CRT 2020: Stage 3 kidney injury after TAVI leads to seven times higher mortality

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Howard M Julien

Patients who develop stage 3 acute kidney injury (AKI) following transcatheter aortic valve implantation (TAVI) have seven times higher adjusted one-year mortality than patients who do not develop AKI. Researchers also found that more than 10% of patients develop some degree of AKI, although the vast majority only experience mild renal insufficiency.

The findings were outlined at a late breaking session at the Cardiac Resynchronisation Therapy meeting (CRT 2020; 23–25 February, Washington DC, USA) by Howard M Julien (Pen Heart and Vascular Center, University of Pennsylvania, Philadelphia, USA) who pointed out: “Knowledge of factors associated with the development of AKI may help identify patients at risk of the most severe form of AKI and may prompt prevention strategies focused on these characteristics.”

Using data from the Society of Thoracic Surgeons (STS) National Database and the American College of Cardiology’s (ACC) National Cardiovascular Data Registry (NCDR), Julien and colleagues looked at trends in the incidence of AKI over time, as well as attempting to identify factors associated with the development of AKI after TAVI and determining the association between incident stage 3 AKI after TAVI and one-year all-cause mortality.

Julien explained: “Acute kidney injury is a known potential complication of invasive angiographic procedures, with reported rates of AKI after TAVI in small observational studies varying widely between 3%, 4%, and 57% such that the incidence and outcomes of AKI in real-world clinical practice is currently unknown.”

The researchers used the data from the STS/ACC TVT Registry to calculate the unadjusted annual incidence of AKI using AKIN criteria from 2012–2018. Data from January 2016 to June 2018 were used to create a predictive model, with a starting population of 133,696 patients at more than 600 sites. The final number of patients included in the model was 107,814 based on the highest creatinine measurement recorded, with 1,212 in stage 3, 314 in stage 2 (more than two or three-fold increase in creatinine), and 10,220 in stage 1 (≥1.5–2-fold increase or 0.3–4mg/dl change). and 96,248 with normal kidney function.

Direct Centers for Medicare and Medicaid Services (CMS) linkage was used to evaluate longitudinal outcomes, and three step multivariable modeling to assess predictors of AKI. Covariates were the standard STS/ACC TVT-Registry mortality model, and outcomes of interest were death at one year.

Julien et al found that, for those who developed stage 3 AKI after TAVI, among the highest predictors of further injury to kidneys after TAVI were factors associated with patient instability: conversion to open heart surgery, procedure status (other vs. elective), use of preprocedural inotropes, and cardiogenic shock within 24 hours.

Other notable risk factors for developing stage 3 AKI included: non-femoral access method (other vs. percutaneous), use of general anaesthesia (general vs. moderate sedation) diabetes mellitus, anaemia (haemoglobin <10g/dl), black race, and self- expanding valve use (self-expanding vs. balloon expanding).”

Under the one-year mortality model, the adjusted hazard ratio (aHR) for stage three acute kidney injury (renal failure) was 7.035 (95% confidence interval [CI] 6.006–8.24, p<0.001); for stage 2 AKI (renal injury) it was 10.386 (95% CI 6.977–15.409, p<0.001) and for stage 1 AKI (risk of renal injury) it was 2.674 (95% CI 2.512–2.847, p<0.001).

Limitations of the study were that residual confounding could not be completely eliminated given the retrospective nature of the study design, researchers were unable to discern the underlying cause of AKI for patients in the cohort, due to database limitations, and that CMS linkage was only available for a subset of patients.


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