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慢性肾损伤的进展机制。

Mechanisms of progression of chronic renal damage.

作者信息

Klahr S

机构信息

Washington University School of Medicine, and Barnes-Jewish Hospital, St. Louis, MO 63110, USA.

出版信息

J Nephrol. 1999 Jul-Aug;12 Suppl 2:S53-62.

PMID:10688403
Abstract

The amount of protein in the urine is a strong predictor of subsequent loss of renal function. Proteinuria and tubular atrophy have been linked with progressive renal insufficiency. In the last few years several studies have indicated that smoking is also a risk factor in the progression of renal disease. In addition, a number of studies have suggested that higher levels of blood pressure are associated with a faster decline in renal function. A number of cytokines, vasoactive compounds, chemoattractant molecules and growth factors are upregulated during the course of progressive renal disease in experimental animals. Recent data indicate that vasoconstrictor substances have a key role in the initial phases of this process. In particular, angiotensin II is increased following the development of renal injury. Angiotensin in turn upregulates the expression of other factors including: transforming growth factor beta, tumor necrosis alpha, nuclear factor kappaB and several chemoattractant compounds. Other vasoactive compounds (endothelin, thromboxane A2 and prostaglandins) may also be upregulated during the course of progressive renal disease

摘要

尿蛋白量是肾功能随后丧失的有力预测指标。蛋白尿和肾小管萎缩与进行性肾功能不全有关。在过去几年中,多项研究表明吸烟也是肾病进展的一个危险因素。此外,一些研究表明,血压升高与肾功能更快下降有关。在实验动物进行性肾病过程中,多种细胞因子、血管活性化合物、趋化分子和生长因子上调。最近的数据表明,血管收缩物质在这一过程的初始阶段起关键作用。特别是,肾损伤发生后血管紧张素II增加。血管紧张素进而上调其他因子的表达,包括:转化生长因子β、肿瘤坏死因子α、核因子κB和几种趋化化合物。在进行性肾病过程中,其他血管活性化合物(内皮素、血栓素A2和前列腺素)也可能上调

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