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Editorial
Originally Published 20 August 2018
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Acute Kidney Injury After Transcatheter Aortic Valve Replacement: Better Understanding the Role of Aortic Atherosclerosis

See Article by Shishikura et al
Despite increasing awareness and strategies to limit iodinated contrast dye exposure, acute kidney injury (AKI) remains a common source of morbidity after invasive cardiology procedures. Although attention tends to focus on the most dreaded complication of acute dialysis, even milder forms of AKI result in prolonged average hospital stay, increased healthcare costs, and most importantly, increased morbidity and mortality in the short and long run.1 The relationship between AKI and outcomes is clearly evident in the setting of AKI after transcatheter aortic valve replacement (TAVR). Patients undergoing TAVR are older and sicker than the typical patient undergoing other types of common angiographic procedures. Published rates of post-TAVR AKI typically vary from 10% to 30% in the reported literature.2 Despite increasing awareness of an association between AKI and morbidity after TAVR, the pathophysiology remains murky at best. In this issue, Shishikura et al3 describe a novel method to identify patients at risk for AKI after TAVR through quantitative measurement of aortic atheroma volume. The authors report that total atheroma volume, but more importantly percent atheroma volume (PAV), specifically above the renal arteries (PAVabove renal arteries) were statistically significant predictors of the occurrence of AKI as well as a higher likelihood of attenuated recovery of kidney function post-AKI.
Detailed in their study, Shishikura et al3 report that 33% of the patients in their single-center cohort developed AKI of some degree. Although this incidence of AKI is high, the majority were stage I. AKI in this setting could be multifactorial, with 3 main contributors being ischemic tubular injury, contrast-induced nephrotoxicity, and cholesterol emboli. Though attributing AKI events to any of these mechanisms is tricky, the association of atheroma burden above the renal arteries in this study points to cholesterol emboli as a primary culprit. Indeed, a Dutch group reported the association of total atherosclerotic burden, especially noncalcified atherosclerosis, with AKI in a cohort of 210 patients, of whom 51 developed AKI (25%).4 Similarly, Kandathil et al5 studied a cohort of 106 patients and found that atherosclerosis, especially renal artery stenosis, was a predictor of AKI in 19% who did develop AKI. These are small single-center studies, but an increased incidence of AKI in suprarenal atheroma volume versus infrarenal atheroma volume merits attention in Shishikura et al’s3 model. Although overall total atheroma volume likely identifies patients of higher morbidity, the finding that only PAVabove renal arteries correlated with AKI provides a strong case for cholesterol emboli causing AKI. Nevertheless, this data requires validation in a larger population.
The severity of AKI described in this study deserves further attention. Seventeen patients (18.5% of all patients with AKI and 6% overall) developed stage III AKI. Of these, 8 patients (3% of overall cohort) required temporary hemodialysis. But does stage I and II AKI matter? Indeed, all AKI staging criteria include such small changes in creatinine for their prognostic value, but does preventing small changes in creatinine reduce clinical morbidity?6 The answer to this question, disappointingly, is no. In a meta-analysis of interventions that decreased rates of milder varieties of AKI, Coca et al7 found no difference in subsequent renal outcomes or mortality.
If the association of PAVabove renal arteries with post-TAVR AKI is validated, the question remains as to whether this study’s methodology to calculate PAVabove renal arteries is generalizable and feasible for all institutions performing TAVR and potentially other large bore arterial access. Although the authors’ postprocessing software is widely available and frequently used for TAVR preprocedural planning, their atheroma volume measurements were performed manually. Currently, this approach would be feasible for only a few specialized TAVR institutions. However, if calculations of PAVabove renal arteries prove to be a reproducible predictor of AKI, then one would hope that demand for this information could spur innovation in image processing and software for rapid acquisition. Until then, providers must manually outline atheroma themselves to try and replicate these results.
Although this study demonstrates a relationship between atheroma volume above the renal arteries and AKI, it is not clear if it is specific to the quantity of overall atheroma volume above the renal arteries or whether there is qualitative importance to the specific location of atheroma. What role do renal arterial aorto-ostial stenoses play in TAVR-related AKI? Were they excluded or inadvertently included in one group over another? This is unclear. In addition, one may ask if there is any prognostic importance in the histology of atheroma? Does elevated PAVabove renal arteries of uniform highly lipid atheroma impart any different risk of embolization than highly fibrotic or calcified atheroma? Calculating atheroma volume does not account for descriptive features such as eccentricity, mobility, or ulceration, which arguably could influence the probability of plaque embolization. Areas of future study could include whether additional targeted measures such as plaque eccentricity, calcium volumetric analysis, or further regionalization of atheroma may better predict AKI.
The most important question is whether identifying elevated PAVabove renal arteries can reduce the risk of AKI after TAVR? Awareness of elevated atheroma volume could influence an operator to more gently traverse the aorta. If this is even possible, the benefit may be limited given that passage of bulky catheters still needs to occur. During shared decision-making discussions between patient and physician, atheroma assessment may provide patients a better estimation of procedural risk. Perhaps this may influence low-risk patients to consider surgical valve replacement, but it is not clear that these measurements impact a patient’s prognosis if TAVR is deferred given the lack of data evaluating causation versus correlation. The authors’ suggestion that high-dose statins may reduce the risk of plaque embolization seems optimistic in patients who have been developing atheroma for decades. Dedicated embolic protection devices exist to reduce the risk of periprocedural embolic stroke during TAVR, but it is unclear if similar approaches in the descending aorta can lower the risk of AKI.8
In conclusion, the study by Shishikura et al3 provides meaningful knowledge in our understanding of periprocedural AKI during TAVR by demonstrating that elevated atheroma volume in the aorta, specifically above the renal arteries, may confer a higher risk of AKI. In many ways, this study raises more questions than answers in regards to causation and potential preventive strategies, but hopefully, clarity will be achieved now that we better appreciate that a relationship may exist between aortic atheroma and kidney function.

