OBJECTIVE: Acute kidney injury is common among hospitalized patients and likely leads to inflated reports of the incidence of CT contrast agent-induced nephropathy as a cause of acute kidney injury. For a more accurate estimation, we compared the incidence of acute kidney injury immediately after contrast agent administration and a few days afterward in the same population. We also controlled for a creatinine level increase starting before and continuing after CT, which may be incorrectly associated with the scan itself. MATERIALS AND METHODS: After excluding patients undergoing dialysis, we included all adults who underwent CT from January 2006 through May 2013 in our health region. The incidence of acute kidney injury (Acute Kidney Injury Network stages) and dialysis after acute kidney injury were assessed in the immediate period (24-48 hours) and in a delayed period (72-96 hours) after the scan. New acute kidney injury in either period occurred if the creatinine level had increased at a greater rate than that in a preceding 24-hour interval. The incidence of acute kidney injury and dialysis after acute kidney injury attributable to CT were calculated by subtracting the delayed incidence from the immediate incidence. RESULTS: Incidences of acute kidney injury and dialysis after acute kidney injury attributable to contrast-enhanced CT were statistically insignificant across glomerular filtration rate (GFR) subgroups. Acute kidney injury incidences (Acute Kidney Injury Network stage I or worse) were 0.5% (95% CI, -0.4% to 1.4%) for GFR greater than 60 mL/min/1.73 m(2), 2.4% (95% CI, -0.7% to 5.6%) for GFR 30-59 mL/min/1.73 m(2), -4.3% (95% CI, -19.8% to 11.3%) for GFR 15-29 mL/min/1.73 m(2), and 0% (95% CI, -24.5% to 24.5%) for GFR less than 15 mL/min/1.73 m(2). CONCLUSION: There appears to be a minimal risk of CT contrast agent-induced nephropathy at mild to moderate levels of renal dysfunction.
OBJECTIVE:Acute kidney injury is common among hospitalized patients and likely leads to inflated reports of the incidence of CT contrast agent-induced nephropathy as a cause of acute kidney injury. For a more accurate estimation, we compared the incidence of acute kidney injury immediately after contrast agent administration and a few days afterward in the same population. We also controlled for a creatinine level increase starting before and continuing after CT, which may be incorrectly associated with the scan itself. MATERIALS AND METHODS: After excluding patients undergoing dialysis, we included all adults who underwent CT from January 2006 through May 2013 in our health region. The incidence of acute kidney injury (Acute Kidney Injury Network stages) and dialysis after acute kidney injury were assessed in the immediate period (24-48 hours) and in a delayed period (72-96 hours) after the scan. New acute kidney injury in either period occurred if the creatinine level had increased at a greater rate than that in a preceding 24-hour interval. The incidence of acute kidney injury and dialysis after acute kidney injury attributable to CT were calculated by subtracting the delayed incidence from the immediate incidence. RESULTS: Incidences of acute kidney injury and dialysis after acute kidney injury attributable to contrast-enhanced CT were statistically insignificant across glomerular filtration rate (GFR) subgroups. Acute kidney injury incidences (Acute Kidney Injury Network stage I or worse) were 0.5% (95% CI, -0.4% to 1.4%) for GFR greater than 60 mL/min/1.73 m(2), 2.4% (95% CI, -0.7% to 5.6%) for GFR 30-59 mL/min/1.73 m(2), -4.3% (95% CI, -19.8% to 11.3%) for GFR 15-29 mL/min/1.73 m(2), and 0% (95% CI, -24.5% to 24.5%) for GFR less than 15 mL/min/1.73 m(2). CONCLUSION: There appears to be a minimal risk of CT contrast agent-induced nephropathy at mild to moderate levels of renal dysfunction.
Entities:
Keywords:
CT; IV contrast agent; contrast agent–induced nephropathy
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