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慢性肾衰竭患者血清胆汁酸水平升高的潜在机制。

Mechanism underlying an elevated serum bile acid level in chronic renal failure patients.

作者信息

Chu Lei, Zhang Kangkang, Zhang Yingying, Jin Xunbo, Jiang Huaxin

机构信息

Department of Minimally Invasive Urology Center, Provincial Hospital Affiliated to Shandong University, 9677 Jingshi Road, Jinan, Shandong, China.

出版信息

Int Urol Nephrol. 2015 Feb;47(2):345-51. doi: 10.1007/s11255-014-0901-0. Epub 2014 Dec 25.

DOI:10.1007/s11255-014-0901-0
PMID:25539619
Abstract

INTRODUCTION

Bile acids play an important role in the digestion of dietary lipids. Bile acid metabolism is regulated by the digestive system. The kidney is an important organ of the urinary system and is believed to play a minor role in bile acid excretion; however, many recent studies have reported an increased serum bile acid level and alterations in bile acid homeostasis in both clinical and animal model studies on chronic renal failure. The existing research findings on the mechanisms underlying this phenomenon were mostly derived from animal model studies, but clinical investigations have been limited.

MATERIALS AND METHODS

Kidney tissues and serum and urine samples from CRF patients and normal controls were studied.

RESULTS

We found increased serum bile acid levels and decreased urine bile acid output levels in chronic renal failure patients. Mesangial cell and endothelial cell proliferation, glomerular sclerosis, renal interstitial fibrosis, and intrarenal vascular sclerosis were observed based on hematoxylin-eosin and Masson trichrome staining pathology analysis. Scatter diagram and Pearson correlation analysis showed that in chronic renal failure patients, the estimated glomerular filtration rate and serum bile acid level were interrelated. Reverse transcription polymerase chain reaction and Western blotting results indicated that reabsorption and secretion of bile acid at the apical surface of the proximal renal tubular did not contribute to the elevated serum BA level.

CONCLUSION

The increase in plasma bile acid is due to decreased bile acid filtration through the kidneys in CRF patients.

摘要

引言

胆汁酸在膳食脂质消化中起重要作用。胆汁酸代谢受消化系统调节。肾脏是泌尿系统的重要器官,一般认为其在胆汁酸排泄中作用较小;然而,最近许多研究报告称,在慢性肾衰竭的临床和动物模型研究中,血清胆汁酸水平升高且胆汁酸稳态发生改变。关于这一现象潜在机制的现有研究结果大多来自动物模型研究,但临床研究有限。

材料与方法

对慢性肾衰竭患者及正常对照者的肾组织、血清和尿液样本进行研究。

结果

我们发现慢性肾衰竭患者血清胆汁酸水平升高,尿胆汁酸排出水平降低。基于苏木精 - 伊红染色和马松三色染色病理分析,观察到系膜细胞和内皮细胞增殖、肾小球硬化、肾间质纤维化及肾内血管硬化。散点图和皮尔逊相关分析表明,在慢性肾衰竭患者中,估计肾小球滤过率与血清胆汁酸水平相关。逆转录聚合酶链反应和蛋白质印迹结果表明,近端肾小管顶端表面胆汁酸的重吸收和分泌并非血清胆汁酸水平升高的原因。

结论

慢性肾衰竭患者血浆胆汁酸升高是由于经肾脏的胆汁酸滤过减少所致。

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