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非糖尿病肾病患者中,短期抗蛋白尿反应对血管紧张素转换酶抑制剂治疗的反应在预测肾小球滤过率下降方面的预后价值。

Prognostic value of the short-term antiproteinuric response to ACE inhibition for prediction of GFR decline in patients with nondiabetic renal disease.

作者信息

Wapstra F H, Navis G, de Jong P E, de Zeeuw D

机构信息

Groningen Institute of Drug Studies, (GIDS), Department of Medicine, State University, The Netherlands.

出版信息

Exp Nephrol. 1996;4 Suppl 1:47-52.

PMID:9001897
Abstract

In chronic renal disease, the severity of proteinuria is associated with the rate of renal function loss. Proteinuria, therefore, was postulated to play a role in the final common pathway of chronic renal function loss. If so, reduction of proteinuria would improve long-term renal outcome. Improvement of long-term renal function outcome has been obtained in several intervention trials; in these studies; regimens providing better renoprotection were associated with more effective reduction of poteinuria than control regimens. As the reduction of proteinuria is mostly associated with a fall in blood pressure, however, it is difficult to delineate the respective roles of the lowering of blood pressure and of proteinuria. Interestingly, the initial reduction of proteinuria (but not of blood pressure) by antihypertensive treatment appears to predict long-term renal outcome in man as well as in experimental renal disease. This suggests that an intervention strategy aimed not only at the normalization of blood pressure, but also specifically at elimination of proteinuria, might be able to improve long-term renal outcome in proteinuric patients. If so, this would provide further evidence in support of the hypothesis that proteinuria is causally involved in the progression of long-term renal function loss.

摘要

在慢性肾脏疾病中,蛋白尿的严重程度与肾功能丧失的速率相关。因此,蛋白尿被假定在慢性肾功能丧失的最终共同途径中起作用。如果是这样,降低蛋白尿将改善长期肾脏结局。在几项干预试验中已经取得了长期肾功能结局的改善;在这些研究中,提供更好肾脏保护作用的治疗方案与比对照方案更有效地降低蛋白尿相关。然而,由于蛋白尿的降低大多与血压下降相关,因此难以区分降低血压和降低蛋白尿各自的作用。有趣的是,抗高血压治疗最初降低蛋白尿(而非血压)似乎可预测人类以及实验性肾脏疾病的长期肾脏结局。这表明,一种不仅旨在使血压正常化,而且特别旨在消除蛋白尿的干预策略,可能能够改善蛋白尿患者的长期肾脏结局。如果是这样,这将为支持蛋白尿因果性参与长期肾功能丧失进展这一假说提供进一步证据。

相似文献

1
Prognostic value of the short-term antiproteinuric response to ACE inhibition for prediction of GFR decline in patients with nondiabetic renal disease.非糖尿病肾病患者中,短期抗蛋白尿反应对血管紧张素转换酶抑制剂治疗的反应在预测肾小球滤过率下降方面的预后价值。
Exp Nephrol. 1996;4 Suppl 1:47-52.
2
Titrating for antiproteinuric effect: the clue to renoprotection?滴定以获得抗蛋白尿效果:肾脏保护的线索?
J Hum Hypertens. 1996 Oct;10(10):669-73.
3
Renoprotection by blockade of the renin-angiotensin-aldosterone system in diabetic and non-diabetic chronic kidney disease. Specific involvement of intra-renal angiotensin-converting enzyme activity in therapy resistance?糖尿病和非糖尿病慢性肾脏病中通过阻断肾素-血管紧张素-醛固酮系统实现的肾脏保护作用。肾内血管紧张素转换酶活性在治疗抵抗中的具体作用?
Minerva Med. 2004 Oct;95(5):395-409.
4
Long-term effects of antihypertensive agents on proteinuria and renal function.抗高血压药物对蛋白尿和肾功能的长期影响。
Arch Intern Med. 1995 May 22;155(10):1073-80.
5
[Are all antihypertensive drugs renoprotective?].[所有抗高血压药物都具有肾脏保护作用吗?]
Herz. 2004 May;29(3):248-54. doi: 10.1007/s00059-003-2508-6.
6
[ACE inhibitors and the kidney].[血管紧张素转换酶抑制剂与肾脏]
Wien Med Wochenschr. 1996;146(11):231-4; discussion 234-5.
7
Proteinuria predicts end-stage renal failure in non-diabetic chronic nephropathies. The "Gruppo Italiano di Studi Epidemiologici in Nefrologia" (GISEN).蛋白尿可预测非糖尿病慢性肾病患者的终末期肾衰竭。“意大利肾脏病流行病学研究组”(GISEN)。
Kidney Int Suppl. 1997 Dec;63:S54-7.
8
ACE polymorphism does not determine short-term renal response to ACE-inhibition in proteinuric patients.血管紧张素转换酶(ACE)基因多态性并不能决定蛋白尿患者对ACE抑制治疗的短期肾脏反应。
Nephrol Dial Transplant. 1997;12 Suppl 2:42-6.
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Angiotensin converting enzyme insertion/deletion polymorphism and short-term renal response to ACE inhibition: role of sodium status.血管紧张素转换酶插入/缺失多态性与ACE抑制的短期肾脏反应:钠状态的作用
Kidney Int Suppl. 1997 Dec;63:S23-6.
10
A randomized and double-blind comparison of isradipine and spirapril as monotherapy and in combination on the decline in renal function in patients with chronic renal failure and hypertension.一项关于伊拉地平与螺普利作为单一疗法及联合疗法对慢性肾衰竭合并高血压患者肾功能下降影响的随机双盲对照研究。
Clin Nephrol. 2001 May;55(5):375-83.

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