The relation between the incidence and severity of acute kidney injury (AKI) and clinical outcomes remains unclear in patients with DeBakey type III acute aortic dissection (AAD). We retrospectively assessed 56 patients admitted to our hospital for type III AAD within 48 hours of the onset of symptoms. The presence of AKI was identified, and its severity was staged on the basis of changes in serum creatinine (SCr) levels within 7 days after admission. We investigated the relations between AKI and clinical presentations, in-hospital complications, and predischarge renal function; AKI was observed in 20 patients (36%). After adjusting for age, gender, and body mass index, the incidence of AKI was associated with a history of hypertension, electrocardiographic ST-T changes, DeBakey type IIIb, and SCr level on admission. Maximum white blood cell count and serum C-reactive protein level were higher in patients with AKI than in those without AKI. AKI was associated with a greater incidence of in-hospital complications (70% vs 39%, p = 0.03) and higher SCr levels at discharge (1.1 [range 1.0 to 2.0] vs 0.9 [range 0.7 to 1.0] mg/dl, p = 0.0001). These associations were more pronounced in patients with relatively severe AKI. Multivariate analysis revealed that SCr level on admission and DeBakey type IIIb with renal artery involvement were major predictors of AKI. In conclusion, renal function on admission and renal artery involvement were significant risk factors for AKI, which was associated with poor outcomes and enhanced inflammatory response during hospitalization in patients with type III AAD.
Acute aortic dissection (AAD) is an uncommon but potentially devastating condition that necessitates immediate and intensive management to prevent catastrophic complications. Patients with uncomplicated DeBakey type III (or Stanford type B) AAD can be treated with aggressive medical management that includes strict control of blood pressure and heart rate. However, some patients with type III AAD experience severe complications, such as aortic rupture, visceral ischemia due to malperfusion of a branch vessel, or limb ischemia, for which emergent surgical treatment is usually required. In addition, respiratory failure due to acute lung injury or pleural effusion sometimes occurs in association with enhanced systemic inflammatory reactions after AAD. Acute kidney injury (AKI), which is associated with adverse outcomes in critically ill patients, is also reported to occur in some patients with AAD. Although postoperative AKI is reported to be a significant predictor of mortality in surgically treated patients with AAD, the clinical significance of AKI has not yet been determined in medically treated patients with type III AAD. Thus, in the present study, we investigated the incidence and severity of AKI and the association between AKI and in-hospital outcomes in patients with type III AAD.
Methods
From March 2003 to December 2012, a total of 74 consecutive patients were admitted to the intensive care unit at the Tokyo Saiseikai Central Hospital for DeBakey type III AAD. Patients who were admitted >48 hours after symptom onset (n = 15) were excluded, because this study focused on the incidence of AKI and its clinical implications in the early phase of AAD. Patients who died of aortic rupture on admission (n = 2) and those with end-stage chronic kidney disease on hemodialysis (n = 1) were also excluded from this study. None of the patients were excluded because of data incompleteness. Finally, we enrolled 56 patients. The local Institutional Review Board of the hospital approved this retrospective study and waived the need for individual consent.
We reviewed patients’ medical records and laboratory results to evaluate the following clinical characteristics: age; gender; body mass index; risk factors for atherosclerosis including hypertension, diabetes mellitus, dyslipidemia, and cigarette smoking; history of previous coronary artery disease, stroke, aortic disease, Marfan syndrome, or cancer; time elapsed from symptom onset to hospital admission; vital signs including blood pressure and heart rate on arrival; and electrocardiographic findings. AAD was verified by contrast-enhanced computed tomography (CT) and categorized as types I, II, or III according to the DeBakey classification. Type III AADs were further subclassified, depending on whether the dissection was limited to the descending thoracic aorta (IIIa) or extended below the diaphragm to involve the abdominal aorta (IIIb). According to the enhancement of the false lumen, the thrombosed type was defined as a completely thrombosed false lumen or intramural hematoma and the open type was defined as a nonthrombosed or partially thrombosed false lumen. The perfusion status of the major branches from the dissected aorta, including the renal arteries, was also assessed. All data from CT scans were analyzed by 2 independent radiologists without the knowledge of the patients’ backgrounds. During the acute phase, arterial blood pressure was monitored and systolic blood pressure was controlled between 100 and 120 mm Hg with intravenous administration and/or oral intake of antihypertensives such as β blockers, calcium antagonists, sodium nitroprusside, or nitroglycerin. Blood samples for measurements of white blood cell (WBC) count and serum creatinine (SCr), glucose, and C-reactive protein (CRP) levels were obtained on admission and then every day for at least 7 days.
