Acute Kidney Injury after Transcatheter Aortic Valve Replacement

Abstract

Since its introduction in 2002, more than 150,000 patients have undergone transcatheter aortic valve replacement (TAVR) globally. The results of randomized trials and observational studies have positioned TAVR as 1) treatment of choice for inoperable patients with severe symptomatic aortic stenosis and 2) an attractive alternative to surgical aortic valve replacement (SAVR) in high-risk patients [1]. As TAVR results continue to improve with the introduction of smaller delivery systems and other technological advances, it is increasingly considered an option for younger and lower-risk patients. Acute kidney injury (AKI) frequently complicates SAVR and is associated with increased mortality, infectious complications, and prolonged hospital stay in the short term [2] and serious adverse cardiovascular events and mortality in the long term [3,4]. Because cardiopulmonary bypass (CPB), required for SAVR, is a major predictor of increased risk for AKI, the less invasive TAVR without CPB was predicted to reduce this AKI risk. However, TAVR requires use of large delivery devices in the aorta with the potential for associated micro-embolism, large volumes of radiographic contrast material, and rapid ventricular pacing that induces hypotension, all of which also increase the risk of AKI. Indeed, in the original trial of TAVR leading to FDA approval (PARTNER B Trial), AKI occurred in only 4.8% of cases and AKI requiring dialysis in only 2.9%. Yet practitioners recognize that AKI frequencies with AVR by either technique are indeed high (~40%) and vary widely depending on the definition used and the patient characteristics. Clearly the relative rates of AKI comparing TAVR with SAVR are critically important, particularly as TAVR moves into a younger population with less surgical risk. Recently, a large analysis (12 studies of >90,000 SAVR patients and 26 studies of >6000 TAVR patients) confirmed that the frequency of AKI was highly dependent on the definition used [5]. They noted that frequencies of AKI ranged from 3.4% to 43% with SAVR as 2.5% required dialysis, and from 3.4% to 57% with TAVR. Independent predictors of AKI were baseline kidney failure, EUROSCORE, diabetes, hypertension, chronic obstructive pulmonary disease, anemia, peripheral vascular disease, heart failure, surgical priority, CPB time, re-operation, use of intra-aortic balloon pump, re-exploration, contrast volume, transapical access, transfusion, postoperative thrombocytopenia, postoperative leukocytosis, age, and female sex. The 30-day mortality rates for AKI following SAVR ranged from 5.5% to 46% (or 3- to 16-fold higher vs. patients without AKI). Patients developing AKI after TAVR had mortality rates ranging from 7.8% to 29% (or 2- to 8-fold higher vs. patients without AKI). Development of AKI confers up to a 4-fold increase in 1-year mortality, and the AKI-associated mortality with SAVR appears to be higher vs. TAVR. Finally, the length of hospital stay was longer among patients developing AKI vs. those without AKI in both the SAVR and TAVR groups. In the current issue of this journal [6], a meta-analysis of 3 randomized controlled trials (RCTs) with 1852 patients and 14 cohort studies with 3113 patients assessed the AKI risk for TAVR. The pooled data for AKI associated with TAVR suggest an ~30% relative risk reduction compared with SAVR. Sensitivity analysis in RCTs and propensity score-based studies using a standard AKI definition supported an association between TAVR and lower AKI risk (RR: 0.35; 95% CI 0.25-0.50). Interestingly, associations between TAVR and reduced risks of severe AKI requiring dialysis were not found. The authors concluded that TAVR is associated with lower AKI risk.