A novel rat model of contrast-induced nephropathy based on dehydration

Liu, Kun; Zhou, Lingyun; Li, Dai-Yang; Cheng, Wenjing; Wu, Yin; Wang, Jianglin; Zuo, Shi; Chen, Linhua; Zhang, Ge; Zuo, Xiaoxia

doi:10.1016/j.jphs.2019.09.003

Cited by 12 publications

(13 citation statements)

References 19 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Those authors also found that IOCM was associated with fewer adverse events than LOCM. Similarly, in different rat models of CIN, iohexol induced more severe kidney injury than iodixanol [ 42 , 43 ]. However, the recent meta-analysis by Han et al showed no significant difference between IOCM and LOCM in the incidence of CIN among diabetic patients, although a significant reduction in the risk of CIN was observed in the iodixanol group compared with the iohexol group [ 40 ].…”

Section: Risk Factorsmentioning

confidence: 99%

The Pathophysiology and the Management of Radiocontrast-Induced Nephropathy

Cho

2022

Diagnostics

View full text Add to dashboard Cite

Contrast-induced nephropathy (CIN) is an impairment of renal function that occurs after the administration of an iodinated contrast medium (CM). Kidney dysfunction in CIN is considered transient and reversible in most cases. However, it is the third most common cause of hospital-acquired acute kidney injury and is associated with increased morbidity and mortality, especially in high-risk patients. Diagnostic and interventional procedures that require intravascular CM are being used with increasing frequency, especially among the elderly, who can be particularly susceptible to CIN due to multiple comorbidities. Therefore, identifying the exact mechanisms of CIN and its associated risk factors is crucial not only to provide optimal preventive management for at-risk patients, but also to increase the feasibility of diagnostic and interventional procedure that use CM. CM induces kidney injury by impairing renal hemodynamics and increasing the generation of reactive oxygen species, in addition to direct cytotoxicity. Periprocedural hydration is the most widely accepted preventive strategy to date. Here, we review the latest research results on the pathophysiology and management of CIN.

show abstract

Section: Risk Factorsmentioning

confidence: 99%

The Pathophysiology and the Management of Radiocontrast-Induced Nephropathy

Cho

2022

Diagnostics

View full text Add to dashboard Cite

show abstract

“…The experimental mice were randomly divided into four groups (n = 18 in each group) as follows: control group, EPO group, CIN group, and EPO+CIN group. The mouse model of CIN was a modified version of a previously described model (14,15). In brief, after 7 days of acclimation to the experimental area and 24 h of water deprivation, mice were injected with indomethacin (10 mg/kg; MedChemExpress, NJ, USA) and N G -nitro-L-arginine methyl ester (10 mg/kg; MedChemExpress, NJ, USA) intraperitoneally before iohexol (6.0 g/kg organically bound iodine, General Pharmaceutical Co., Ltd., Shanghai, China).…”

Section: Animals and Contrast-induced Acute Kidney Injury Modelmentioning

confidence: 99%

Erythropoietin Attenuates Experimental Contrast-Induced Nephrology: A Role for the Janus Kinase 2/Signal Transducer and Activator of Transcription 3 Signaling Pathway

et al. 2021

View full text Add to dashboard Cite

The aim of the present study was to investigate the effect of erythropoietin (EPO) on contrast-induced nephrology (CIN) in vivo and in vitro. Male C57BL/6J mice were divided into four groups: control, CIN (iohexol 6.0 g/kg), EPO (3,000 IU/kg), and CIN+EPO. Hematoxylin and eosin (H&E) staining and biochemical index analyses were performed to evaluate renal injury. The cellular proliferation rate was detected using the Cell Counting Kit-8 (CCK-8) assay. In addition, a terminal deoxynucleotidyl transferase-mediated dUTP nick end labeling (TUNEL) assay and flow cytometric assay were used to assess the apoptosis of tissue and cells, respectively. Renal protein expression associated with apoptosis, pyroptosis, and signaling pathways was determined by Western blot (WB) assays for tissues and cells. The results showed that EPO significantly decreased serum creatinine, blood urea nitrogen, and cystatin C levels and alleviated renal histological changes in vivo. The protein levels of Janus kinase 2/signal transducer and activator of transcription 3 (JAK2/STAT3) signaling pathway components were overexpressed in the EPO treatment group. Furthermore, EPO suppressed the cell apoptosis and pyroptosis; decreased the protein levels of cleaved caspase-3, Bax, gasdermin D (GSDMD), and caspase-1; and enhanced the expression of Bcl-2. In summary, EPO could exert renoprotective effect by activating the JAK2/STAT3 signaling pathway, which may be a novel potential therapy for the treatment of CIN in the clinic.

show abstract

“…Several models reported dehydrating the rats for 24 to 48 hours prior to contrast administration (31)(32)(33)(34)(35)(36)(37). Efrati et al demonstrated that the renal physiological changes in response to CM are most pronounced in the dehydrated animal (38).…”

Section: Pre-test Conditionsmentioning

confidence: 99%

Experimental rat models for contrast-induced nephropathy; a comprehensive review

et al. 2020

View full text Add to dashboard Cite

Contrast-induced nephropathy (CIN) is an iatrogenic disease caused by the parenteral administration of iodinated contrast media (CM). A number of agents are currently being assessed to minimise or prevent CIN. Such agents are typically assessed using rat models. The aim of this study was to provide a comprehensive review of the rat models of CIN used in pre-clinical research. The MEDLINE, EMBASE, Web of Science and Cochrane databases were systematically searched. Articles reporting rat models of CIN were included for assessment. Study designs, contrast agents and outcome measures were assessed. Of the assessed studies, a majority report a requirement for pre-existing renal impairment prior to the administration of CM. Outcome measures are heterogenous between studies, but typically include assessment and quantification of serum biochemical markers, cellular oxidative stress and histopathological changes. The significant variation in methodology reported in the current literature highlights the lack of consensus. The use of a reliable pre-contrast insult appears critical to result in the development of contrast nephropathy. The use of acceptable outcome measures appears to include serum laboratory markers, quantification of reactive oxygen species (ROS) and objective histopathological outcomes. ABSTRACT Implication for health policy/practice/research/medical education:Contrast-induced nephropathy (CIN) is an iatrogenic disease caused by the parenteral administration of iodinated contrast media. A number of agents are currently being assessed to minimise or prevent CIN, of which initial assessment of these agents are typically assessed using rat models. We provide a comprehensive review outlining previously utilised rat models for the assessment of CIN. This paper is of benefit, as it highlights the different approaches to studying this model and provides a framework for future trials assessing novel agents. Please cite this paper as: Perera M, Ischia J, Bolton D, Shulkes A, Baldwin GS, Patel O. Experimental rat models for contrast-induced nephropathy; a comprehensive review. J Nephropathol. 2020;9(2):e12.

show abstract

A novel rat model of contrast-induced nephropathy based on dehydration

Cited by 12 publications

References 19 publications

The Pathophysiology and the Management of Radiocontrast-Induced Nephropathy

The Pathophysiology and the Management of Radiocontrast-Induced Nephropathy

Erythropoietin Attenuates Experimental Contrast-Induced Nephrology: A Role for the Janus Kinase 2/Signal Transducer and Activator of Transcription 3 Signaling Pathway

Experimental rat models for contrast-induced nephropathy; a comprehensive review

Contact Info

Product

Resources

About