NEW ORLEANS -- Contrast-enhanced CT angiography (CTA) reduced acute kidney injury (AKI) in patients with suspected coronary artery disease, researchers reported here.
In a cohort of patients with suspected coronary artery disease (CAD), contrast-induced AKI occurred in 6% of the patients who received coronary CTA with intravenous contrast (95% CI 3-10%) compared with 13% of patients who received invasive coronary angiography (ICA) with intracoronary contrast (95% CI 8-19%, P=0.023), according to Marc Dewey, MD, of Charité Medical University Berlin, and colleagues.
Action Points
- Note that this study was published as an abstract and presented at a conference. These data and conclusions should be considered to be preliminary until published in a peer-reviewed journal.
"If I was to put the findings in a 30-second elevator pitch, I would say that coronary CTA with intravenous contrast reduces acute kidney injury in patients with suspected coronary artery disease compared with cardiac catheterization," Dewey said in a presentation at ASN Kidney Week 2017.
He added that patients prefer CTA because it's less invasive, while physicians prefer it because it's an easier and shorter procedure. "It's a win-win for patients -- and maybe a loss for people doing cardiac catheterization," he said.
Commenting on the study, Oisin O'Corragain, MD, of Temple University Lewis Katz School of Medicine in Philadelphia, said "Overall, this study did nicely show that digital subtraction angiography has nearly double the risk of AKI versus CT angiography -- a not unexpected finding -- and did show that those with AKI did progress to [chronic kidney disease or CKD] faster, or had more significant progression of pre-existing CKD compared with those without."
However, "based on the information provided in the presentation, it was an unnecessary [randomized, controlled trial] with vague findings that does not contribute a huge amount to the area," O'Corragain, who was not involved in the study, told 鶹ý.
Swapnil Hiremath, MD, MPH, of the University of Ottawa in Canada, commented that the "trial pushes back against the growing narrative that contrast-induced AKI does not exist ... it fits with the mechanistic understanding of how contrast causes kidney damage.
"Caveats are that the risk was higher mainly in the subgroup who underwent angiogram via the femoral route, suggesting this may have been driven by atheroembolic damage rather than contrast," note Hiremath, who was not involved in the study.
Dewey's group recruited patients from Charite University Hospital Berlin from February 2009 to August 2015. Patients were eligible if they had suspected CA and a clinical indication for ICA based on atypical chest pain.
Patients were randomized 1:1 to ICA with intracoronary contrast (N=162) or to CTA with intravenous contrast (N=165). The same low-osmolar non-ionic contrast agent was used for both imaging procedures. Baseline estimated glomerular filtration rates were not significantly different between patients in the CTA (84.3±17.2 mL/min/1.73 m2) and the ICA group (87.1±16.7 mL/min/1.73 m2; P=0.14).
The primary outcome was defined as contrast-induced AKI within 3 days following contrast agent administration and an increase in serum creatinine of ≥0.5 mg/dL or 25% after 18-24 hours or 46-50 hours.
The researchers found that follow-up creatinine after 18-24 hours or 46-50 hours was available for 159 patients (98%) in the ICA group and 161 (98%) in the CTA group.
When only patients without obstructive CAD were analyzed, contrast-induced AKI occurred less often in the CTA group (4.3%) compared with the cardiac catheterization group (11.9%, P=0.024).
Importantly, blood tests completed after a median duration of 1.9 years showed a greater proportion of patients with AKI still had increased creatine compared with those without AKI (38% versus 6%; P<0.001).
Dewey listed several issues that may have led to the results, including a smaller contrast agent volume (66 ml for CTA versus 87 ml for ICA, P=0.01), microshowers of cholesterol emboli into renal arteries, and that femoral access increased AKI by 2% in acute coronary syndrome.
Study limitations included a large variability in adherence to hydration recommendations and an inability to use invasive measurement for guiding fluid administration.
Hiremath cited the limited data on baseline kidney function, which prevented study generalizability, as another limitation. O'Corragain agreed that background data were limited, with only a passing mention that the majority of these patients had near normal eGFR.
Dewey concluded that the findings should be "considered for clinical decision-making in patients who have a clinical indication for imaging procedures with intravenous or intraarterial contrast agent administration" and that further randomized trials in other patient cohorts are warranted.
Disclosures
Dewey disclosed non-U.S. government support.
Primary Source
ASN Kidney Week 2017
Dewey M, et al "Kidney injury after intravenous or intracoronary contrast agents for noninvasive or invasive coronary angiography: An industry-independent, phase 3, randomized controlled trial" ASN 2017; Abstract SA-OR123.