The mechanism causing sodium retention in nephrotic syndrome remains controversial. There is an increasing evidence that sodium retention is directly due to an intrarenal mechanism. Atrial natriuretic peptide (ANP), realized from the heart during hypervolaemia, increases glomerular filtration rate, renal sodium and water elimination in both experimental animals and healthy men. In attempt to clarify the possible role of ANP in the mechanism of sodium retention in nephrotic syndrome we carried out this study. The purpose was: a) to determine plasma concentrations of ANP and values of creatinine clearance (CCr), natriuresis and diuresis both in basal conditions and after remission of the ilness, and b) to analyze the influence of acute hypervolaemia on ANP, Ccr, diuresis and natriuresis. A group of 12 children (aged 2-13 years) was studied during relapse and remission of nephrotic syndrome. In addition, 8 patients were studied during acute hypervolaemia due to intravenous infusion of 12% albumine. Twelve healthy children served as control group. Our results showed that in nephrotic syndrome group ANP was higher than in control group. Creatinine clearance, diuresis and natriuresis were significantly lower during relapse than in remission. The increase in Ccr, diuresis and natriuresis were observed during infusion of albumine, but no correlation was found between increased ANP and other parameters. This study showed that during relapse of nephrotic syndrome plasma concentrations of ANP are moderately elevated, but Ccr, diuresis nad natriuresis are blunted. We speculate that natriuretic and diuretic effects of ANP are impaired in children with nephrotic syndrome.

摘要

肾病综合征中导致钠潴留的机制仍存在争议。越来越多的证据表明,钠潴留直接归因于肾脏内的机制。心房利钠肽(ANP)在血容量过多时从心脏释放,可增加实验动物和健康男性的肾小球滤过率、肾脏钠和水的排泄。为了阐明ANP在肾病综合征钠潴留机制中可能的作用,我们进行了这项研究。目的是:a)测定基础状态以及疾病缓解后ANP的血浆浓度、肌酐清除率(CCr)、尿钠排泄和利尿的值,b)分析急性血容量过多对ANP、CCr、利尿和尿钠排泄的影响。对一组12名儿童(年龄2至13岁)在肾病综合征复发和缓解期间进行了研究。此外,对8名因静脉输注12%白蛋白导致急性血容量过多的患者进行了研究。12名健康儿童作为对照组。我们的结果显示,肾病综合征组的ANP高于对照组。复发期间的肌酐清除率、利尿和尿钠排泄显著低于缓解期。输注白蛋白期间观察到CCr、利尿和尿钠排泄增加,但未发现ANP升高与其他参数之间存在相关性。这项研究表明,在肾病综合征复发期间,ANP的血浆浓度适度升高,但CCr、利尿和尿钠排泄受到抑制。我们推测,肾病综合征患儿中ANP的利钠和利尿作用受损。

相似文献

1
[Atrial natriuretic peptide in children with nephrotic syndrome].[肾病综合征患儿的心房利钠肽]
Srp Arh Celok Lek. 1995 Nov-Dec;123(11-12):291-4.
2
Atrial natriuretic peptide, sodium retention, and proteinuria in nephrotic syndrome.心房利钠肽、钠潴留与肾病综合征中的蛋白尿
Nephrol Dial Transplant. 1996 Jun;11(6):1034-42.
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Regulation of renal sodium and water excretion in the nephrotic syndrome and cirrhosis of the liver.肾病综合征和肝硬化时肾脏对钠和水排泄的调节
Dan Med Bull. 1997 Apr;44(2):191-207.
4
Plasma concentration and renal effect of human atrial natriuretic peptide in nephrotic syndrome.肾病综合征中人心房利钠肽的血浆浓度及肾脏效应
Nihon Jinzo Gakkai Shi. 1989 Jun;31(6):661-9.
5
Renal response to atrial natriuretic peptide in nephrotic syndrome.
Nephrol Dial Transplant. 1987;2(6):510-4.
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Hormonal regulation of water metabolism in children with nephrotic syndrome.肾病综合征患儿水代谢的激素调节
Kidney Int Suppl. 1987 Aug;21:S83-9.
7
Cellular basis for blunted volume expansion natriuresis in experimental nephrotic syndrome.实验性肾病综合征中容量扩张性利钠减弱的细胞基础。
J Clin Invest. 1992 Oct;90(4):1302-12. doi: 10.1172/JCI115995.
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Attenuated diuretic and natriuretic effects of atrial natriuretic peptide in rats with heart failure.心房利钠肽在心力衰竭大鼠中的利尿和利钠作用减弱。
Horm Metab Res. 1989 Apr;21(4):185-8. doi: 10.1055/s-2007-1009187.
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Effect of posture on sodium excretion and diuretic efficacy in nephrotic patients.姿势对肾病患者钠排泄及利尿效果的影响。
Am J Kidney Dis. 2000 Oct;36(4):719-27. doi: 10.1053/ajkd.2000.17616.
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Bolus injections of synthetic atrial natriuretic peptide in patients with chronic renal failure or nephrotic syndrome.对慢性肾衰竭或肾病综合征患者进行合成心房利钠肽的推注注射。
J Cardiovasc Pharmacol. 1989 May;13(5):682-90.