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DOI: 10.1055/s-0035-1544349
Further Insights in Acute Kidney Injury after Transcatheter Aortic Valve Implantation: Time of Onset of Kidney Injury is Crucial for Severity and Mortality Risk
Objective: Acute kidney Injury (AKI) is a frequent complication after transcatheter aortic valve implantation (TAVI) affecting outcome and mortality. The Valve academic research consortium adjusted the VARC II criteria now recommending a postoperative observation period of 7 days for Acute kidney injury (AKI) (VARC I: 72 hours). However, little is known about potential differences concerning the timing of the occurence of AKI after TAVI and whether this fact takes influence on the outcome.
Methods: Data of 436 patients after TAVI at our institution were analyzed according to VARC II criteria to gain further insight into 1) the incidence and severity (stages) of early- AKI (EAKI) (onset < 72 hours after TAVI) and late-AKI (LAKI) (>72 hour), 2) the impact of EAKI and LAKI on mortality and 3) to identify risk factors for the occurence of E- or LAKI.
Results: 36.3% developed postoperative AKI with a higher incidence of EAKI (66.7% versus LAKI 32.3%). Severe AKI (stages II + III) occurred more frequently in EAKI patients (31.3% vs 7.8% lAKI, p = 0.001). 30-day overall mortality was 8.2% with a mortality of 15.2% in EAKI-patients versus 0% in LAKI patients resulting in a 4.57 fold increased mortality risk after EAKI (95%CI 1.98–10.56; p < 0.001). LAKI did not influence early mortality. Kaplan Meier analysis revealed a significant impact of EAKI (p = 0.016) on one- and three-year survival, wheras LAKI did not affect mid-term survival (p = 0.269). Multivariate analyisis identified serum-creatiine > 1.1 mg/dl as independent predictor for E- and LAKI (EAKI:OR 4.67 95%CI 2.53–8.64 p < 0.001 + LAKI: OR 3.27 95%CI 1.60–6.68 p = 0.001). Additionally, contrast administration (> 135 ml/procedure) (OR 2.71 95%CI 1.22–6.02; p = 0.014) and diabetes (OR 1.4 95%CI 1.05–1.89; p = 0.023) were associated with EAKI.
Conclusion: AKI occurring within 72 hours postopertiely significantly affects short and midterm survival, in contrast to a later onset. Our clinical data suggest different pathophysiological mechanisms for the occurrence of E- or LAKI. Furher inverstigation is needed to completey understand the mechanisms of AKI after TAVI and to develop preventive strategies.