Consensus Report from Oncology Advisory Board Meeting

18 • Strategies for Prevention and Management of CI-AKI and the Role of Contrast in Oncology CT Settings non-ionic, low-osmolar contrast agents, such as iohexol, iopamidol, iopromide, and ioversol; 80–150 ml, depending on body region. Patients were hydrated with normal saline at the rate of 40–60 ml/hour. AKI was defined as a serum Cr increase of ≥25% or ≥0.5 mg/dl over 48–72 hours. The incidence rate of CI-AKI in the study patients was 8% (Fig. 4). However, the authors acknowledged that exclusion of patients without Cr follow-up measurements may have influenced this incidence rate. Except for liver cirrhosis which was more prevalent in AKI-positive patients than non-AKI patients (9.1% vs 3.6%, respectively), there was no difference in comorbidities between the two groups. Furthermore, no relationship was found between the development of AKI and the type of CT, volume of CM used or number of CT scans performed. Mortality was higher in patients who developed AKI than those who did not (10.6% vs 2.3%, respectively; p=0.002) . Based on the findings, it was concluded that even in patients with normal or “near normal” baseline serum Cr levels, the rate of AKI could be substantial. Similarly, a prospective Turkish study has assessed the specific risk of CI-AKI in cancer patients with normal or near- normal kidney function at baseline [3]. The study patients had GFR >50 ml/min, were well-hydrated prior to undergoing CECT, and were not receiving nephrotoxic drugs other than chemotherapy. Contrast agent employed was iopromide or iohexol, in the amount of 50–100 ml depending on body region. AKI was defined as ≥25% or ≥0.5 mg/dl increase in serum Cr within 72 hours of CECT. The rate of AKI in this study was quite high (20%) compared with other reports, even though the patient population was selected to have good renal function at baseline. AKI developed in 26% patients who received chemotherapy vs 11% who did not receive it (p=0.1). The time between the last chemotherapy treatment and contrast administration, showed a significant association with the development of AKI. While the mean time between CECT and the last chemotherapy administration was 27 days (median 10, range 1–160) in patients who developed AKI, it was 66 days (median 25, range 1–350) in those who did not (p=0.1) develop it. The risk of AKI was significantly increased in patients who had CECT within 45 days vs those who had CECT >45 days after the last chemotherapy administration or those who never had chemotherapy (Fig. 5). Also, the risk of AKI was significantly increased among patients who had CECT within 45 days vs all other patients in the study. On logistic regression analysis, only CT within 45 days Fig. 3. Risk of AKI in cancer patients: MD Anderson analysis. AKI: acute kidney injury (≥50% increase in serum creatinine); CM: contrast medium; ICU: intensive care unit; IV: intravenous Source: [1] Fig. 4. AKI incidence in cancer patients in an emergency settings. *Non-simultaneous CECT performed 24–72 hours after first scan AKI: acute kidney injury (serum creatinine increase of ≥25% or ≥0.5 mg/dl over 48–72 hours); BUN/Cr: blood–urea–nitrogen/creatinine ratio; CECT: contrast- enhanced computed tomography; CT: computed tomography Source: Figure adapted from [2] Fig. 5. Effect of chemotherapy and CM on the incidence of AKI in hospitalized cancer patients undergoing CECT. AKI: acute kidney injury (≥25% or ≥0.5 mg/dl increase in serum creatinine within 72 hours); CECT: contrast-enhanced computed tomography; CM: contrast medium; OR: odds ratio Source: [3] JB6810 01-2016AKI in cancerpatients 0 5 10 15 20 25 30 35 40 ≤45 days since last chemotherapy >45 days since last chemotherapy No chemotherapy ≤45 days + no chemotherapy AKI incidence, % Effect of chemotherapy and CM on the incidence of AKI in hospitalised cancer patients undergoing CECT Cicin I et al. Eur Radiol 2014; 24 : 184 – 190. AKI: acute kidney injury (≥25% or ≥0.5 mg/dl increase in serum creatinine within 72 hours); CECT: contrast-enhanced computed tomography; CM: contrast medium; OR: odds ratio 35% 10% 11% 11% OR 5.4, p=0.033 OR 4.5, p=0.005 OR 4.0, p=0.019 JB6810 01-2016AKI in cancerpatients Risk of AKI in cancer patients: MD Anderson analysis Salahudeen AK et al. Clin J Am Soc Nephrol 2013; 8 : 347 – 54. AKI: acute kidney injury (≥50% i cr ase in s rum creatinine) CM: contrast medium ICU: intensive care unit IV: intravenous 0 1 2 3 4 5 6 Odds ratio (95% confidence interval) Multivariate analyses for factors associated with AKI in 3,558 patients admitted to MD Anderson Cancer Center Antibiotics Chemotherapy Diabetes Hyponatraemia Transfer to ICU IV CM 1.52 (1.15 – 2.02), p=0.004 1.61 (1.26 – 2.05), p<0.001 1.89 (1.51 – 2.36), p<0.001 1.97 (1.57 – 2.47), p<0.001 2.34 (1.66 – 3.31), p<0.001 4.55 (3.51 – 5.89), p<0.001 JB6810 01-2016AKI in cancerpatients Risk factors for AKI in cancer patients in an emergency setting Figure adapted from Hong SI et al. Support Care Cancer 2016; 24 : 1011 – 1017. *Non-simultaneous CECT performed 24 – 72 hours after first scan AKI: acute kidney injury (serum creatinine increase of ≥25% or ≥0.5 mg/dl over 48 – 72 hours); BUN/Cr: blood – urea – nitrogen/creatinine ratio; CECT: contrast-enhanced computed tomography; CT: computed tomography 0 3 6 9 12 15 Odds ratio (95% confidence interval) Overall AKI incidence: 8.0% (66/820 patients) Peritoneal seeding BUN/Cr >20 Liver cirrhosis Hypotension before CT Consecutive CECT* 1.75 (1.01 – 3.00) 2.54 (1.44 – 4.46) 2.82 (1.06 – 7.55) 3.95 (1.77 – 8.83) 4.09 (1.34 – 12.56)