Suppr超能文献

高盐摄入的自发性高血压大鼠肾小管损伤的早期尿液生物标志物

Early urinary biomarkers for renal tubular damage in spontaneously hypertensive rats on a high salt intake.

作者信息

Hosohata Keiko, Yoshioka Daisuke, Tanaka Akira, Ando Hitoshi, Fujimura Akio

机构信息

Departments of Clinical Pharmacolo.gy, School of Medicine, Jichi Medical University, Tochigi, Japan.

Departments of Pathology, School of Medicine, Jichi Medical University, Tochigi, Japan.

出版信息

Hypertens Res. 2016 Jan;39(1):19-26. doi: 10.1038/hr.2015.103. Epub 2015 Sep 17.

Abstract

A high salt intake exacerbates hypertension and accelerates renal tubular damage in hypertensive patients. However, data concerning early biomarkers for renal tubular change induced by a high salt intake are limited. The objective of this study was to clarify the time course of new biomarkers for renal tubular damage during high salt intake in spontaneously hypertensive rats (SHR). Male SHR received a regular or high-salt diet from 9 to 17 weeks of age. At 10 weeks of age, a high salt intake caused renal tubular damage, which was further exacerbated at 17 weeks of age. Although albuminuria was detected in salt-loaded SHR at 14 weeks of age, urinary excretion of vanin-1 and neutrophil gelatinase-associated lipocalin (NGAL) was elevated in these animals from 10-17 weeks of age. However, kidney injury molecule-1 (Kim-1) was elevated at 15 weeks of age in salt-loaded SHR. These results suggest that urinary vanin-1 and NGAL are potentially early biomarkers for renal tubular damage in SHR under a high salt intake.

摘要

高盐摄入会加重高血压患者的高血压病情并加速肾小管损伤。然而,关于高盐摄入引起的肾小管变化的早期生物标志物的数据有限。本研究的目的是阐明自发性高血压大鼠(SHR)在高盐摄入期间肾小管损伤新生物标志物的时间进程。雄性SHR从9周龄到17周龄接受正常或高盐饮食。在10周龄时,高盐摄入导致肾小管损伤,在17周龄时进一步加重。虽然在14周龄时在高盐负荷的SHR中检测到蛋白尿,但这些动物在10至17周龄时vanin-1和中性粒细胞明胶酶相关脂质运载蛋白(NGAL)的尿排泄量升高。然而,在高盐负荷的SHR中,肾损伤分子-1(Kim-1)在15周龄时升高。这些结果表明,尿vanin-1和NGAL可能是高盐摄入下SHR肾小管损伤的潜在早期生物标志物。

文献AI研究员

20分钟写一篇综述,助力文献阅读效率提升50倍。

立即体验

用中文搜PubMed

大模型驱动的PubMed中文搜索引擎

马上搜索

文档翻译

学术文献翻译模型,支持多种主流文档格式。

立即体验