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肾病综合征及缓解后的肾脏多巴胺能系统

Renal dopaminergic system in nephrotic syndrome and after remission.

作者信息

Pestana M, Jardim H, Afonso C, Serrão P, Santos N, Guerra L, Soares-da-Silva P

机构信息

Nephrology Department, Institute of Pharmacology and Therapeutics, Faculty of Medicine, Porto, Portugal.

出版信息

Nephrol Dial Transplant. 1998 Oct;13(10):2559-62. doi: 10.1093/ndt/13.10.2559.

Abstract

BACKGROUND

Although intrarenal dopamine is known to behave as an endogenous natriuretic hormone the role of the renal dopaminergic system in the sodium handling of nephrotic oedema remains unknown.

STUDY DESIGN

We monitored the daily urinary excretion of free dopamine, L-DOPA-its precursor, and its metabolites, DOPAC and HVA, during sodium retention accompanying the nephrotic state and natriuresis leading to oedema mobilization in eight patients (mean age 8.0+/-2.4 years) with drug-induced remission of minimal-change nephrotic syndrome (MCNS).

RESULTS

During natriuresis the urinary levels of dopamine did not increase in parallel with sodium excretion in any of the eight patients studied. Moreover, after remission of the nephrotic syndrome the urinary levels of dopamine were significantly lower than during the nephrotic state (1565.3+/-361.7 vs 2416.1+/-558.4, P= 0.02). In contrast, the urinary excretion of L-DOPA increased markedly during natriuresis resulting from remission of proteinuria (from 87.0+/-40.5 up to 296.9+/-86.3 nmol/24 h; P< 0.01).

CONCLUSION

We conclude that the natriuretic response resulting from drug-induced remission of proteinuria in MCNS is accompanied by a decrease in the renal uptake/decarboxylation of L-DOPA to dopamine.

摘要

背景

尽管已知肾内多巴胺可作为一种内源性利钠激素,但肾多巴胺能系统在肾病性水肿钠代谢中的作用仍不清楚。

研究设计

我们监测了8例药物诱导缓解的微小病变肾病综合征(MCNS)患者(平均年龄8.0±2.4岁)在肾病状态伴钠潴留以及利尿导致水肿消退过程中,游离多巴胺、其前体L-多巴及其代谢产物3,4-二羟基苯乙酸(DOPAC)和高香草酸(HVA)的每日尿排泄量。

结果

在利尿过程中,所研究的8例患者中,无一例多巴胺尿水平与钠排泄量呈平行增加。此外,肾病综合征缓解后,多巴胺尿水平显著低于肾病状态时(1565.3±361.7对2416.1±558.4,P = 0.02)。相反,蛋白尿缓解导致利尿时,L-多巴的尿排泄量显著增加(从87.0±40.5增至296.9±86.3 nmol/24小时;P<0.01)。

结论

我们得出结论,MCNS中药物诱导的蛋白尿缓解所导致的利钠反应伴随着L-多巴向多巴胺的肾摄取/脱羧作用降低。

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