1. Systemic inflammation and oxidative stress contribute to acute kidney injury after transcatheter aortic valve implantation
- Author
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Arunraj Navaratnarajah, Philip MacCarthy, Emma Alcock, Amit Bhan, Olaf Wendler, Mark J. Monaghan, Ajay M. Shah, Rafal Dworakowski, and Tracy Dew
- Subjects
medicine.medical_specialty ,medicine.medical_treatment ,Renal function ,030204 cardiovascular system & hematology ,medicine.disease_cause ,Systemic inflammation ,Transcatheter Aortic Valve Replacement ,03 medical and health sciences ,0302 clinical medicine ,Internal medicine ,medicine ,Humans ,Interleukin 6 ,Peroxidase ,Inflammation ,biology ,Interleukin-6 ,Tumor Necrosis Factor-alpha ,business.industry ,Acute kidney injury ,Aortic Valve Stenosis ,General Medicine ,Acute Kidney Injury ,medicine.disease ,Acetylcysteine ,Oxidative Stress ,C-Reactive Protein ,Treatment Outcome ,Cytokine ,Aortic Valve ,Cardiology ,biology.protein ,Tumor necrosis factor alpha ,medicine.symptom ,Cardiology and Cardiovascular Medicine ,Complication ,business ,Biomarkers ,Oxidative stress - Abstract
Background: Acute kidney injury (AKI) is a frequent complication of transcatheter aortic valve implantation (TAVI) and has been linked to preexisting comorbidities, peri-procedural hypotension, and systemic inflammation. The extent of systemic inflammation after TAVI is not fully understood. Our aim was to characterize the inflammatory response after TAVI and evaluate its contribution to the mechanism of post-procedural AKI. Methods: One hundred and five consecutive patients undergoing TAVI at our institution were included. We analyzed the peri-procedural inflammatory and oxidative stress responses by measuring a range of biomarkers (including C-reactive protein [hsCRP], cytokine levels, and myeloperoxidase [MPO]), before TAVI and 6, 24, and 48 hours post-procedure. We correlated this with changes in renal function and patient and procedural characteristics. Results: We observed a significant increase in plasma levels of pro-inflammatory cytokines (hsCRP, interleukin 6, tumor necrosis factor alpha receptors) and markers of oxidative stress (MPO) after TAVI. The inflammatory response was significantly greater after trans-apical (TA) TAVI compared to trans-femoral (TF). This was associated with a higher incidence of AKI in the TA cohort compared to TF (44% vs. 8%, respectively, p < 0.0001). The incidence of AKI was significantly lower when N-acetylcysteine (NAC) was given peri-procedurally (12% vs. 38%, p < 0.005). In multivariate analysis, only the TA approach and no use of NAC before the procedure were independent predictors of AKI. Conclusions: TAVI creates a significant post-procedural inflammatory response, more so with the TA approach. Mechanisms of AKI after TAVI are complex. Inflammatory response, hypoperfusion, and oxidative stress may all play a part and are potential therapeutic targets to reduce/prevent AKI.
- Published
- 2022