AKI was defined according to the following criteria, which are based on the AKI Network criteria : either an increase in SCr level by ≥0.3 mg/dl within 48 hours or an increase in SCr level to ≥1.5 times the reference level obtained on admission. It is also recommended that AKI be defined according to the urine output; however, the urine output was not used in this study because retrospectively collected data have the potential to be inaccurate. AKI was staged for severity according to the following criteria: stage 1, an increase in SCr level to 1.5 to 2.0 times the reference level or an increase by ≥0.3 mg/dl; stage 2, increase in SCr level to 2.0 to 3.0 times the reference level; and stage 3, increase in SCr level to >3.0 times the reference level or an increase in SCr level to ≥4.0 mg/dl with an acute increase by at least 0.5 mg/dl.
Patients were divided into 2 groups according to the presence or absence of AKI during hospitalization; stages 2 and 3 AKIs were considered relatively severe. We then investigated the relations between the presence and severity of AKI and a variety of clinical outcomes, including in-hospital complications such as organ or limb malperfusion, acute lung injury, acute coronary syndrome, and stroke; duration of the hospital stay; maximum WBC count and serum CRP levels; and renal function (SCr) at discharge. The indications for surgical therapy included aortic wall rupture, malperfusion syndromes such as visceral or limb ischemia, progression of dissection, enlarging aneurysm, and refractory pain. Patients with life-threatening complications underwent urgent repair, and the remaining patients underwent elective surgery. Renal infarction was defined as the perfusion defect of the focal or global renal parenchyma on contrast-enhanced CT scan associated with symptoms such as abdominal or flank pain. Acute lung injury was defined as the lowest PaO 2 /fractional inspired oxygen ratio of ≤200 mm Hg. Acute coronary syndrome was defined as unstable angina or acute myocardial infarction according to the American College of Cardiology/American Heart Association criteria. The diagnosis of myocardial infarction was determined by increased cardiac biomarkers (creatine kinase-MB or troponin) with electrocardiographic changes indicative of myocardial ischemia. Stroke was defined as an ischemic cerebral infarction caused by an embolic or thrombotic occlusion of a major intracranial artery.
Categorical variables are expressed as the number of patients (%). Normally distributed continuous data are presented as mean ± SD, whereas non-normally distributed continuous data are presented as median (interquartile range). Fisher’s exact test or the chi-square test was used to compare categorical variables, and the unpaired Student t test, Mann-Whitney U test, or Kruskal-Wallis rank test was used to compare continuous variables. Bonferroni corrections were used for post hoc multiple tests. To determine predictors of AKI, as a first step, multiple logistic regression analysis adjusted for age, gender, and body mass index was performed with each variable with p <0.10 by univariate analyses (model 1). Subsequently, a new logistic regression model (model 2) was built with independent variables including those with p <0.05 in model 1 plus age, gender, and body mass index. In addition, DeBakey type IIIb AADs were divided into the 2 subgroups according to the presence or absence of renal artery involvement, which were incorporated into the separate model (model 3). Statistical significance was defined as a p value of <0.05. All statistical analyses were performed using StatView, version 5.0 (SAS Institute, Cary, North Carolina), or SPSS, version 20 (SPSS, Inc., Chicago, Illinois).
