Department of Radiology and Biomedical Imaging, University of California San Francisco, Box 0628, M-372, 505 Parnassus Avenue, San Francisco, CA, 94143-0628, USA.
Division of Cardiology, San Francisco Veterans Affairs Medical Center, 4150 Clement Avenue, San Francisco, CA, 94121, USA.
Abdom Radiol (NY). 2016 Jan;41(1):91-9. doi: 10.1007/s00261-015-0611-9.
To compare the incidence of contrast-induced nephropathy (CIN) for intravenous vs. intra-arterial administration of iodixanol, compared to non-administration.
We retrospectively identified 650 patients who had intravenous iodixanol-enhanced CT, 695 with intra-arterial iodixanol cardiac catheterization, 651 with unenhanced CT, and those who also had baseline and follow-up serum creatinine within 5 days of the exam. From the medical records, we recorded the gender, age, baseline and follow-up serum creatinine/eGFR; underlying renal injury risk factors; indication for imaging; contrast material administration volume, concentration, and route of administration; and use of pre-imaging prophylactic measures for CIN. Univariate and multivariate models were used to determine predictors of CIN.
Baseline eGFR was lower for patients undergoing unenhanced CT than intravenous or intra-arterial patients (68 vs. 74.6 and 72.2, respectively, p < 0.01) and not different between intravenous and intra-arterial patients (p = 0.735). Simple logistic regression did not show a difference in the rate of CIN in patients who received intravenous vs. intra-arterial iodixanol (28 of 650, 4%, vs. 28 of 695, 4%, respectively, p = 0.798), nor a higher rate of CIN than seen with unenhanced CT (45 of 651, 7%, p = 0.99 and p = 0.98 by one-sided t test). Multivariate regression modeling showed that only elevated baseline creatinine or decreased eGFR and low hematocrit/hemoglobin were associated with CIN incidence (odds ratio 1.28 and 2.5; p < 0.023 and <0.006, respectively).
Elevation in serum creatinine due to intravenous and intra-arterial iodixanol administration is infrequent and is not more common than after unenhanced CT scans.
比较静脉内与动脉内给予碘克沙醇后对比剂诱导肾病（CIN）的发生率，与未给予碘克沙醇者相比。
我们回顾性地确定了 650 例接受静脉内碘克沙醇增强 CT、695 例接受动脉内碘克沙醇心导管检查、651 例接受未增强 CT 检查且在检查后 5 天内有基线和随访血清肌酐的患者。从病历中，我们记录了性别、年龄、基线和随访血清肌酐/肾小球滤过率（eGFR）；潜在的肾损伤危险因素；影像学适应证；造影剂给予量、浓度和途径；以及 CIN 影像学前预防性措施的使用。采用单变量和多变量模型确定 CIN 的预测因素。
与静脉内或动脉内患者相比，行未增强 CT 检查的患者基线 eGFR 更低（分别为 68 与 74.6 和 72.2，p < 0.01），但静脉内与动脉内患者间 eGFR 无差异（p = 0.735）。简单的逻辑回归分析显示，接受静脉内与动脉内碘克沙醇的患者 CIN 发生率无差异（分别为 650 例中的 28 例，4%，与 695 例中的 28 例，4%，p = 0.798），也不比未增强 CT 更高（651 例中的 45 例，7%，单侧 t 检验 p = 0.99 和 p = 0.98）。多变量回归模型显示，只有基线肌酐升高或 eGFR 降低及低血细胞比容/血红蛋白与 CIN 发生率相关（比值比 1.28 和 2.5；p < 0.023 和 <0.006）。
静脉内和动脉内给予碘克沙醇后血清肌酐升高不常见，且不比未增强 CT 扫描更常见。
