Contrast-induced acute kidney injury (CI-AKI) is a serious complication that is difficult to predict in patients with chronic kidney disease (CKD) undergoing percutaneous coronary intervention (PCI). The aim of this study was to investigate predictors and clinical outcomes of CI-AKI in patients with CKD after PCI. A total of 297 patients with CKD who underwent PCI from September 2006 to December 2011 were enrolled. CI-AKI was defined as serum creatinine level either ≥25% or ≥0.5 mg/dl from baseline within 72 hours after PCI. The primary outcome was all-cause death. The median follow-up duration was 26 months (interquartile range 12 to 40), and CI-AKI occurred in 55 patients (19%). In multivariate logistic regression analyses, the development of CI-AKI was associated with female gender, left ventricular systolic dysfunction, acute myocardial infarction, PCI for left main disease, serum hemoglobin level, and a contrast volume to creatinine clearance ratio >6.0. The development of CI-AKI was significantly associated with increased in-hospital mortality (18.2% vs 3.7%, p = 0.001). Cox proportional-hazard analysis showed that the incidence of all-cause death was significantly higher in patients who developed CI-AKI than in those without CI-AKI (41.8% vs 16.1%, adjusted hazard ratio 3.0, 95% confidence interval 1.6 to 5.6, p <0.001). In conclusion, female gender, left ventricular systolic dysfunction, acute myocardial infarction, PCI for left main disease, serum hemoglobin level, and contrast volume to creatinine clearance ratio >6.0 are independent predictors of CI-AKI. The development of CI-AKI is significantly associated with increased in-hospital and long-term adverse clinical outcomes in patients with CKD undergoing PCI.
Contrast-induced acute kidney injury (CI-AKI) is the third leading cause of hospital-acquired acute kidney injury and has been recognized as a serious complication of percutaneous coronary intervention (PCI), which may be associated with increased morbidity and mortality. The overall incidence of CI-AKI is reported to be 3.3% in patients after PCI ; however, this value is variable depending on the presence of preexisting risk factors. Recent studies try to prevent the development of CI-AKI such as remote ischemic conditioning and well established risk factors of CI-AKI include diabetes, congestive heart failure, acute hypotension, advanced age, ST-elevation myocardial infarction (MI), volume depletion, the amount of contrast administered, the type of contrast media, and the simultaneous use of nephrotoxic medications in unselected patients after PCI. Chronic kidney disease (CKD) is also an important risk factor for the occurrence of CI-AKI, which is caused by a decrease in compensatory mechanisms to maintain filtration function and a smaller number of nephrons to excrete the contrast load. However, the risk factors for the development of CI-AKI after systemic exposure of contrast media in patients with CKD after PCI has been not well established. In the present study, we aimed to investigate the predictors of CI-AKI and the association of CI-AKI with adverse clinical outcomes in patients with CKD after PCI.
Methods
This was a retrospective, single center, observational study. The subjects were recruited from the cardiovascular catheterization database of Samsung Medical Center (Seoul, South Korea). From September 2006 to December 2011, a total of 471 consecutive patients with CKD underwent PCI with drug-eluting stent. Patients on dialysis, patients who died within 72 hours after the procedure, and patients who had no available data were excluded. Baseline clinical, laboratory, and angiographic characteristics were collected from the databases and medical records. The institutional review board approved the present study, and informed consent was waived.
Experienced operators performed all procedures using standard interventional techniques. Patients who had not previously taken antiplatelet agents were administered loading doses of aspirin (300 mg) and clopidogrel (300 to 600 mg). Anticoagulation therapy during PCI was performed following the current practice guidelines of the Korean Society of Interventional Cardiology. The type of drug-eluting stent and glycoprotein IIb/IIIa receptor antagonist to be use depended on the operator’s discretion. Nonionic low-osmolar agents (iopamidol, iopromide, and iobitridol) and iso-osmolar agent (iodixanol) were used in all angiography procedures. In the elective PCI, patients with CKD routinely received intravenous hydration with isotonic saline solution at 1 ml/kg/hour for 12 hours before the diagnostic procedure and for 12 hours after procedure according to local institute protocol. In the emergency PCI, hydration was performed during the diagnostic procedure using isotonic saline solution and was continued at a rate of 1 ml/kg/hour for at least 12 hours. Duration of dual antiplatelet therapy was determined by the operators.
