Methods Sixty Sprague-Dawley rats were randomly divided into a model group and a control group, with 30 rats in each group. The model group was injected with 50% glycerin saline at 10 ml/kg intramuscularly, and the control group was injected with 0.9% saline at 10 ml/kg intramuscularly. At 0.5, 2, 6, 12, and 24 h after injection, six rats in each group were examined by CEUS. Renal cortical and medullary time-intensity curve (TIC) and related quantitative parameters [ascending slope (AS), area under the curve (AUC), descending slope (DS), descending time/2 (DT/2), peak intensity (PI)] were obtained to analyze the CEUS characteristics at different time points. Blood was collected from the inferior vena cava at the end of the examination to detect the serum levels of urea nitrogen, creatinine, cystatin C, and creatine kinase, and pathological sections were prepared for observation after renal tissue was fixed. The t-test or Mann Whitney U test was used to compare the differences in relevant quantitative parameters and serum biochemical indexes between groups, and one-way ANOVA or Kruskal-Wallis H test was used to compare the differences in various indexes at different time points within the groups.
Results Compared with the control group, the levels of serum creatinine, urea nitrogen, and creatine kinase at 0.5, 2, 6, and 12 h and the levels of serum cystatin C at 2 and 6 h were significantly increased in the model group (serum creatine kinase: Z=-2.242, P=0.025; Z=-2.882, P=0.004; Z=-2.882, P=0.004; Z=-2.562, P=0.010; urea nitrogen: t=4.288, P=0.002; t=4.450, P=0.001; t=10.812, P＜0.001; t=5.260, P＜0.001; creatinine: t=6.327, P=0.001; t=10.577, P＜0.001; t=2.612, P=0.035; t=4.694, P=0.001; cystatin C: t=3.460, P=0.009; t=2.391, P=0.038). In the model group, the cortical AUC at 0.5 h was significantly increased [(2636.84±150.99) dB·s vs (2308.20±210.50) dB·s, t=3.107, P=0.011], the cortical DS at 2, 6, and 12 h and cortical AS at 6, 12, and 24 h were significantly decreased [DS: (0.16±0.05) dB/s vs (0.23±0.03) dB/s, t=-3.342, P=0.007; (0.16±0.03) dB/s vs (0.23±0.04) dB/s, t=-3.542, P=0.005; (0.16±0.05) dB/s vs (0.23±0.03) dB/s, t=-3.226, P=0.009; AS: (0.54±0.22) dB/s vs (0.84±0.15) dB/s, t=-2.733, P=0.021; (0.58±0.21) dB/s vs (0.86±0.20) dB/s, t=-2.318, P=0.043; (0.67±0.20) dB/s vs (0.96±0.13) dB/s, t=-2.809, P=0.019], and the cortical DT/2 at 12 h was significantly increased [(55.78±12.28) s vs (40.09±6.29) s, t=2.789, P=0.019]. The medullary AUC at 0.5, 2, 6, and 12 h was significantly increased [(2382.40±189.84) dB·s vs (1910.82±140.13) dB·s, t=5.025, P=0.001; (2637.35±258.55) dB·s vs (1999.88±409.52) dB·s, t=3.217, P=0.009; (2424.63±409.39) dB·s vs (1910.47±263.59) dB·s, t=2.669, P=0.0024; (2353.54±348.2) dB·s vs (1958.43±95.37) dB·s, t=3.014, P=0.013], the medullary DS and AS at 2 and 6 h were significantly decreased [DS: 0.13 (0.07, 0.15) dB/s vs 0.22 (0.19, 0.24) dB/s, Z=-2.892, P=0.004; 0.13 (0.11, 0.16) dB/s vs 0.21(0.20, 0.23) dB/s, Z=-2. 585, P=0.010; AS: (0.44±0.22) dB/s vs (0.77±0.14) dB/s, t=-3.063, P=0.015; (0.41±0.21) dB/s vs (0.80±0.10) dB/s, t=-4.042, P=0.005], and the medullary DT/2 at 2, 6, and 12 h was significantly increased [(61.44±15.52) s vs (38.88±8.80) s, t=3.105, P=0.011; (54.60±12.47) s vs (37.59±8.71) s, t=2.724, P=0.021; (56.08±14.57) s vs (38.42±6.00) s, t=3.003, P=0.013]. The pathological examination showed that the glomerular and tubular structures were normal in the control group. In the model group, the glomerular structure did not change significantly, the brush border of some tubules was sloughed off, the epithelial cells were flattened, the dilation of the tubular lumen was obvious starting at 0.5 h, with the distal tubules being the most prominent one, tubular cast appeared at 2 h, and the pathological changes were aggravated with the prolongation of time, being the most severe at 24 h.