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离子型对比剂在糖尿病肾病中比非离子型对比剂诱导更多的细胞凋亡。

Ionic contrast media induced more apoptosis in diabetic kidney than nonionic contrast media.

机构信息

Division of Cardiology, Department of Internal Medicine, Kaohsiung Medical University Hospital, Kaohsiung - Taiwan.

出版信息

J Nephrol. 2011 May-Jun;24(3):376-80. doi: 10.5301/JN.2010.5784.

DOI:10.5301/JN.2010.5784
PMID:20890877
Abstract

BACKGROUND

Contrast-induced nephropathy is a major cause of hospital-acquired acute renal failure, and its risk is significantly increased in patients with diabetes mellitus. This study aimed to examine both the role of apoptosis in low-osmolar contrast media-induced kidney injury in normal and diabetic rats and the difference in the induced kidney injury between ionic and nonionic contrast media.

METHODS

Normal and streptozotocin-induced diabetic Wistar rats were administered with ionic low-osmolar ioxaglate, nonionic low-osmolar iopromide or normal saline injection. Apoptosis in kidney tubular cells was determined by the presence of positive terminal deoxynucleotidyl transferase-mediated dUTP in situ nick end-labeling (TUNEL) stain.

RESULTS

At 24 hours after administration, both ioxaglate and iopromide injections induced more apoptosis in diabetic (49.7% vs. 25.3% for ioxaglate; 37.7% vs. 25.3% for iopromide; both p<0.001) and normal (36.2% vs. 27.4%, p=0.002, for ioxaglate; 33.6% vs. 27.4%, p=0.029, for iopromide) kidney tubular cells than normal saline injections. Additionally, ioxaglate induced more apoptotic tubular cells in diabetic kidneys than in normal kidneys (p<0.001). Moreover, ioxaglate significantly induced more apoptotic cells than iopromide in diabetic kidneys, but not in normal kidneys (p<0.001, for diabetic rats; p=0.345, for normal rats).

CONCLUSION

Ionic low-osmolar contrast media induced more apoptosis in tubular cells in diabetic kidneys than in normal kidneys. Notably, ionic contrast media induced more apoptosis than nonionic contrast media in diabetic kidneys.

摘要

背景

对比剂肾病是医院获得性急性肾衰竭的主要原因,糖尿病患者的风险显著增加。本研究旨在探讨凋亡在正常和糖尿病大鼠低渗造影剂诱导的肾损伤中的作用,以及离子型和非离子型造影剂诱导的肾损伤的差异。

方法

正常和链脲佐菌素诱导的糖尿病 Wistar 大鼠分别给予离子型低渗碘海醇、非离子型低渗碘普罗胺或生理盐水注射。通过末端脱氧核苷酸转移酶介导的 dUTP 原位缺口末端标记(TUNEL)染色确定肾小管细胞凋亡。

结果

给药后 24 小时,碘海醇和碘普罗胺注射均可诱导糖尿病大鼠(碘海醇为 49.7%对 25.3%;碘普罗胺为 37.7%对 25.3%;均<0.001)和正常大鼠(碘海醇为 36.2%对 27.4%,p=0.002;碘普罗胺为 33.6%对 27.4%,p=0.029)肾小管细胞凋亡增加,高于生理盐水注射组。此外,碘海醇在糖尿病肾脏中诱导的肾小管细胞凋亡多于正常肾脏(p<0.001)。此外,碘海醇在糖尿病肾脏中诱导的凋亡细胞明显多于碘普罗胺,但在正常肾脏中无差异(糖尿病大鼠,p<0.001;正常大鼠,p=0.345)。

结论

离子型低渗造影剂在糖尿病肾脏中诱导的肾小管细胞凋亡多于正常肾脏。值得注意的是,离子型造影剂在糖尿病肾脏中诱导的凋亡多于非离子型造影剂。

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