Acute kidney injury post-PCI: Might a small behaviour change make a big difference?
CIN. CI-AKI. CA-AKI. PC-AKI? While the exact nature of the relationship between the administration of contrast media and post-procedural AKI is debated, some things are clear.
Firstly, CM are nephrotoxic.1 After administration, direct cytotoxicity to the renal tubular cells, medullary vasoconstriction, and oxidative stress can all contribute to potential kidney damage.1
Secondly, post-procedural AKI can have serious consequences. With no effective means of reversing injury once it has occurred, AKI following coronary interventions is associated with long-term worsening of kidney function, as well as increased cardiovascular morbidity and mortality.2
And thirdly, as the volume of contrast goes up, so too does the risk of AKI. Indeed, for every 100 ml of CM, the risk of developing post-procedural AKI can increase between 12 and 28%.3
It’s because of this well-documented association that contrast volume is included in most published risk models for AKI.2 Moreover, its inclusion in the guidelines of primary cardiological societies, including the EHC, AHA, ACC, and SCAI, suggests contrast volume is a risk factor that can be modified.2,4
Patients’ baseline renal function is a critical factor.2 Contrast is freely filtered, and in healthy kidneys, it is completely eliminated just 30 to 60 minutes after injection.2,5 But when GFR is reduced, contrast remains in circulation for a longer period of time.2
With fewer working nephrons, each has a larger load of CM to filter and the exposure burden per nephron is increased.2 As a result, a lower volume of CM may result in adverse effects in patients with pre-existing renal impairment, with the risk of AKI up to 10-fold greater when compared to those with normal kidney function.4,6
So how much contrast can be safely administered in these high-risk patients? To calculate a safe dose, equations that use patient-specific factors, such as serum creatinine and body weight, can be a useful guide.7,8 And while there isn’t a ‘one size fits all’ solution, a general rule is that the amount of CM used shouldn’t exceed two to three times a patient’s eGFR.5
One might expect that patients at higher risk of AKI would be treated with less contrast.8
Yet analysis of over 1.3 million patients included in the NCDR Cath PCI Registry found little evidence that physicians were limiting the amount of contrast in patients at higher risk of AKI.9
There were, however, substantial variations in AKI incidence (0 to 30%) and contrast volumes used (79 ml to 487 ml) among individual physicians performing PCIs.9 Some procedures, such as coronary angiography and stent insertion, may require more contrast.7 But interestingly, the variation in AKI remained even after accounting for the complexity of the procedure, or the degree to which patients were compromised, implying differences were due to physician practices.9
The authors concluded that the variation among physicians and the absence of an adjustment in contrast volume for patients at higher risk underscores an important opportunity to reduce AKI.9
So where to begin? A recent survey of international cardiologists suggests simply measuring contrast volume used would be a starting point for many.10 Among 506 cardiology practices, only 62% accurately measured volume. By implementing tools to track and report how much contrast has been used, feedback on areas for contrast reduction could be provided and best practices identified.11
Ultimately, AKI has serious clinical consequences.2 While the causality of the relationship between contrast volume and post-procedural AKI continues to be debated, the association is sufficient to warrant caution.3 Crucially, having any limit on contrast is probably more important than having none at all.2 And with only small changes making a potentially big difference, addressing the volume problem might just be an opportunity to tip the scales in favour of both cardiologists and their patients.10,12
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Abbreviations
ACC: American College of Cardiology AHA: American Heart Association AKI: acute kidney injury
CA-AKI: contrast-associated AKI
CI-AKI: contrast-induced AKI
CIN: contrast-induced nephropathy
CM: contrast media
ESC: European Society of Cardiology
eGFR: estimated GFR
GFR: glomerular filtration rate
NCDR: ACC National Cardiovascular Data Registry
PC-AKI: post-contrast AKI
PCI: percutaneous coronary intervention
SCAI: Society for Cardiovascular Angiography & Interventions
References
1. Seeliger E et al. Eur Heart J 2012; 33(16): 2007-15.
2. Solomon R. Am J Nephrol 2021; 52: 261-3.
3. Azzalini L et al. Can J Cardiol 2016; 32(2): 247-55.
4. Mullasari A, Victor SM. e-J Cardiol Pract 2014; 13(4).
5. Faggioni M, Mehran R. Interv Cardiol 2016; 11(2): 98-104.
6. Almendarez M et al. JACC Cardiovasc Interv 2019; 12(19): 1877-88.
7. Aoun J et al. Curr Opin Hypertens 2018; 27(2): 121-9.
8. Keaney JJ et al. Nephrol Dial Transplant 2013; 28(6): 1376-83.
9. Amin AP et al. JAMA Cardiol 2017; 2(9): 1007-12.
10. Prasad A et al. Catheter Cardiovasc Interv 2017; 89: 383-92.
11. Cox CE. Highs and Lows: Contrast Volume in PCI Varies Greatly Among US Physicians. Available at: https://www.tctmd.com/news/highs-and-lows-contrast- volume-pci-varies-greatly-among-us-physicians. Accessed on: 14.09.21.
12. Singh R, Zughaib M. Cardiol Res Pract 2019; 2019: 9238124.
