Suppr超能文献

尿足细胞表面蛋白,用于检测肥胖早期肾脏变化的新型生物标志物。

Urinary podocalyxin, the novel biomarker for detecting early renal change in obesity.

作者信息

Suwanpen Chayanut, Nouanthong Phonethipsavanh, Jaruvongvanich Veeravich, Pongpirul Krit, Pongpirul Wannarat Amornnimit, Leelahavanichkul Asada, Kanjanabuch Talerngsak

机构信息

Department of Internal Medicine, Faculty of Medicine, Chulalongkorn University, 254 Phayathai Road, Pathumwan, Bangkok, 10330, Thailand.

Pasteur Institute du Laos, Samsenthai Road, Ban Kao-Gnot, Sisattanak district, P.O Box 3560, Vientiane, Lao PDR.

出版信息

J Nephrol. 2016 Feb;29(1):37-44. doi: 10.1007/s40620-015-0199-8. Epub 2015 Apr 24.

Abstract

BACKGROUND

The prevalence of obesity is increasing during the past decade along with obesity-related glomerulopathy (ORG), glomeruli injury due to the obesity. The major pathogenesis of ORG is the shedding of podocytes from the glomerular cell barrier into urine. Podocalyxin (PCX), a main surface antigen of podocyte, correlates well with glomerulosclerosis progression and glomerular injury severity, and might be a potential biomarker for early renal alteration in obesity. In addition, vascular endothelial growth factor (VEGF) and alpha-smooth muscle actin (α-SMA) also play a role in promoting glomerulosclerosis. The aim of this study was to explore whether obese subjects without other diseases excrete more PCX-positive (PCX+) cells than non-obese individuals, in comparison with urine protein-creatinine ratio (UPCR) and glomerular filtration rate (GFR) as traditional renal markers. Moreover, the effect of body mass index (BMI) on urinary VEGF, PCX or α-SMA positive cells was also investigated.

METHODS

Forty-eight obese and 13 non-obese adults were included. Exfoliated cells from fresh first void morning urine were harvested, stained with PCX, VEGF, and α-SMA antibody, and quantified by flow cytometry. Correlation between interested urinary biomarkers (cells positive for PCX, VEGF plus PCX and α-SMA), UPCR and GFR with BMI and metabolic risk factors were analyzed.

RESULTS

Obese patients had significantly higher PCX+ cells than non-obese [0.62 (0.00-13.13) vs. 0.15 (0.00-0.72) cells/ml × mg cr, p < 0.05]. There was no significant difference in GFR and UPCR between the groups. Of interest, BMI demonstrated a correlation with PCX+ cells (r = 0.343, p = 0.008) and cells positive for PCX plus VEGF (r = 0.374, p = 0.004).

CONCLUSION

Obese subjects without other diseases and with normal UPCR and GFR showed evidence of renal alteration through the detection of a higher number of PCX+ cells. Increasing BMI also resulted in higher number of PCX+ cells.

摘要

背景

在过去十年中,肥胖症的患病率不断上升,与此同时,肥胖相关肾小球病(ORG),即因肥胖导致的肾小球损伤也日益增多。ORG的主要发病机制是足细胞从肾小球细胞屏障脱落进入尿液。足细胞表面主要抗原足ocalyxin(PCX)与肾小球硬化进展及肾小球损伤严重程度密切相关,可能是肥胖早期肾脏改变的潜在生物标志物。此外,血管内皮生长因子(VEGF)和α-平滑肌肌动蛋白(α-SMA)在促进肾小球硬化方面也发挥作用。本研究的目的是探讨无其他疾病的肥胖受试者与非肥胖个体相比,是否比非肥胖个体排泄更多的PCX阳性(PCX+)细胞,并将尿蛋白肌酐比值(UPCR)和肾小球滤过率(GFR)作为传统肾脏标志物进行比较。此外,还研究了体重指数(BMI)对尿VEGF、PCX或α-SMA阳性细胞的影响。

方法

纳入48名肥胖成年人和13名非肥胖成年人。收集清晨首次晨尿中的脱落细胞,用PCX、VEGF和α-SMA抗体染色,通过流式细胞术进行定量分析。分析感兴趣的尿生物标志物(PCX阳性细胞、VEGF加PCX阳性细胞和α-SMA阳性细胞)、UPCR和GFR与BMI及代谢危险因素之间的相关性。

结果

肥胖患者的PCX+细胞明显高于非肥胖患者[0.62(0.00 - 13.13)对0.15(0.00 - 0.72)个细胞/ml×mg肌酐,p < 0.05]。两组间GFR和UPCR无显著差异。有趣的是,BMI与PCX+细胞(r = 0.343,p = 0.008)以及PCX加VEGF阳性细胞(r = 0.374,p = 0.004)存在相关性。

结论

无其他疾病且UPCR和GFR正常的肥胖受试者通过检测到更多的PCX+细胞显示出肾脏改变的证据。BMI升高也导致PCX+细胞数量增加。

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