4. Discussion 

The main findings of the study were: (1) The volume of CM administered during TAVI  and the cumulative volume of CM administered within seven days or 30 days from TAVI were not associated with AKI post-TAVI; and (2) None of the tested risk assessment models that included a CM module, were independently associated with post-TAVI AKI. (3) eGFR was the only independent predictor for AKI.

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AKI is a serious complication, commonly encountered following TAVI with an incidence of any level of AKI, reported from large registries and metanalyses, at around 20% [1,3]. The development of AKI, following TAVI, significantly increases the risk of both short-term and long-term deleterious complications, such as myocardial infarction, life-threatening bleeding, permanent renal dysfunction necessitating renal replacement therapy, and mortality [1,3–5,20–23]. Various baseline characteristics, co-morbidities, and peri-procedural factors have been linked with TAVI-related AKI. Some of the most reported are the baseline decreasing level of hemoglobin, chronic kidney dysfunction, acute bleeding necessitating blood transfusions, and hemodynamic instability during the procedure [2,5,22,24,25]. Still, there is much uncertainty with a multitude of proposed risk factors previously associated with AKI following other procedures in which CM is used and the role they play in the development of AKI following TAVI with conflicting reported results. For instance, while some studies demonstrated a relationship between increasing age and AKI development following TAVI, other studies did not [3,6,7,10,25]. While in some studies LVEF was dis-concordantly associated with post-TAVI AKI, in other publications it was not [6,7,10,23,25,26]. Even decreasing baseline eGFR and chronic kidney dysfunction have an uncertain magnitude of effects on post-TAVI AKI [3,6–8,10,25–27]. The relationship between CM volume and TAVI-related AKI is also controversial. In several previous studies, there was no significant difference in the volume of CM delivered during TAVI,  between AKI+ patients and AKI− patients, nor between CM dose and post-procedural AKI [2,4,5,8,16]. Conversely, other studies described higher dosages of CM in AKI+ patients compared to AKI, and an association between the volume of CM delivered during TAVI  and the subsequent development of AKI [6,9,10,25,26].

The uncertain association between administered CM volume and AKI has been described with other medical procedures utilizing radiographic CM. In patients with eGFR above 30 mL/min/1.73 m2 who underwent CT testing, there was no significant difference in the incidence of AKI between those who received intravenous CM and those who did not,  and the results for patients with eGFR less than 30 mL/min/1.73 m2 were conflicting [28,29]. An analysis of observational studies concluded that radiocontrast use in CT scanning was not causally related to changes in kidney function [30]. These results were echoed in the most recent update of the American College of Radiology consensus statement in which it was declared that the risk of AKI developing following exposure to intravenous iodinated CM has been exaggerated and that the true risk of AKI, related to CM administration,  remains uncertain even for patients with severe kidney disease [31]. It has been suggested that intravenous administration of CM, like with CT angiography, may impose a different risk of AKI than the one associated with arterial administration of CM, like with PCI and TAVI; however, the data is inconclusive [32–37].

CM-related AKI has been extensively studied in the context of PCI. However, assessing the true impact of CM on the development of AKI, following PCI, has proven to be a  difficult task. Studies that evaluated this coupling between CM and AKI widely differed in the type, chemical characteristics, pharmacokinetics, and volume of CM, the route it was administered, the medical procedure it was given, and, the definition used to diagnose AKI [38]. Notably, a broad range of contrast volume (from below 100 mL to above 800 mL) has been associated with post-PCI nephropathy [12,13,39–41]. There are several fundamental differences between patients treated with TAVI and patients treated with PCI  which, potentially, position the former at a higher risk to develop AKI than the latter. Patients undergoing TAVI are usually elderly, fragile, frequently suffering from multiple co-morbidities and have reduced GFR [7,42]. Additionally, PCI-treated patients are usually exposed to CM once during their index procedure. TAVI-treated patients, however, are frequently exposed to a large cumulative volume of CM during several diagnostic and interventional procedures and over a relatively short period. Interestingly, despite these differences, Venturi et al. found that AKI occurred less frequently in patients undergoing TAVI than in patients undergoing PCI, even after propensity score matching [7]. Following  TAVI, unlike other procedures that utilize CM, there is an immediate and sustained improvement in hemodynamics increasing cardiac output and systemic perfusion [43–45]. Still, even though this can translate into a reduced incidence of AKI following TAVI, the rate of immediate kidney function improvement after TAVI was found to be small in a recent publication (5%) [46].

The diagnosis of AKI tends to lag after the index exposure to CM, with gradual worsening of kidney function over the ensuing days. Accordingly, the assessment for CM-associated nephrotoxicity was traditionally made within 48 to 72 h of exposure and according to VARC-3 consensus statements, this time frame has been further extended to seven days [13,17,39]. Thus far, the effect of CM on kidney function was tested for CM  delivered during TAVI alone, while the possible effect inflicted by near past exposures to CM was overlooked. This led us to test for an additive effect of preceding exposures to CM on the incidence of AKI following TAVI. In this study, the volume of CM administered during TAVI alone, during 7 days, or 30 days, did not significantly differ between AKI+ patients and AKI− patients, nor did it independently predict the development of AKI. Similarly, in a recent study, assessing the effect of multiple exposures to CM during recurrent diagnostic and interventional coronary procedures, although over several years, worsening of renal function was associated with known risk factors for the progression of kidney disease but not with cumulative CM volume [47].

