Department of Cardiac Surgery, University of Michigan Medical School, Ann Arbor, Michigan.
Department of Cardiac Surgery, University of Michigan Medical School, Ann Arbor, Michigan.
Ann Thorac Surg. 2019 Feb;107(2):486-492. doi: 10.1016/j.athoracsur.2018.07.054. Epub 2018 Sep 21.
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.
急性 B 型主动脉夹层(ABAD)后导致急性肾损伤(AKI)的机制包括肾脏灌注不良或潜在的肾功能障碍。我们对 ABAD 后的 AKI 进行了特征描述,并评估了其对不良临床和主动脉结局的潜在影响。
1995 年至 2016 年间,478 名无透析需求的患者(平均年龄 62.1 岁;60.5%为男性)出现 ABAD。87 例(18.2%)存在肾灌注不良。采用肾脏病:改善全球结局(KDIGO)标准评估 AKI。
252 例(52.7%;130 例为 1 期,71 例为 2 期,51 例为 3 期)出现 AKI,与住院时间延长相关(AKI 组为 11 天,无 AKI 组为 7 天,p=0.008)。AKI 的独立预测因素包括高血压(比值比[OR],1.69)、慢性肾脏病(OR,3.98)、充血性心力衰竭(OR,2.36)以及内脏(OR,2.19)、肾(OR,3.18)或肢体灌注不良(OR,2.18,均 p<0.05)。44 例(9.2%)发生早期死亡,且 2 期(OR,4.38)和 3 期 AKI(OR,6.30;均 p<0.03)是独立的死亡预测因素。10 年生存率为 46.5%,晚期死亡的独立预测因素包括主动脉直径(OR,1.02)、慢性阻塞性肺疾病(OR,2.02)、慢性肾脏病(OR,3.51)以及 2 期(OR,2.74)和 3 期 AKI(OR,2.26,均 p<0.01)。10 年免于主动脉破裂、再次夹层或需要再次干预的生存率为 39.8%。晚期主动脉事件的独立预测因素包括高血脂(OR,1.55)、糖尿病(OR,0.38)、主动脉直径(OR,1.03)和结缔组织疾病(OR,2.54,均 p<0.03),但与 AKI 无关(p=0.149)。
ABAD 后 AKI 很常见,增加了早期死亡率和住院时间,降低了晚期生存率。尽管 AKI 对生存率有不利影响,但与晚期主动脉事件无关。