Review of: "Acute kidney injury and acute kidney recovery following Transcatheter Aortic Valve Replacement"

References Authors ​ ​Marilou Peillex, Benjamin Marchandot, Kensuke Matsushita, Eric Prinz, Sebastien Hess, Antje Reydel, Marion Kibler, Adrien Carmona, Antonin Trimaille, Joe Heger, Helène Petit-Eisenmann, Annie Trinh, Laurence Jesel, Patrick Ohlmann, Olivier Morel. Reference ​ ​Peillex M, Marchandot B, Matsushita K, Prinz E, Hess S, Reydel A, et al. (2021) Acute kidney injury and acute kidney recovery following Transcatheter Aortic Valve Replacement. PLoS ONE 16(8): e0255806. https://doi.org/10.1371/ journal.pone.0255806 Published August 2021


How was it executed -the methodology?
This is a retrospective, observational, unblinded, single-center study that included 584 TAVI patients for severe aortic stenosis.
AKI was defined as an increase in serum creatinine ≥0.3 mg/dL or ≥ 50% increase in serum creatinine up to 72 hours after TAVR.
AKR was mirroring defined as 1) an absolute decrease ≥0.3 mg/dL or a relative decrease ≥ 50% in serum creatinine up to 72H or 2) a 25% improvement of eGFR over 72H after TAVR.
The primary endpoint was the incidence of AKI and AKR following TAVI.
The secondary endpoints included the incidence of all-cause mortality and a composite endpoint of cardiac death, stroke, myocardial infarction and rehospitalization for heart failure at follow-up among AKI, AKR and unchanged renal function groups.

What is the main result?
AKI occurred in 8.3%, while AKR in 15.7 % of patients.
By univariate analysis basal creatinine, procedure duration and major bleeding were predictors of AKR, with baseline creatinine level that remained the sole independent predictor after multivariate analysis was performed (HR: 1; 95% CI 1 to 1.1 p < 0.001).

Critical reading and relevance for clinical practice
This report increases the knowledge about AKR in an all-comers real-world TAVI population. Indeed, conflicting results have been provided on AKR predictors and clinical implications. AKR after TAVI was firstly defined by Azarbal et al [2]as a 25% improvement in eGFR at 48 hours after TAVI. Based on a population of 366 patients, AKR resulted to be predicted by lack of chronic beta-blocker use, male gender, CKD. The same authors on a 1502 TAVI population from the Northern New England registry, reported AKR to occur in 25% of the procedures and to be predicted by CKD, COPD and previous aortic valve surgery, while DM, anaemia and high STS score (>6.1) were less likely linked with AKR. In this report AKR was defined as an increase of GFR >25% at discharge as compared to the admission value [3]. Qeios, CC-BY 4.0 · Review, September 20, 2021 Qeios ID: 1LM5U2 · https://doi.org/10.32388/1LM5U2 2/3 Nijenhuis et al, on a 639 TAVI population, using a different definition criteria of AKR (post to pre-TAVR ratio within 48H ≤0.80) reported a potential protective on two-year mortality rate ( HR 0.53, 95%CI 0.30-0.93) compared with a stable kidney function. In this report also the predictors of AKR were conflicting with previous experience: indeed independent predictors were female gender, preserved kidney function, haemoglobin level and absence of atrial fibrillation [4].
Conversely, Pighi et al on a 674 TAVI population, defining AKR as for Azarbal's definition an increase of GFR >25% at discharge, reported an incidence of AKR of 14.5%; in this analysis the association between extravalvular cardiac damage (EVCD), AKI, AKR and their interaction with clinical outcomes was analyzed.
Advanced EVCD was related to a higher rate of AKR (23.8% vs. 12.8%; p<0.01), as well as CKD. AKR had no significant impact on reduction of 12-month all-cause mortality but was associated with an improvement of renal function at 12-months [5].
In conclusion, it is necessary to emphasize that at present a validated and shared definition of AKR is lacking and consequently different and conflicting predictors have been proposed, with conflicting interaction with clinical outcomes at long-term follow-up. Thus a shared and common effort is needed in order to provide a valid definition, with clear pathogenic basis and the consequent impact on cardiac and non-cardiac clinical outcomes.