e24 Abstracts / Journal of the American Society of Hypertension 8(4S) (2014) e23–e25

healthy people, CAVI was related to age, systolic blood pressure and body

mass index.

Keywords: Asia; Cardio-ankle vascular index; Blood pressure; Women

FP-17

MicroRNA-29b protected renal fibrosis

Deye Yang,1 Jialin Pan.2 1Hangzhou Normal University, Hangzhou, China;2Wenzhou Medical University, Wenzhou, China

It has been demonstrated that the Angiotensin II (Ang II) contents and its

receptor density in the kidney of young spontaneously hypertensive rats

(SHRs) were significantly higher than in age-matched Wistar-Kyoto rats

(WKYs). Ang II has been proved to induce Epithelial-Mesenchymal

Transition (EMT). The present study was aimed at testing the role of

miRNA-29b (miR-29b) in Ang II-induced EMT. Differential expression

of miR-29b in renal cortex between 15-weeks SHRs and age-matched

WKYs was determined by real-time quantitative polymerase chain reac-

tion (RT-qPCR). The effect of miR-29b on EMT-associated genes such

as transforming growth factor (TGF-b), a-smooth muscle actin (a-

SMA), CollagenI (ColI) was examined after transfecting miR-29b mimics

(24 h before treatment with 10-7M Ang II) and miR-29b inhibitor into

cultured renal tubular epithelial cells line_NRK-52E cells. Analysis of

these genes expression was confirmed by RT-qPCR, western blot and

immunofluorescence staining. Downregulation of miR-29b in renal cortex

of SHRs was demonstrated by RT-qPCR compared with that of WKYs.

Transfection of miR-29b inhibitor significantly increased the expression

of TGF-b, a-SMA and ColI, while transfection of miR-29b mimics in-

hibited Ang II-induced upregulation of these genes expression. Expression

of miR-29b in renal cortex of SHRs was decreased. The miR-29b may play

a crucial role in EMT. Downregulation of miR-29b may exert a similar ef-

fect on NRK-52E cells as those seen in treatment of Ang II, while upregu-

lation of miR-29b may protect NRK-52E cells from EMT induced by

Ang II.

Keywords: MicroRNA-29b; Angiotensin II; Epithelial-Mesenchymal

Transition; Spontaneously hypertensive rats

FP-18

Incidence and risk factors of acute kidney injury after thoracic

endovascular aortic repair for type B aortic dissection

Songyuan Luo,1 Jianfang Luo,1 Zhen Liu,2 Bingrong Nie,1 Yuan Liu,1

Wenhui Huang,1 Ling Xue,1 Yingling Zhou,1 Ruixin Fan,1 Jiyan Chen.11Guangdong Academy of Medical Sciences, Guangdong General Hospital,Guangzhou, China; 2Zhongshan School of Medicine, Sun Yat-Sen

University, Guangzhou, China

Background: Aortic dissection is a life-threatening complication of hyper-

tension. Thoracic endovascular aortic repair (TEVAR) becomes an

emerging treatment modality for acute type B aortic dissection (AD) in

recent years. The risk of acute kidney injury after TEVAR , however,

has been not widely established.

Methods: We retrospectively studied the clinical records of 312 consecu-

tive patients who submitted to our institution and were performed TEVAR

for Stanford type B AD between May 2011 and September 2012. The pa-

tients were routinely monitored the renal function pre-operation until 7

days after TEVAR. The KDIGO criteria was used for acute kidney injury

(AKI).

Results: Incidence of AKI TEVAR was 26.9%. Risks of stage 1.2.3 of AKI

were 18.3%, 5.1%, and 3.5%, respectively. There were higher incidence of

AKI in patients with history of stroke (P<0.001), and carotid-subclavian