Results
The patients’ clinical characteristics are presented in Table 1 . The mean age of the patients was 64 ± 13 years, 40 (71%) were men, 43 (77%) had a history of hypertension, and 41 (73%) had smoked or were current smokers. The time elapsed from symptom onset to hospital admission was 1.7 hours (0.9 to 5.6). Presenting symptoms included chest pain (55%), back pain (88%), and abdominal pain (34%). Systolic blood pressure and heart rate on arrival were 184 ± 34 mm Hg and 78 ± 16 beats/min, respectively. CT findings revealed that 35 patients (63%) had thrombosed-type AAD and that the AAD in 40 patients (71%) could be classified as DeBakey type IIIb. The SCr level on admission was 0.8 mg/dl (0.7 to 1.0).
| Variable | No AKI (n = 36) | AKI (n = 20) | p Value ∗ | AKI Stage 1 (n = 12) | AKI Stage 2/3 (n = 8) | p Value † |
|---|---|---|---|---|---|---|
| Age (yrs) | 65 ± 13 | 64 ± 13 | 0.82 | 65 ± 14 | 63 ± 10 | 0.93 |
| Men | 23 (64%) | 17 (85%) | 0.09 | 9 (75%) | 8 (100%) | 0.12 |
| Body mass index (kg/m 2 ) | 23.3 ± 3.3 | 25.2 ± 3.6 | 0.06 | 24.4 ± 3.3 | 26.4 ± 4.0 | 0.08 |
| Body mass index ≥25 kg/m 2 | 12 (33%) | 10 (50%) | 0.35 | 5 (42%) | 5 (63%) | 0.31 |
| Hypertension | 24 (67%) | 19 (95%) | 0.02 | 12 (100%) | 7 (88%) | 0.04 ‡ , § |
| Dyslipidemia | 14 (39%) | 10 (50%) | 0.42 | 6 (50%) | 4 (50%) | 0.72 |
| Diabetes mellitus | 2 (6%) | 3 (15%) | 0.34 | 1 (8%) | 2 (25%) | 0.22 |
| Cigarette smoker | 25 (69%) | 16 (80%) | 0.39 | 11 (92%) | 5 (63%) | 0.25 |
| Known coronary artery disease | 3 (8%) | 1 (5%) | 1.00 | 0 | 1 (13%) | 0.51 |
| Previous stroke | 4 (11%) | 0 | 0.29 | 0 | 0 | 0.30 |
| Previous aortic disease | 5 (14%) | 1 (5%) | 0.40 | 1 (8%) | 0 | 0.49 |
| Marfan syndrome | 1 (3%) | 0 | 1.00 | 0 | 0 | 0.75 |
| Cancer | 7 (19%) | 1 (5%) | 0.24 | 0 | 1 (13%) | 0.25 |
| Time from onset to admission (h) | 1.8 (1.0–7.3) | 1.4 (0.9–3.6) | 0.27 | 1.4 (1.0–2.2) | 3.0 (0.8–7.5) | 0.48 |
| Presenting symptoms | ||||||
| Chest pain | 20 (56%) | 11 (55%) | 0.97 | 9 (75%) | 2 (25%) | 0.09 |
| Back pain | 31 (86%) | 18 (90%) | 0.67 | 11 (92%) | 7 (88%) | 0.88 |
| Abdominal pain | 13 (36%) | 6 (30%) | 0.64 | 4 (33%) | 2 (25%) | 0.83 |
| Vital signs on admission | ||||||
| Systolic blood pressure (mm Hg) | 183 ± 39 | 185 ± 30 | 0.81 | 192 ± 34 | 174 ± 22 | 0.55 |
| Systolic blood pressure ≥180 mm Hg | 16 (44%) | 12 (60%) | 0.26 | 9 (75%) | 3 (38%) | 0.14 |
| Heart rate (beats/min) | 76 ± 16 | 80 ± 16 | 0.40 | 72 ± 9 | 92 ± 15 | 0.01 § , ‖ |
| Respiratory rate (/min) | 19 ± 5 | 19 ± 4 | 0.92 | 19 ± 3 | 19 ± 5 | 0.96 |
| Body temperature (°C) | 36.5 ± 0.7 | 36.3 ± 1.0 | 0.53 | 36.0 ± 0.9 | 36.8 ± 1.1 | 0.10 |
| Electrocardiographic findings on admission | ||||||
| Sinus rhythm | 33 (92%) | 20 (100%) | 0.55 | 12 (100%) | 8 (100%) | 0.41 |
| Atrial fibrillation | 3 (8%) | 0 | 0.55 | 0 | 0 | 0.41 |
| Left ventricular hypertrophy | 7 (19%) | 6 (30%) | 0.51 | 3 (25%) | 3 (38%) | 0.54 |
| ST-T changes | 9 (25%) | 13 (65%) | 0.003 | 7 (58%) | 6 (75%) | 0.01 § |
| CT findings on admission | ||||||
| Thrombosed type | 24 (67%) | 11 (55%) | 0.39 | 9 (75%) | 2 (25%) | 0.05 |