The difficulties in predicting AKI following TAVI led to the development of risk assessment models. Incorporating several parameters to form a  risk model, can potentially improve the predictive power beyond that of the individual modules included in it. AKI risk prediction models have been developed, tested, and validated for coronary procedures [11–14,48,49]. Sadly, only a few of these models have been specifically designed to assess the risk of post-TAVI AKI. For instance, Zivcovic et al. introduced an AKI risk calculator that was meant to be utilized before TAVI and therefore did not include a CM  component [27]. As in this study, several previous studies tested the effectiveness of CMbased, non-TAVI dedicated risk models in predicting AKI following TAVI [6,15,16,24,26,50]. In our study, none of the CM-based risk models we tested independently predicted postTAVI AKI. Mach et al. reported that none of the six tested CM-based risk models (including the Mehran risk model) were significantly different between AKI+ and AKI− patients or,  similarly to our results, independently predicted AKI [16]. Rosa et al. describe that all of their tested risk models, of which four included a CM module and two did not, had poor accuracy in terms of predicting the occurrence of any AKI. However, there was an improvement in AKI risk prediction for more advanced stages of AKI. By univariable logistic regression analysis, only risk models with a CM module were associated with AKI. The results of multivariable logistic regression coefficients of risk for any AKI or the different stages of AKI were not reported [15]. In contrast, a small study of 93 patients, of which AKI was diagnosed in 24 of them, found in a univariable analysis that the Mehran risk model, as well as CM volume, predicted post-TAVI AKI. The authors also reported that in multivariable analysis, CM volume, the Mehran score, SCr, and eGFR were all independently associated with AKI [6]. However, the study was of limited sample size and,  given the low number of endpoints achieved, was underpowered to accurately explore the aforementioned endpoints.

In our study, decreasing eGFR, as previously described by others, was significantly and independently associated with AKI across most analyses [5,8]. It was the only independent predictor for AKI. Therefore, with caution, we suggest that the AKI predictive power of risk score models containing a CM volume module is almost entirely limited to pre-procedural eGFR.

Limitations: This is an individual center report and has limitations associated with retrospective analysis. Given the relatively small number of AKI events, our study was underpowered to evaluate the most severe stages of AKI. The assessment of baseline sCr was made before TAVI and not before the first exposure to CM within the assessed time interval. Additionally, most patients were discharged before seven days had elapsed from their procedure, and therefore, even though it is our institutional practice to discharge the patient after kidney function has stabilized, it is possible that further deterioration in kidney function ensued after discharge without being recorded. The use of drugs with nephrotoxic properties close to contrast media exposure was also not recorded.

5. Conclusions

Neither the volume of CM delivered during TAVI nor the cumulative amount of CM  delivered during a period that starts either seven days or 30 days before TAVI and ends with TAVI are associated with AKI. The power of non-TAVI dedicated CM-based risk models, in predicting AKI, is limited to pre-procedural kidney dysfunction.

Author Contributions: Conceptualization, D.S. and I.M.; Methodology, D.S., L.G.-R., E.Y.B., and I.M.; Validation, D.S., L.G.-R., A.L., and I.M.; Formal Analysis, D.S., L.G.-R., and I.M.; Investigation, D.S., Y.D., F.K., A.L., M.G., W.K., and I.M.; Resources, D.S., W.K., E.H., M.G., and I.M.; Data Curation, D.S. and A.L.; Writing—Original Draft Preparation, D.S.; Writing—Review and Editing, D.S., L.G.-R., E.Y.B., A.L., and I.M.; Visualization, D.S., L.G.-R., A.L., and E.Y.B.; Supervision, E.Y.B., and I.M.; Project Administration, D.S.; All authors have contributed to preparing the manuscript by the International Committee of Medical Journal Editors (ICMJE) criteria for authorship. All authors have read and agreed to the published version of the manuscript.

Funding: This research received no external funding. 

Institutional Review Board Statement: The study was conducted according to the guidelines of the Declaration of Helsinki, and approved by the Institutional Review Board of Padeh Medical Center (Protocol code POR-0099-14; Approval date: 30 December 2019).

Informed Consent Statement: Informed consent was obtained from all subjects involved in the study. 

Data Availability Statement: The data presented in this study was obtained from PMC’s local TAVI  prospective registry and is available on request from the corresponding author.

Conflicts of Interest: D.S. received a speakers’ fee from Abbott Medical Laboratories, Sanofi, Novartis, and Novo Nordisk; E.Y.B. received a speakers’ honoraria from CTS, and Novo Nordisk received research support paid to the University of Pennsylvania by Medtronic Inc. and Impulse Dynamics Ltd.

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