Systemic inflammation and oxidative stress contribute to acute kidney injury after transcatheter aortic valve implantation

Figures

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  Figure 1. A. Incidence of acute kidney injury (AKI) according to access site (transfemoral [TF] vs. transapical [TA]). There was a significantly higher frequency of AKI in the transapical group (chi-square test, p < 0.005); B. Kaplan-Meier curves for patient with AKI and with no post-procedural AKI (Wilcoxon test, p < 0.05). There was higher mortality in the group developing AKI; *p < 0.005.

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  Figure 2. Levels of inflammatory markers and oxidative stress after transcatheter aortic valve implantation (TAVI) by stage of acute kidney injury (AKI); A. 22–26 h after TAVI; B. 44–52 h after TAVI. One-way ANOVA, followed by Tukey post-hoc test performed if ANOVA was significant, *p < 0.05 from post hoc test significant difference against group with no postprocedural AKI. The magnitude of inflammatory reaction measured by levels of tumor necrosis factor alpha (TNFα) and its receptors, myeloperoxidase (MPO) and C-reactive protein (CRP) 22–26 h after TAVI was higher in all patients who developed AKI regardless of its severity. On the other hand, 44–52 h after TAVI inflammatory markers remained high, but only in patients who developed AKI stage 2/3.

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  Figure 3. Changes in inflammatory markers and oxidative stress after transfemoral (TF) and transapical (TA) group 4–6 h, 22–26 h, and 44–52 h post-procedure. A. High-sensitivity C-reactive protein (hsCRP); B. Myeloperoxidase (MPO); C. Aldosterone; D. Tumor necrosis factor alpha (TNFα); E. TNFαR1; F. TNFαR2. Two-way ANOVA followed by Bonferroni post hoc test, *p < 0.05. Levels of hsCRP, MPO, aldosterone, and TNFαR1 and TNFαR2 were significantly higher after TA transcatheter aortic valve implantation.

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  Figure 4. Changes in neurohormonal activation in acute kidney injury (AKI) and no AKI group 4–6 h, 22–26 h, and 44–52 h post-procedure. A. Neutrophil gelatinase-associated lipocalin (NGAL); B. Interleukin 6; C. N-terminal pro-B-type natriuretic peptide (NT-proBNP), D. Receptor for interleukin 33 (ST2); Two-way ANOVA followed by Bonferroni post hoc test, *p < 0.05. NGAL levels were higher pre-transcatheter aortic valve implantation (TAVI) and were rising after the procedure significantly more in the AKI group. Interleukin 6 levels increase after TAVI from 4–6 h continuing rise over next hours. The rise in interleukin 6 levels was significantly higher in the AKI group at 22–26 h and 44–52 h. BNP and ST2 levels were rising significantly only in the AKI group at 22–26 h and 44–52 h.

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  Figure 5. Changes in basic hemodynamics in acute kidney injury (AKI) and no AKI group 4–6 h and 22–26 h post-procedure; A. Heart rate (HR); B. Cardiac output (CO); C. Systemic vascular resistance (SVR); D. Systolic blood pressure (SBP); E. Diastolic blood pressure (DBP); F. Mean blood pressure (MBP). No significant difference was observed in the first 24 h in HR, CO, SBP, DBP, and MBP in either group. The SVR was significantly lower at baseline and remained lower in patients who developed AKI.