| DeBakey type IIIb | 23 (64%) | 17 (85%) | 0.09 | 9 (75%) | 8 (100%) | 0.12 |
| Renal artery involvement | 1 (3%) | 6 (30%) | 0.006 | 1 (8%) | 5 (63%) | <0.0001 § , ‖ |
| Laboratory findings on admission | ||||||
| SCr (mg/dl) | 0.7 (0.6–0.8) | 1.0 (0.9–1.2) | 0.0002 | 0.9 (0.8–1.1) | 1.1 (0.9–1.2) | 0.007 ‡ , § |
| WBC (/μl) | 9,800 (7,600–11,750) | 11,500 (7,450–13,775) | 0.26 | 8,450 (6,750–12,325) | 13,350 (11,125–16,950) | 0.02 § |
| Serum CRP (mg/dl) | 0 (0–1.0) | 0 (0–0.4) | 0.86 | 0 (0–0.4) | 0 (0–0.7) | 0.94 |
| Blood glucose (mg/dl) | 129 (113–154) | 149 (137–161) | 0.02 | 137 (131–159) | 161 (148–187) | 0.02 § |
| Antihypertensives after admission | ||||||
| Intravenous β blockers | 26 (72%) | 14 (70%) | 1.00 | 8 (67%) | 6 (75%) | 0.91 |
| Oral β blockers | 35 (97%) | 19 (95%) | 0.86 | 12 (100%) | 7 (88%) | 0.30 |
| Intravenous calcium antagonists | 34 (94%) | 19 (95%) | 1.00 | 11 (92%) | 8 (100%) | 0.72 |
| Oral calcium antagonists | 30 (83%) | 20 (100%) | 0.08 | 12 (100%) | 8 (100%) | 0.15 |
| Sodium nitroprusside | 9 (25%) | 11 (55%) | 0.02 | 6 (50%) | 5 (63%) | 0.07 |
| Nitroglycerin | 8 (22%) | 9 (45%) | 0.08 | 6 (50%) | 3 (38%) | 0.17 |
∗ Compared between no AKI and AKI.
† Compared between no AKI, AKI stage 1, and AKI stage 2/3.
‡ p <0.05 when compared between no AKI and AKI stage 1.
§ p <0.05 when compared between no AKI and AKI stage 2/3.
‖ p <0.05 when compared between AKI stage 1 and AKI stage 2/3.
AKI was observed in 20 patients (36%). AKIs were classified into stage 1 (n = 12), stage 2 (n = 2), and stage 3 (n = 6) according to their severity. Patients with AKI were more likely to have a history of hypertension than those without AKI. Although the heart rate on arrival was similar in patients with and without AKI, it was higher in patients with relatively severe AKI (stage 2 or 3) than in those without AKI or those with AKI stage 1. ST-T changes on electrocardiogram were more common in patients with AKI, particularly those with relatively severe AKI, compared with those without AKI. Renal artery involvement occurred more frequently in patients with AKI, particularly those with relatively severe AKI, than in those without AKI. Narrowing or occlusion of 1 or both renal arteries was caused by either flow-limiting compression of the true lumen from which the renal artery originated by the expanding false lumen (n = 6) or thrombotic occlusion of the false lumen from which the renal artery arose (n = 1). On admission, the SCr level was significantly higher in the AKI group than in the non-AKI group. The blood glucose level was also higher in the AKI group than in the non-AKI group. In addition, SCr and blood glucose levels were higher in patients with relatively severe AKI than in those without AKI. The WBC count and serum CRP level on admission were comparable between the AKI and non-AKI groups, but patients with relatively severe AKI had a higher WBC count on admission than those without AKI. Sodium nitroprusside was administered more frequently in patients with AKI than in those without AKI, although the rates of other antihypertensives use were comparable between the 2 groups.
