Acute Kidney Injury in Acute Type B Aortic Dissection: Outcomes Over 20 Years

Mechanisms contributing to acute kidney injury (AKI) after acute type B aortic dissection (ABAD) include renal malperfusion or underlying renal dysfunction. We characterized AKI after ABAD and evaluated its potential for adverse clinical and aortic outcomes.

Between 1995 and 2016, 478 patients without prior dialysis requirement (mean age, 62.1 years; 60.5% male) presented with ABAD. Renal malperfusion was identified in 87 (18.2%). AKI was assessed by the Kidney Disease: Improving Global Outcomes criteria.

AKI was seen in 252 (52.7%; stage 1 in 130, stage 2 in 71, stage 3 in 51) and was associated with increased hospitalization (11 days vs 7 days with no AKI, p = 0.008). Independent predictors of AKI included hypertension (odds ratio [OR], 1.69), chronic kidney disease (OR, 3.98), congestive heart failure (OR, 2.36), and visceral (OR, 2.19), renal (OR, 3.18), or limb malperfusion (OR, 2.18, all p < 0.05). Early mortality occurred in 44 (9.2%) and was independently predicted by stages 2 (OR, 4.38) and 3 AKI (OR, 6.30; both p < 0.03). The 10-year survival was 46.5%, and independent predictors of late death included aortic diameter (OR, 1.02), chronic obstructive pulmonary disease (OR, 2.02), chronic kidney disease (OR, 3.51), and stages 2 (OR, 2.74) and 3 AKI (OR, 2.26, all p < 0.01). The 10-year freedom from aortic rupture, repeat dissection, or need for reintervention was 39.8%. Independent predictors of late aortic events included hyperlipidemia (OR, 1.55), diabetes (OR, 0.38), aortic diameter (OR, 1.03), and connective tissue disease (OR, 2.54, all p < 0.03), but not AKI (p = 0.149).

AKI is common after ABAD and increases early mortality and hospital stay and diminishes late survival. Despite its adverse effect on survival, AKI is not associated with late aortic events.