Author + information
- Kaiser Permanente Los Angeles Medical Center, and the David Geffen School of Medicine, University of California-Los Angeles, Los Angeles, California
- ↵∗Address for correspondence:
Dr. Somjot S. Brar, Kaiser Permanente Los Angeles Medical Center, 4867 Sunset Boulevard, Third Floor, Room 3753, Los Angeles, California 90027.
Contrast-induced acute kidney injury (CI-AKI) remains a serious complication of cardiac catheterization. CI-AKI results in prolonged hospitalization, increased health care costs, heightened risk of myocardial infarction, renal replacement therapy, and death. Thus, the CI-AKI rate after cardiac catheterization is a quality improvement metric that is becoming increasingly important as the health care environment shifts to value-based care. Systematically measuring CI-AKI rates in the catheterization laboratory and being able to compare across centers and operators can provide insight into variations of care and identify opportunities for quality improvement (1).
A common impediment to reducing the rate of CI-AKI post-procedure is often the lack of adequate risk assessment and absence of institutional protocols. Adoption of simple low-cost strategies has been shown to markedly reduce the CI-AKI rate in a large network of hospitals (2). Effective CI-AKI prevention strategies include calling out the estimated glomerular filtration rate (eGFR), contrast threshold, and fluid administration strategy during the pre-procedure timeout. Doing so in a systematic fashion has been shown to contribute to a reduction in the volume of contrast administered, increase the volume of fluid administered, and significantly lower the CI-AKI rate (2). A standardized fluid administration protocol should be integrated into the electronic medical record or as a pre-printed order set to improve compliance in eligible patients. Furthermore, each catheterization laboratory should have a process to track the CI-AKI rate; risk-adjusted CI-AKI metrics are available through quality improvement programs such as the National Cardiovascular Data Registry/CathPCI registry.
The report by Maioli et al. (3) in this issue of the Journal describes a novel fluid administration strategy for CI-AKI prevention based on bioimpedance vector analysis (BIVA), a noninvasive measure of total body fluid. The investigators used BIVA to identify patients with low total body fluid levels who were scheduled for elective coronary angiography. Patients were randomized to receive an isotonic saline (0.9% sodium chloride) infusion at 1 versus 2 ml/kg/h for 12 h before and after the procedure. The incidence of CI-AKI was significantly lower with the higher fluid administration rate: 11.5% versus 22.3% (p = 0.015). These results are consistent with a growing body of evidence that higher rates of fluid administration are more effective in reducing the contrast-induced CI-AKI rate. For example, higher fluid administration rates (up to 5 ml/kg/h), guided by the left ventricular end-diastolic pressure, result in a significant reduction in CI-AKI (4). However, invasive hemodynamic parameters are not available for all patients, such as those undergoing noncardiac procedures. Thus, BIVA, a noninvasive measure of total body fluid volume, could be used to guide fluid administration in settings in which cardiac hemodynamic parameters are not readily available.
The choice of an endpoint in a clinical trial affects the interpretation of the results and the ability to compare event rates with other studies. Maioli et al. (3) chose a novel endpoint; CI-AKI was defined as an increase in cystatin C of ≥10% 24 h after contrast exposure. The principal advantage of this endpoint is the potential early detection of CI-AKI and thus the need for 1 blood test 24 h post-procedure. Although obtaining 1 sample shortly after the procedure is clearly convenient for the patient and decreases missing data in a trial, more research is needed to confirm whether a single cystatin C measurement can replace the more common regimen of 2 serum creatinine samples obtained on days 1 to 4 post-procedure, a protocol that is common in many CI-AKI prevention trials. Moreover, whether a ≥10% increase in cystatin C from baseline is the optimal threshold that best correlates with major adverse clinical events warrants further investigation. Although cystatin C has shown some promise as an early biomarker of kidney injury, more research is needed; whether it will be the long-sought-after marker of early kidney injury, as troponin is for cardiac injury, remains to be seen (5).
In general, it is desirable to use endpoints that are standardized or frequently reported to facilitate comparison between trials. It would have been preferable had the investigators (3) also reported the CI-AKI rate by using the commonly used CI-AKI definition of a 25% relative increase or 0.5 mg/dl absolute increase in serum creatinine. In patients with stable angina, unstable angina, or non–ST-segment elevation acute coronary syndrome, the CI-AKI rate using this definition is ∼10% to 20% (4,6–8). Reporting the event rate using this commonly used CI-AKI definition would have facilitated comparison of the findings of the present report with previously published studies. Event rates significantly lower or higher than those observed in previous trials may raise concerns about the generalizability of the findings. Fortunately, the investigators do report CI-AKI using other definitions. The CI-AKI rate defined as a ≥0.5 mg/dl increase in serum creatinine level within 72 h was 3.4% versus 7.4%, a difference that did not reach statistical significance (p = 0.19), but the event rate in the control group was similar to other trials, which is somewhat reassuring.
It is also imperative that CI-AKI prevention studies recruit patients at reasonable risk for this complication. Most trials enroll patients with an estimated GFR of ≤60 ml/min/1.73 m2 because values higher than this one are associated with low rates of CI-AKI. There is a concerning trend in which patients with little to no baseline renal impairment are being recruited into CI-AKI prevention trials. Although using this approach considerably accelerates recruitment, it makes the findings of such trials difficult to interpret, especially when positive. In some populations such as ST-segment elevation myocardial infarction, in which cardiogenic shock is more prevalent, CI-AKI occurs at higher levels of renal function, but the mechanism of renal injury is likely multifactorial; acute tubular necrosis, related to hemodynamic compromise, likely plays a more significant role. In the present report (3), all patients were stable, as those needing urgent or emergency procedures were excluded. Therefore, it is somewhat concerning that only 42% of the randomized study population had creatinine clearance <60 ml/min. Despite these limitations, the findings from this report are consistent with the growing body of literature that more aggressive fluid administration decreases the rate of CI-AKI.
Although fluid administration is a key strategy in CI-AKI prevention, the duration of fluid administration has practical implications. Prolonged fluid administration, such as the 24 h required in the present report (3), can be challenging in many health care settings. In an era of increasing health care costs, a 24-h fluid administration protocol is not practical for patients undergoing elective cardiac catheterization. Research should focus on higher rates of fluid administration over significantly shorter time periods.
Although significant progress has been made in understanding and mitigating the risk of CI-AKI, vulnerable populations remain for whom novel solutions are still needed. Unfortunately, fluid administration strategies are not feasible or safe for all patients. Those recently treated for a heart failure exacerbation, with severe valvular heart disease, or in hemodynamic distress may not be suitable candidates for aggressive fluid administration. CI-AKI prevention strategies in these groups are lacking.
Perhaps the key message for CI-AKI prevention is to keep the strategy simple: incorporate a discussion of eGFR and CI-AKI risk into the timeout, minimize contrast volume, use higher rates of intravenous fluids in appropriate patients, and track the institutional and operator CI-AKI rates. These simple, low-cost strategies are best incorporated into an institutional protocol (a sample protocol is shown in Table 1). Doing so results in a lower rate of CI-AKI, improved quality of care, and decreased costs for the health care system.
↵∗ Editorials published in the Journal of the American College of Cardiology reflect the views of the authors and do not necessarily represent the views of JACC or the American College of Cardiology.
Dr. Brar has reported that he has no relationships relevant to the contents of this paper to disclose.
- 2018 American College of Cardiology Foundation
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