The in-hospital outcomes, displayed according to the presence and severity of AKI, are presented in Table 2 . Malperfusion syndromes, such as intestinal ischemia, renal infarction, or limb ischemia, occurred more frequently in patients with AKI than in those without AKI. Renal infarction occurred in 4 patients with relatively severe AKI, whereas it occurred in only 1 patient in the non-AKI group. Three patients with relatively severe AKI underwent surgery: 1 for progressive intestinal ischemia and renal infarction 4 days after admission, 1 for progressive limb ischemia and renal infarction 7 days after admission, and 1 for chronic limb ischemia 3 months after admission. All of them had AKI before surgery. Only 1 patient without AKI underwent elective surgery for enlarging aneurysm. Acute lung injury occurred in 28 of 56 patients with type III AAD (46%) and 8 of them (31%) were treated with noninvasive positive pressure ventilation or mechanical ventilation. We did not find a significant difference in the incidence of acute lung injury between the AKI and non-AKI groups, although there was a trend toward increased frequency of this complication in patients with relatively severe AKI compared with those without AKI (p = 0.11). Five patients with AKI had acute coronary syndrome (n = 2) or stroke (n = 3) during hospitalization, but none of the patients without AKI had such events (31% vs 0%, p = 0.004). Patients with AKI had a greater incidence of any AAD-related complications (malperfusion syndrome or acute lung injury) or adverse cerebrocardiovascular event (acute coronary syndrome or stroke) compared with those without AKI. Only 1 patient with relatively severe AKI required temporary hemodialysis. No patients died during the hospital stay. Duration of the hospital stay was longer in patients with relatively severe AKI than in those without AKI or those with AKI stage 1.
| In-Hospital Outcome | No AKI (n = 36) | AKI (n = 20) | p Value ∗ | AKI Stage 1 (n = 12) | AKI Stage 2/3 (n = 8) | p Value † |
|---|---|---|---|---|---|---|
| In-hospital complications | ||||||
| Malperfusion syndrome | 1 (3%) | 5 (25%) | 0.02 | 0 | 5 (63%) | <0.0001 ‡ , § |
| Intestinal ischemia | 0 | 1 (5%) | 0.36 | 0 | 1 (13%) | 0.05 |
| Renal infarction | 1 (3%) | 4 (20%) | 0.05 | 0 | 4 (50%) | <0.0001 ‡ , § |
| Limb ischemia | 0 | 2 (10%) | 0.12 | 0 | 2 (25%) | 0.002 ‡ |
| Acute lung injury | 14 (39%) | 12 (60%) | 0.13 | 6 (50%) | 6 (75%) | 0.17 |
| Requiring NPPV/mechanical ventilation | 3 (8%) | 5 (25%) | 0.12 | 2 (17%) | 3 (38%) | 0.10 |
| Acute coronary syndrome | 0 | 2 (10%) | 0.12 | 1 (8%) | 1 (13%) | 0.14 |
| Stroke | 0 | 3 (15%) | 0.04 | 1 (8%) | 2 (25%) | 0.02 ‡ |
| Any of the aforementioned complications | 14 (39%) | 14 (70%) | 0.03 | 7 (58%) | 7 (88%) | 0.04 ‡ |
| Duration of the hospital stay (days) | 19 (16–26) | 23 (18–37) | 0.24 | 18 (14–30) | 39 (23–62) | 0.02 ‡ , § |
∗ Compared between no AKI and AKI.
† Compared between no AKI, AKI stage 1, and AKI stage 2/3.
‡ p <0.05 when compared between no AKI and AKI stage 2/3.
§ p <0.05 when compared between AKI stage 1 and AKI stage 2/3.
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