ArticleBMC nephrology2019
A novel simple experimental model for low-osmolar contrast-induced acute kidney injury using different definitions based on the levels of serum creatinine and cystatin C.
Article in BMC nephrology, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.
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Who cites it
4 citing papers in PubMed.
- The Association of Intraindividual Difference Between Cystatin- and Creatinine-Based Estimated GFR and Contrast-Associated Acute Kidney Injury.Clinical interventions in aging · 2024Article
- Signal pathways involved in contrast-induced acute kidney injury.Frontiers in physiology · 2024Review
- Establishment and assessment of a preclinical model of acute kidney injury induced by contrast media combined acute myocardial ischemia reperfusion surgery.Experimental and therapeutic medicine · 2023Article
- Research progress on animal models of contrast-induced acute kidney injury.Zhong nan da xue xue bao. Yi xue ban = Journal of Central South University. Medical sciences · 2023Article
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Authors and funding
8 authors.
Funding
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Abstract
backgroundIt remained lack of a kind of contrast-induced acute kidney injury (CI-AKI) model which was widely used in clinical practice and comparable to CI-AKI in humans.
methodsFifty Sprague-Dawley rats were divided into five groups of 10 rats each: (1) sham group (normal saline [NS] + NS); (2) NS plus low osmolality contrast medium (CM15) (NS + CM15); (3) furosemide (FM) plus NS (FM + NS); (4) FM + CM10; and (5) FM + CM15.We measured the levels of serum creatinine (SCr), cystatin C (cys-C) and histopathological scores of kidney tissues.
resultsSCr level in the FM + CM15 group were significantly increased after CM exposure compared with baseline levels (32.9 ± 4.57 vs. 158.7 ± 14.48 μmol/L, p < 0.001). Minor changes were found about the SCr levels between the pre- and post-exposure CM or NS treatment in the other groups. Additionally, the cys-C levels after CM exposure were increased compared with pretreatment levels in the FM + CM15 group (0.08 ± 0.03 vs. 0.18 ± 0.05 mg/L, p < 0.001). Minor changes were noted in the FM + NS group before and after NS administration. Only rats in the FM + CM15 group developed CI-AKI with the definitions of SCr or cys-C. Comparing to the FM + NS group, the histopathological scores were significantly increased in the FM + CM15 group.
conclusionsA simple and reliable animal model for low osmolality contrast medium-induced AKI was established, which is similar to clinical CI-AKI based on different definitions for AKI.
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