References

1.
James MT, Ghali WA, Knudtson ML, Ravani P, Tonelli M, Faris P, Pannu N, Manns BJ, Klarenbach SW, Hemmelgarn BR; Alberta Provincial Project for Outcome Assessment in Coronary Heart Disease (APPROACH) Investigators. Associations between acute kidney injury and cardiovascular and renal outcomes after coronary angiography. Circulation. 2011;123:409–416. doi: 10.1161/CIRCULATIONAHA.110.970160
2.
Najjar M, Salna M, George I. Acute kidney injury after aortic valve replacement: incidence, risk factors and outcomes. Expert Rev Cardiovasc Ther. 2015;13:301–316. doi: 10.1586/14779072.2015.1002467
3.
Shishikura D, Kataoka Y, Pisaniello AD, Delacroix S, Montarello JK, Nicholls SJ, Worthley SG. The extent of aortic atherosclerosis predicts the occurrence, severity, and recovery of acute kidney injury after transcatheter aortic valve replacement: a volumetric multislice computed tomography analysis. Circ Cardiovasc Interv. 2018;11:e006367. doi: 10.1161/CIRCINTERVENTIONS.117.006367
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van Rosendael PJ, Kamperidis V, van der Kley F, Katsanos S, Al Amri I, Regeer MV, Schalij MJ, de Weger A, Marsan NA, Bax JJ, Delgado V. Atherosclerosis burden of the aortic valve and aorta and risk of acute kidney injury after transcatheter aortic valve implantation. J Cardiovasc Comput Tomogr. 2015;9:129–138. doi: 10.1016/j.jcct.2015.01.012
5.
Kandathil A, Abbara S, Hanna M, Minhajuddin A, Wehrmann L, Merchant AM, Mills R, Fox AA. Atherosclerosis on CT angiogram predicts acute kidney injury after transcatheter aortic valve replacement. AJR Am J Roentgenol. 2018;17:1–7.
6.
Basile DP, Donohoe D, Roethe K, Osborn JL. Renal ischemic injury results in permanent damage to peritubular capillaries and influences long-term function. Am J Physiol Renal Physiol. 2001;281:F887–F899. doi: 10.1152/ajprenal.2001.281.5.F887
7.
Coca SG, Zabetian A, Ferket BS, Zhou J, Testani JM, Garg AX, Parikh CR. Evaluation of short-term changes in serum creatinine level as a meaningful end point in randomized clinical trials. J Am Soc Nephrol. 2016;27:2529–2542. doi: 10.1681/ASN.2015060642
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Kapadia SR, Kodali S, Makkar R, Mehran R, Lazar RM, Zivadinov R, Dwyer MG, Jilaihawi H, Virmani R, Anwaruddin S, Thourani VH, Nazif T, Mangner N, Woitek F, Krishnaswamy A, Mick S, Chakravarty T, Nakamura M, McCabe JM, Satler L, Zajarias A, Szeto WY, Svensson L, Alu MC, White RM, Kraemer C, Parhizgar A, Leon MB, Linke A; SENTINEL Trial Investigators. Protection against cerebral embolism during transcatheter aortic valve replacement. J Am Coll Cardiol. 2017;69:367–377. doi: 10.1016/j.jacc.2016.10.023

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Go to Circulation: Cardiovascular Interventions
Circulation: Cardiovascular Interventions
PubMed: 30354790

History

Published in print: August 2018
Published online: 20 August 2018

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Keywords

  1. Editorials
  2. atherosclerosis
  3. creatinine
  4. nephrology
  5. renal artery
  6. transcatheter aortic valve replacement

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Chandan Devireddy, MD, FACC, FSCAI [email protected]
Emory University School of Medicine, Atlanta, GA (C.D.)
Swapnil Hiremath, MD, MPH
University of Ottawa, ON, Canada (S.H.).

Notes

The opinions expressed in this article are not necessarily those of the editors or of the American Heart Association.
Chandan Devireddy, MD, FACC, FSCAI, Emory University Hospital Midtown, MOT 6th Floor, Cardiology, 550 Peachtree St, Atlanta, GA 30308. Email [email protected]

Disclosures

Dr Devireddy serves on the scientific advisory board for Medtronic and has received travel expenses from Medtronic and Edwards Lifesciences. Dr Hiremath reports no conflicts.

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  1. Factors Associated With Acute Kidney Injury in Patients Undergoing Transcatheter Aortic Valve Implantation: A Systematic Review and Meta-Analysis, Cureus, (2023).https://doi.org/10.7759/cureus.45131
    Crossref
  2. Transcatheter Aortic Valve Replacement-Associated Acute Kidney Injury: An Update, Cardiorenal Medicine, (143-157), (2023).https://doi.org/10.1159/000529729
    Crossref
  3. Renal outcomes in valve‐in‐valve transcatheter versus redo surgical aortic valve replacement: A systematic review and meta‐analysis, Journal of Cardiac Surgery, 37, 11, (3743-3753), (2022).https://doi.org/10.1111/jocs.16890
    Crossref
  4. Preventing a nonexistent entity, Current Opinion in Nephrology and Hypertension, 29, 1, (152-160), (2020).https://doi.org/10.1097/MNH.0000000000000562
    Crossref
  5. New Insights Into Mechanisms of Acute Kidney Injury in Heart Disease, Canadian Journal of Cardiology, 35, 9, (1158-1169), (2019).https://doi.org/10.1016/j.cjca.2019.06.032
    Crossref
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Acute Kidney Injury After Transcatheter Aortic Valve Replacement
Circulation: Cardiovascular Interventions
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  • No. 8

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