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We aimed to develop a novel simple experimental model in mice for low-osmolar contrast-induced acute kidney injury (CI-AKI) with different definitions for AKI that would be comparable to CI-AKI in humans.
Fifty Sprague-Dawley rats were divided into five groups of 10 rats each: (1) sham group (normal saline [NS] + NS); (2) NS plus contrast medium (CM15) (NS+CM15); (3) furosemide (FM) plus NS (FM + NS); (4) FM+CM10; and (5) FM + CM15. After they were acclimatized for 7 days, and 6 h before CM administration, FM (10 mL/kg) was administered to groups 3, 4 and 5. Then, after restricted access to water for 6 h in all the groups, groups 2 and 5 received low-osmolality CM (LOCM) (iopromide, 15 mL/kg) in the tail vein, and group 4 received LOCM (10 mL/kg) under ether anesthesia. Serum creatinine (SCr) and cystatin C (cys-C) levels were measured and histopathological scores were determined in kidney tissues.
In the FM + CM15 group, SCr concentration was significantly higher after CM exposure than before (32.9 ± 4.57 vs. 158.7 ± 14.48 μmol/L, p < 0.001). In the other groups, there were minor changes in the SCr levels between the pre- and post- CM or NS exposure. In addition, the cys-C levels were also higher after CM exposure than that before in the FM+CM15 group (0.08 ± 0.03 vs. 0.18 ± 0.05 mg/L, p < 0.001). There were minor changes in the FM + NS group before and after NS administration. Furthermore, only rats in the FM + CM15 group developed CI-AKI based on the definitions for SCr or cys-C. The histopathological scores were significantly higher in the FM + CM15 group than in the FM + NS group.
We developed a simple and reliable animal model for LOCM-induced AKI that is similar to clinical CI-AKI based on different definitions for AKI.