Sheng Liu

CTA and CTP are the most frequently used noninvasive vascular imaging techniques to evaluate acute ischemic stroke (AIS).^1,2 Although previous studies suggest that the risk of contrast-induced acute kidney injury (AKI) secondary to CTA/CTP imaging is relatively low in patients with AIS,^1–3 the potential risk from iodinated contrast exposure is proportional to the dose of contrast medium administered, and multiple, consecutive doses of contrast medium could imply a greater risk for AKI.^4,5 We therefore performed this prospective study to determine whether additional use of contrast during endovascular treatment of AIS increases the risk of AKI.

Our study showed that CTA and endovascular treatment did not increase the rate of AKI in patients with AIS (7.4%) compared with the 1-time use of contrast for CTA (2.3%) (P = .172). Although we observed a trend toward an increased incidence of AKI after using more contrast in the original research, we did not find a significant difference after enlargement of the sample size. Additionally, recent device innovations (like balloon guide catheters and aspiration catheters) have made previously dif­ficult cases easy to manage, and the volume of the iodinated contrast used in the procedure is reduced, which may lower the risk of contrast dose–related AKI.⁶

For lack of midterm and long-term follow-up, our study only presented the incidence of AKI. Currently, we are collecting the 6-month follow-up data to evaluate the delayed kidney injury and the long-term sequelae induced by contrast.

As for the topic of contrast-induced AKI, we also agree with another hypothesis: AKI may be a surrogate marker reflecting critical illness and multimorbidity rather than a factor determining patient outcome.⁷ Accumulating evidence from experimental studies as well as observational studies suggests that stroke may lead to kidney dysfunction via biologic communication through central neural and peripheral humoral pathways.⁸ Therefore, in the setting of AIS, AKI should not be viewed as a single disease, and when AKI is recognized, a critical first step is the prompt evaluation for all possible causes of it.

Because the available evidence showed that a large amount of contrast is less likely to cause AKI in patients with AIS, it is reasonable to save the brain first regardless of the patient’s baseline renal function. It may be more reasonable to treat AKI as a comorbidity of AIS.

References

1. Brinjikji W, Demchuk AM, Murad MH, et al. Neurons over nephrons: systematic review and meta-analysis of contrast-induced nephropathy in patients with acute stroke. Stroke 2017;48:1862–68
2. Ehrlich ME, Turner HL, Currie LJ, et al. Safety of computed tomographic angiography in the evaluation of patients with acute stroke: a single-center experience. Stroke 2016;47:2045–50
3. Demel SL, Grossman AW, Khoury JC, et al. Association between acute kidney disease and intravenous dye administration in patients with acute stroke: a population-based study. Stroke 2017;48:835–39
4. Rao QA, Newhouse JH. Risk of nephropathy after intravenous administration of contrast material: a critical literature analysis. Radiology 2006;239:392–97
5. Krol AL, Dzialowski I, Roy J, et al. Incidence of radiocontrast nephropathy in patients undergoing acute stroke computed tomography angiography. Stroke 2007;38:2364–66
6. Jia ZY, Wang SX, Zhao LB, et al. Risk of acute kidney injury with consecutive, multidose use of iodinated contrast in patients with acute ischemic stroke. AJNR Am J Neuroradiol 2019;40:652–54
7. Li X, Partovi S. Save the brain first: CTA and mechanical thrombectomy in patients at risk for contrast-induced nephropathy. AJNR Am J Neuroradiol 2020;41:637–38
8. Zhao Q, Yan T, Chopp M, et al. Brain-kidney interaction: renal dysfunction following ischemic stroke. J Cereb Blood Flow Metab 2020;40:246–62

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