Contrast-Induced AKI After Intra-aterial and IV Contrast
Results
Between 2001 and 2010, 14287 patients underwent procedures requiring intra-arterial administration of iodinated contrast media in the five participating hospitals. In a total of 8870 patients no CT scan requiring intravenous contrast administration had been performed within one year prior to or after the intra-arterial contrast administration. These patients were excluded from the study as we were only interested in the risk of CI-AKI in patients who underwent both procedures. Another 1006 and 1063 patients were also excluded as the duration between both contrast procedures was less than 7 days or more than 1 year, respectively. Creatinine values were missing in 2354 patients. As a result 170 patients were included in our study (Figure 2).
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Figure 2.
Flow chart.
Patient and procedure characteristics are reported in Table I. Median time between the two contrast procedures was 37 days (2.5–97.5 percentile 7–324). Data on pre-contrast creatinine levels were available with a median of one day prior to both intravascular contrast procedures (2.5–97.5 percentiles: 0–96 for intra-arterial and 0–71 for intravenous contrast administration), with a similar time interval in patients who underwent intra-arterial contrast administration first and in patients in whom the order was the other way around. The duration between contrast administration and post contrast creatinine measurements was also equal in both groups, with a median of 3 days (2.5–97.5 percentile 1–7 for both procedures). Intravenous contrast-enhanced CT was preceded by an intra-arterial contrast procedure in 83/170 patients (49%) and in the remaining 87 patients it was the other way around. Median creatinine values at time of the first and second contrast exposure were 97 μmol/L (2.5–97.5, percentile 46–218) and 96 μmol/L (2.5–97.5, percentile 40–242), respectively.
Short-term Outcomes
In total, 39 patients developed CI-AKI by the definition of a serum creatinine increase >25% or >44 μmol/L. The risk of CI-AKI was 24/170 (14.0%, 95% CI 9.6–20.2) after intra-arterial versus 20/170 (11.7%, 95% CI 7.7–17.5) after intravenous contrast administration, which led to a relative risk of 1.2 (95% CI 0.7–2.1). Also, in 5/170 patients (2.9%, 95% CI 1.1–6.9), CI-AKI occurred after both procedures. Median time between contrast injections in these patients was 20 days (2.5–97.5, percentile 10–102). Furthermore, renal function had recovered after the first CI-AKI event before the second occurred in all five patients. In the entire population, CI-AKI occurred after the first contrast administration in 17.1% of patients (95% CI, 12.1–23.5) and in 8.8% (95% CI, 5.3–14.1) after the second. Patients who developed CI-AKI after the second event had similar baseline creatinine values prior to the first and second contrast procedure (median creatinine 101 μmol/L prior to both contrast procedures). The risk of CI-AKI after intra-arterial contrast administration was slightly higher in patients undergoing coronary catheterization or intervention compared with other procedures requiring intra-arterial contrast injections, with proportions of 18.9% (10/53, 95% CI10.4–31.6) and 12.0% (14/117, 95%CI 7.1–19.2), respectively. However, comparing the risk of CI-AKI in patients undergoing coronary contrast procedures with the risk of CI-AKI in the same patients after intravenous contrast-enhanced CT resulted in a relative risk of 1.3 (95% CI 0.5–2.9), with a CI-AKI risk after CT of 8/53 (15.1%). Moreover, patients in whom the intra-arterial contrast administration was accompanied by a coronary or non coronary intervention were not at increased risk of CI-AKI compared with patients in whom contrast was administered intra-arterially for diagnostic purposes only, with a relative risk of 0.9 (95% 0.4–1.9).
As for secondary outcomes, incidences of CI-AKI according to the two other CI-AKI definitions (serum creatinine increase >44 μmol/L or >100%) are illustrated in Figure 3, and resulted in relative risks comparing the incidences of CI-AKI after intra-arterial with intravenous contrast administrations of 0.6 (95% CI 0.3–1.4), and 0.3 (95% CI 0.4–3.2), respectively. None of the patients with CI-AKI according to the definition of an increase in serum creatinine >25% or >44 μmol/l had a need for dialysis. Median hospital stay duration in patients with CI-AKI was 15.0 days (2.5–97.5 percentile 1–92) after intra-arterial and 15.5 days (2.5–97.5 percentile 0–38) after intravenous contrast administration. However, 12/24 (50%) and 13/20 (65%) patients with CI-AKI after intra-arterial and intravenous contrast administration, respectively, were already admitted to the hospital prior to the contrast procedures for other reasons than CI-AKI. Reasons for admission in patients developing CI-AKI after intra-arterial contrast administration were complications of peripheral artery disease in 7 patients; coronary artery disease in 3; 1 patient was admitted for mitral valve replacement, and another patient, for a hypertensive emergency. For inpatients developing CI-AKI after intravenous contrast administration, reasons for admission were peripheral artery disease in four patients; complications of malignant disease in 2, aortic dissection, dehydration, ischemic stroke, renal transplantation, and ischemic bowel disease in one for each diagnosis, respectively.
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Figure 3.
Incidences of contrast induced-acute kidney injury according to three definitions.
Long-term Outcomes
Mortality data of 3/170 patients (1.8%) were missing. Hundred and fourteen of the 170 patients survived the first year of follow up. Median survival in the 53 patients who died was 155 days (2.5–97.5 percentile 2.0–359). Eight out of 39 (20.5%, 95% CI 10.5–35.8) CI-AKI patients died within 14 days after the diagnosis. Two of them had developed CI-AKI after intra-arterial contrast administration of which one was accompanied by an intervention. Three others had developed CI-AKI after intravenous contrast-enhanced CT and the last 3 after both contrast procedures. In 2 of the latter, the intra-arterial contrast administration was also companied by an intervention. Although cause of death was unknown, mortality risk for patients diagnosed with CI-AKI after either intra-arterial or intravenous contrast administration was compared with that of patients without CI-AKI, adjusting for comorbidity related to both CI-AKI and mortality (Table II). Hazard ratios for patients with CI-AKI after intra-arterial and intravenous contrast administration were 1.6 (95% CI 0.7–3.7) and 1.7 (95% CI 0.7–4.4), respectively.
We calculated renal function recovery rates between two weeks and six months after the CI-AKI diagnosis. Therefore, recovery of renal function was impossible for the eight CI-AKI patients who had died within 2 weeks after the diagnosis. Renal function recovered in 13/24 and 10/20 patients diagnosed with CI-AKI after intra-arterial and intravenous contrast administration, respectively. Renal function recovered after the first and second event in 5/5 and 2/5 patients who had developed CI-AKI after both events, respectively.