A novel rat model of contrast-induced acute kidney injury

Sun, Shiqun; Zhang, Tuo; Nie, Peng; Hu, Liuhua; Yu, Ying; Cui, Mingli; Cai, Zhaohua; Shen, Linghong; He, Ben

doi:10.1016/j.ijcard.2013.12.066

Cited by 22 publications

(31 citation statements)

References 8 publications

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“…Histopathological analysis revealed that all CI-AKI rats developed tubular necrosis and medullary congestion, indicating that this method efficiently leads to AKI in the rats. 13 All animal experimental protocols complied with the guidelines on animal care of Shanghai Jiao Tong University.…”

Section: Ci-aki Rat Modelmentioning

confidence: 99%

“…We hypothesized that the renal-specific miRNAs might be released into circulation during CI-AKI and could be used to detect kidney injury. Based on the rat model of CI-AKI we previously reported, 13 here we explore the changes in miRNA expression in plasma and kidney during CI-AKI. We identify miRNA-188, -30a, and -30e as the most consistently upregulated miRNA during the early stage following CM exposure.…”

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confidence: 99%

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Circulating MicroRNA‐188, ‐30a, and ‐30e as Early Biomarkers for Contrast‐Induced Acute Kidney Injury

Sun

Zhang

Ding

et al. 2016

JAHA

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BackgroundContrast‐induced acute kidney injury (CI‐AKI) is typically defined by an increase in serum creatinine after intravascular administration of contrast medium. Because creatinine is an unreliable indicator of acute changes in kidney function, we assessed whether circulating microRNAs (miRNAs) could serve as biomarkers for early detection of CI‐AKI.Methods and ResultsUsing a rat model of CI‐AKI, we first evaluated the miRNA profile of rat plasma and kidney. Three miRNA species with >1.5‐fold increase in plasma samples of CI‐AKI rats, including miRNA‐188, miRNA‐30a, and miRNA‐30e, were selected as candidate miRNAs. Quantitative real‐time polymerase chain reaction showed that these candidate miRNAs peaked in concentration around 4 hours after contrast medium exposure and were relatively renal‐specific. We compared the plasma levels of these candidate miRNAs in 71 patients who underwent coronary angiography or percutaneous coronary intervention and developed CI‐AKI with those of 71 matched controls. The plasma levels of the 3 candidate miRNAs were significantly elevated in the CI‐AKI group as compared to the control group. Receiver operating characteristic analysis showed that these miRNAs significantly distinguished patients with CI‐AKI from those without CI‐AKI. MiRNA composites were highly accurate for CI‐AKI prediction, as shown in maximized specificity by treble‐positive miRNA composite or maximized Youden index by any‐positive miRNA composite. Moreover, the selected miRNAs changes were associated with Mehran Risk Scores.ConclusionsPlasma levels of candidate miRNAs significantly distinguished patients with CI‐AKI from those without CI‐AKI. Thus, miRNAs are potential biomarkers for early detection of CI‐AKI.

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Section: Ci-aki Rat Modelmentioning

confidence: 99%

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confidence: 99%

Circulating MicroRNA‐188, ‐30a, and ‐30e as Early Biomarkers for Contrast‐Induced Acute Kidney Injury

Sun

Zhang

Ding

et al. 2016

JAHA

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“…In previous studies, pretreatment included introducing ischemic damage to the kidneys [2], some nephrotoxic drugs (e.g., aminoglycoside, cyclosporine A, glycerol, cisplatin, Adriamycin, etc.) [5, 6, 16], and dehydration [8, 10]. The nephrotoxic drug and ischemic damage are confounding factors and interfere with results in research [2].…”

Section: Discussionmentioning

confidence: 99%

A Novel Contrast-Induced Acute Kidney Injury Model Based on the 5/6-Nephrectomy Rat and Nephrotoxicological Evaluation of Iohexol and IodixanolIn Vivo

Liu

Luo

Tan

et al. 2014

Oxidative Medicine and Cellular Longevity

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Contrast-induced acute kidney injury (CI-AKI) is a serious complication in patients after administration of iodinated contrast media. Proper animal models of CI-AKI can help understand the mechanisms involved and prevent the disorder. We used the 5/6-nephrectomized (NE) rat to develop a CI-AKI model and to evaluate differences in the toxic effects on the kidney between iohexol and iodixanol. We found that six weeks after ablative surgery was the preferred time to induce CI-AKI. We compared multiple pretreatment plans and found that dehydration for 48 hours before iodixanol (320, 10 mL/kg) administration was optimal to induce CI-AKI in the 5/6 NE rats. Compared with iodixanol, iohexol induced a significantly greater reduction in renal function, severe renal tissue damage, intrarenal hypoxia, and apoptotic tubular cells. Iohexol and iodixanol resulted in similarly marked increases in levels of inflammation and oxidative stress. In summary, the 5/6 NE rat combined with dehydration for 48 hours is a useful pretreatment to establish a novel and reliable CI-AKI model. Iohexol induced more severe CI-AKI than iodixanol in this model.

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“…6 Furosemide (Harvest Pharmaceutical Co., Shanghai, China) was injected at 10 ml/kg intramuscularly. Omnipaque (350 mg I/ml, GE Healthcare, Shanghai, China), a nonionic low-osmolar contrast media, was injected at 20 ml/kg via tail vein administration over the course no less than 5 min.…”

Section: Induction Of Acute Kidney Injury By Contrast Mediamentioning

confidence: 99%

Xuezhikang ameliorates contrast media-induced nephropathy in rats via suppression of oxidative stress, inflammatory responses and apoptosis

Chu

Wang

et al. 2016

Renal Failure

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Background: The aim of this study was to assess the preventive effect of xuezhikang (XZK) to replace atorvastatin on the contrast media-induced acute kidney injury (CI-AKI). Methods: The male Sprague-Dawley rats were divided into five groups: group 1 (sham), injected with normal saline; group 2 (XZK), treated with XZK; group 3 contrast media (CM), injected with CM; group 4 (CM þ ATO), injected with CM þ pretreatment with atorvastatin; group 5 (CM þ XZK), injected with CM þ pretreatment with XZK. Twenty-four hours after injection with normal saline or CM, the blood sample and the kidneys were collected for the measurement of biochemical parameters, oxidative stress markers, nitric oxide production, inflammatory parameters, as well as renal histopathology and apoptosis detection. Results: Our results indicated that XZK restored the renal function by reducing serum blood urea nitrogen (BUN) and serum creatinine (Scr), depressing renal malondialdehyde (MDA), increasing renal NO production, decreasing TNF-A and IL-6 expression, attenuating renal pathological changes and inhibiting the apoptosis of renal tubular cells. Conclusion: XZK's therapeutic effect is similar, or even better than atorvastatin at the same effectual dose in some parts.

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A novel rat model of contrast-induced acute kidney injury

Cited by 22 publications

References 8 publications

Circulating MicroRNA‐188, ‐30a, and ‐30e as Early Biomarkers for Contrast‐Induced Acute Kidney Injury

Circulating MicroRNA‐188, ‐30a, and ‐30e as Early Biomarkers for Contrast‐Induced Acute Kidney Injury

A Novel Contrast-Induced Acute Kidney Injury Model Based on the 5/6-Nephrectomy Rat and Nephrotoxicological Evaluation of Iohexol and IodixanolIn Vivo

Xuezhikang ameliorates contrast media-induced nephropathy in rats via suppression of oxidative stress, inflammatory responses and apoptosis

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