Risk factors for acute kidney injury and its impact on 3-year mortality after thoracic endovascular repair for type B aortic dissection.

OBJECTIVE

Acute kidney injury (AKI) following thoracic endovascular aortic repair (TEVAR) significantly impacts outcomes. This study aimed to identify independent predictors of AKI after TEVAR for acute Stanford type B aortic dissection (ATBAD) and evaluate its impact on long-term mortality.

METHODS

This retrospective analysis included 745 consecutive patients who underwent TEVAR for ATBAD at the General Hospital of Northern Theater Command between February 2004 and November 2022. Acute kidney injury was diagnosed based on a serum creatinine increase of ≥26.5 μmol/L within 48 h, a ≥1.5-fold increase from baseline within 7 days, or urine output <0.5 mL/kg/h for 6 h. Univariate and multivariate logistic regressions identified risk factors for AKI and all-cause mortality.

RESULTS

AKI occurred in 75 patients (10.1%). The patients who developed AKI had a higher baseline serum creatinine level (85.97 vs. 78.30 μmol/L; P = 0.009), received more contrast volume (246.13 ± 92.00 vs. 221.17 ± 69.92 mL; P = 0.042), and had a higher prevalence of bilateral renal artery involvement (14.3% vs. 5.1%; P = 0.020). After a mean follow-up of 36 months, the multivariate analysis identified the following three independent predictors: bilateral renal artery involvement [odds ratio (OR): 4.381, 95% confidence interval (CI): 1.54-12.45; P = 0.006], serum creatinine >114 μmol/L (OR: 2.86, 95% CI: 1.38-5.93; P = 0.005), and contrast volume >290 mL (OR: 2.36, 95% CI: 1.10-5.09; P = 0.028). All-cause mortality was significantly higher in the AKI group (16.1% vs. 4.4%; P < 0.001). AKI remained an independent predictor of mortality (OR: 3.02, 95% CI: 1.46-6.28; P = 0.003) after adjusting for age, baseline creatinine, and medication use.

CONCLUSIONS

AKI remains highly prevalent in patients undergoing TEVAR for ATBAD. Bilateral renal artery involvement, elevated baseline creatinine, and contrast volume >290 mL independently predicted AKI. Development of AKI was associated with a threefold increase in long-term mortality, emphasizing the importance of risk stratification and nephroprotective strategies.