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Incidence, Predictors, and Effects of Acute Kidney Injury After Percutaneous Valve Implantation

J. García-Lara, MD, E. Pinar-Bermúdez, MD, PhD, J.R. Gimeno-Blanes, MD, PhD, J. Lacunza-Ruiz, MD, J.A. Hurtado Martinez, MD, R. Valdesuso-Aguilar, MD, PhD, M. Valdés-Chávarri, MD, PhD

Keywords
April 2014

Abstract: Background. Acute kidney injury is a common complication after surgical aortic replacement and entails a worse prognosis. Percutaneous valve implantation is an alternative to surgical replacement. We sought to elucidate incidence, predictors, and effects of acute kidney injury after percutaneous aortic valve implantation. Methods. A cohort of consecutive patients who underwent percutaneous aortic valve implantation at one center were studied, excluding those who died in the first 24 hours and those on prior hemodialysis. Results. A total of 131 patients (age, 80.8 ± 6 years; 42% male; Euroscore II, 10.27 ± 6.9) were included. Acute kidney injury was defined as a reduction >25% in glomerular filtration rate (GFR). GFR was 62.09 ± 22 mL/min/1.73 m2 at baseline, 62.7 ± 25 mL/min/1.73 m2 after the procedure, and 68.03 ± 25 mL/min/1.73 m2 at discharge. Acute kidney injury appeared in 17 patients (13%). Of these, 11 recovered and only 6 (4.5%) showed impaired GFR >25% upon discharge. Patients with acute kidney injury showed longer hospitalization length (median 7 days [IQR, 5-12 days] vs 3 days [IQR, 2-6 days]; P=.01) and higher 30-day mortality rate (17.6% vs 0.9%; P=.01). The only independent predictor for acute kidney injury development was Euroscore II (odds ratio, 1.192; confidence interval, 1.042-1.326; P=.01). Conclusion. Incidence of acute kidney injury after transcatheter aortic valve implantation was 13% in our cohort. Patients with acute kidney injury showed longer hospitalization and higher 30-day mortality rate. Euroscore II was an independent predictor of acute kidney injury.

J INVASIVE CARDIOL 2014;26(4):183-186

Key words: kidney, valvular prosthesis, valves

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Acute kidney injury (AKI) is a common complication after surgical aortic valve replacement.1,2 The occurrence of AKI is associated with a worse prognosis, with up to 58% mortality in patients requiring hemodialysis.3 

In the last years, transcatheter aortic valve implantation (TAVI) has shown to be an alternative to surgical aortic replacement in patients with severe aortic stenosis and prohibitive or very high surgical risk.4,5 

The incidence of AKI undergoing TAVI has been studied in small series, showing lower incidence when compared to surgical aortic replacement, especially in patients with previous chronic kidney disease. However, AKI is still a powerful independent predictor of mortality after the procedure.6,7 

Among predictors of AKI, different groups have proposed the transapical approach, blood transfusion, and the amount of administered contrast.6,8-10

The aim of this study was to evaluate the incidence and prognosis of AKI after TAVI according to Valve Academic Research Consortium (VARC) criteria.11,12

Methods

Patients. A cohort of patients with severe aortic stenosis undergoing TAVI with Edwards Sapien prostheses (Edwards Lifesciences, Inc) between July 2008 and February 2013 in a single center was studied. We excluded patients who died within the first 24 hours after the procedure (because it was impossible to collect serial blood samples) as well as those who underwent previous hemodialysis. 

Clinical, analytical, and echocardiographic data were prospectively recorded. 

TAVI procedure. All patients received an Edwards Sapien prosthesis transfemorally according to the previously described procedure.13,14 

Data regarding the procedure were collected prospectively, and included approach (surgical artery exposure or percutaneous), amount of contrast, and complications. 

Determination of renal function. All patients underwent a serum creatinine determination 24 hours before the procedure, 48 hours after the procedure, and before discharge. Glomerular filtration rate (GFR) was calculated according to the MDRD formula.15

Acute kidney injury was defined as the reduction of more than 25%16 in the GFR in the next 48 hours after the procedure. The degree of AKI was determined according to the AKI classification as proposed by the Valve Academic Research Consortium.17-19

Statistics. Results were expressed as mean ± standard deviation for normally distributed continuous variables, median (interquartile range) for continuous variables with non-normal distribution, and number (percentage) for categorical variables. Categorical variable differences were tested using chi-square or the Fisher exact test. Differences among quantitative variables were tested using Student t-test or Mann-Whitney U-test, depending on normality of its distribution. A logistic regression analysis was performed to find the predictors of AKI, including variables with P<.20 in univariate analysis and those variables that have shown to be relevant in the previous literature. All statistical analyses were performed using the statistics software package SPSS 15.0 for Windows (SPSS, Inc).

Results

A total of 131 consecutive patients (age, 80.8 ± 6 years; 42% male; Euroscore II, 10.27 ± 6.9) who underwent TAVI in the same center were included. Baseline characteristics are shown in Table 1. 

A successful procedure was accomplished in 127 patients (97%). The procedure was totally percutaneous in 102 patients (77.8%), whereas a surgical femoral artery exposure was performed in 29 patients (22.2%). The procedure characteristics are shown in Table 2. 

Glomerular filtration rate was 62.09 ± 22 mL/min/1.73 m2 at baseline, 62.7 ± 25 mL/min/1.73 m2 after the procedure, and 68.03 ± 25 mL/min/1.73 m2 upon discharge (Table 3). Upon discharge, 89 patients (68%) had improved GFR compared with the basal rate. Average improvement in GFR was 5.71 ± 15 mL/min/1.73 m2 (confidence interval [CI], 2.23-9.2; P=.01). 

A total of 17 patients (13%) developed AKI after TAVI. Of these patients, 11 improved before discharge, only 6 patients (4.5%) persisted with a deterioration of GFR >25%, and only 1 patient required permanent dialysis. 

Patients who developed AKI had a longer hospitalization with a median of 7 days (IQR, 5-12 days) vs 3 days (IQR, 2-6 days); P=.01. There were no differences by approach technique with a similar AKI incidence in surgical artery exposure (17.9%) vs total percutaneous approach (12.9%; P=.58). Patients under general anesthesia presented with a similar incidence of AKI compared with those on local anesthesia (15% vs 16.7%, respectively; P=.74) (Table 4). 

Three of the 17 patients who developed AKI died from the procedure in 30 days, whereas 1 of the patients who did not develop AKI died (17.6% vs 0.9%; P=.01). All 3 patients died of multiple organ dysfunction with oliguric acute kidney injury. One of them had suffered a retroperitoneal hematoma after the procedure, requiring conservative non-surgical treatment.

In a logistic regression model, variables such as age, gender, body mass index, and those with P.20 in the univariate analysis were introduced. Previously released papers have found an association between AKI and hypertension, chronic obstructive pulmonary disease, and blood transfusion; thus, these variables were also included in the model.6,20-22 

According to this model, the only independent predictor of AKI after TAVI was Euroscore II (odds ratio [OR], 1.192; CI, 1.042-1.326; P=.01). The presence of coronary artery disease showed a strong trend, but was not statistically significant (OR, 10.528; CI, 0.707-157; P=.09). 

Discussion

This paper provides specific information about a homogenous population of patients undergoing TAVI through femoral access with the same type of prosthesis. 

The incidence of AKI after TAVI in patients with severe symptomatic aortic stenosis was 13% in our cohort. Patients who developed AKI had longer hospitalization stays and a higher 30-day mortality rate. The only independent predictor for AKI was Euroscore II. 

Bagur et al described an incidence of AKI of 11.7% in a cohort that included transfemoral and transapical cases, with similar mean age and baseline GFR.  However, reported data show less contrast media administered to our patients (97.6 ± 57 mL vs 143 ± 60 mL) and fewer diabetic patients (23% vs 47.3%), which could explain the higher incidence of AKI in our cohort. In other previously published series, the incidence of AKI after TAVI ranged from 8.3%-29%.9,20-22 

In the present study, the incidence of AKI was associated with longer mean hospital stay, as has been consistently shown by other groups, showing the relevance of the issue in economic terms, with ~50% increase in hospitalization days.20-22

In our cohort, mortality in patients who developed AKI was higher compared to patients without AKI, which is in accordance with another group’s findings.23 

Bagur et al has shown that AKI developing after TAVI was an independent predictor of in-hospital mortality. This relationship has been previously shown in patients undergoing percutaneous coronary interventions, with an increase in hospital mortality in patients who developed AKI after the procedure.24-26

On the other hand, Euroscore II was the only independent predictor of AKI in our cohort. Our paper reinforces this point, which was elucidated in previously published papers. Unlike the largest paper by Nuis et al,8 we used the Euroscore II, which has shown a better predictive performance in patients undergoing TAVI transfemorally.27 

Different investigators found that the number of blood transfusions required,8,9 transapical approach,9,28 and contrast media amount adjusted by weight and baseline creatinine10 to be independent predictors for AKI after TAVI.

In our study, the percentage of patients requiring transfusion was 21.4%, versus another series’ transfusion rates of around 50%,6 which could explain why blood transfusion was not found as a predictor of AKI. 

Yamamoto et al proposed an index (contrast media volume × baseline serum creatinine) / (weight) to predict AKI after TAVI with a threshold of 2.7. In our patients, 29 (22.1%) had a Yamamoto index of 2.7; however, there was no difference in this index between patients who developed AKI and those who did not (2.20 ± 1.11 vs 2.24 ± 1.12; P=.90). 

Study limitations. Our results are limited by the small sample size (131 patients), which limits the statistical power to detect differences between groups. Similarly, all TAVI procedures were performed in a single center, which could limit the external validity of the conclusions. 

Conclusion

AKI after TAVI in patients with severe symptomatic aortic stenosis has an incidence of 13% in our cohort. Patients who developed AKI had longer hospital stay and higher mortality. The only independent predictor for AKI after TAVI was Euroscore II risk score. 

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From the Servicio de Cardiología, Hospital Universitario Virgen de la Arrixaca, Murcia, Spain.

Disclosure: The authors have completed and returned the ICMJE Form for Disclosure of Potential Conflicts of Interest. Dr Valdés-Chávarri reports personal consulting fees from Edwards Lifesciences. The remaining authors report no conflicts of interest regarding the content herein.

Manuscript submitted September 13, 2013, provisional acceptance given October 10, 2013, final version accepted October 24, 2013.

Address for correspondence: Dr Juan García-Lara, Unidad de Hemodinamica- Servicio de Cardiologia, Hospital Universitario Virgen de la Arrixaca, Carretera Cartagena SN 30110 Murcia, Spain. Email: jgarciadelara@gmail.com

 


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