Serum creatinine was measured before PCI and daily during 3 days after PCI. Estimated glomerular filtration rate (eGFR) was obtained using the equation from the Modification of Diet in Renal Disease formula: eGFR = 175 × serum creatinine −1.154 × age −0.203 × (0.742, if female). CKD was defined as eGFR <60 ml/min/1.73 m 2 for 3 months, which is the accepted cutoff value of CKD by the National Kidney Foundation Kidney Disease Outcomes Quality Initiative guidelines. CI-AKI was defined as serum creatinine level either ≥25% or ≥0.5 mg/dl from baseline within 72 hours after contrast exposure. The contrast volume to creatinine clearance (V/CrCl) ratio was calculated by dividing the volume of contrast media used for PCI by the patient’s baseline eGFR. Left ventricular (LV) systolic dysfunction was defined as an LV ejection fraction <55%.
All-cause death was defined as any death after 72 hours after PCI and was considered to be of cardiac origin unless a definite noncardiac cause could be established. MI was defined as an elevation of cardiac enzymes (troponin I or myocardial band fraction of creatinine kinase) with ischemic symptoms or electrocardiographic findings of ischemia. Target lesion revascularization was defined as a repeat PCI of the lesion within 5 mm of stent deployment.
The follow-up clinical status was documented by review of hospital records, telephone interviews, or contacting general practitioners. The primary outcome of this study was to compare the incidences of all-cause death during follow-up between subjects who developed CI-AKI and those who did not develop CI-AKI. The secondary outcomes were the need for dialysis, cardiac death, recurrent MI, and target lesion revascularization.
Categorical variables are presented as numbers and percentages and were compared using the chi-square test and Fisher’s exact test. Continuous variables are expressed as mean ± SD and were compared using the Student t test and Mann-Whitney U test, as appropriate. The variables associated with the development of CI-AKI in univariate analysis were entered into a stepwise forward binary logistic regression to assess independent predictors of CI-AKI. Receiver-operator characteristics analysis was used to determine the optimal cutoff value for contrast V/CrCl. Event-free survival was compared between patients with CKD who developed CI-AKI and those who did not develop CI-AKI using the Kaplan-Meier estimate with the log-rank test. Adjusted hazard ratios for outcomes were estimated using the Cox multivariate proportional hazards model comparing the 2 groups. Adjusted covariates included age, gender, body surface area, LV systolic dysfunction, clinical presentation, diabetes mellitus, type of contrast media, contrast V/CrCl >6.0, eGFR, serum hemoglobin, number of inserted stents, shock, PCI for left main (LM) coronary artery disease, and hydration before the procedure. Statistical analyses were performed with PASW Statistics 18 (SPSS Inc., Chicago, Illinois). All tests were 2-tailed, and p <0.05 was considered statistically significant.
Results
Of the consecutive 471 patients with CKD who underwent PCI, 174 were excluded (56 patients on dialysis, 4 patients who died within 72 hours after procedure, 40 patients who had no information of contrast media, and 74 patients who had no laboratory data within 72 hours after procedure). Among the included 297 patients, 55 patients developed CI-AKI (19%). Baseline clinical and angiographic characteristics are listed in Table 1 . Overall, patients in the CI-AKI group were high-risk subjects. Compared with patients in the no CI-AKI group, those who developed CI-AKI had a higher prevalence of acute myocardial infarction (AMI), shock, multivessel disease, and LM disease. They also had lower LV ejection fraction, eGFR, and hemoglobin levels than those without CI-AKI. Female gender was common in the CI-AKI group. The amount of contrast media used in the procedure showed no significant difference between the 2 groups but the contrast V/CrCl was higher in patients with CI-AKI than patients who did not develop CI-AKI.
| Variable | Contrast-Induced AKI | p value | |
|---|---|---|---|
| No (n = 242) | YES (n = 55) | ||
| Age (years) | 70.9 ± 10.2 | 69.2 ± 11.4 | 0.27 |
| Female | 73 (30.2%) | 24 (43.6%) | 0.06 |
| Body surface area (m 2 ) | 1.69 ± 0.18 | 1.68 ± 0.16 | 0.75 |
| Current smoker | 31 (12.8%) | 8 (14.6%) | 0.83 |
| Clinical presentation | <0.001 | ||
| Stable angina pectoris | 101 (41.7%) | 11 (20.0%) | |
| Unstable angina pectoris | 46 (19.0%) | 2 (3.6%) | |
| NSTEMI | 68 (28.1%) | 32 (58.2%) | |
| STEMI | 27 (11.2%) | 10 (18.2%) | |
| Diabetes mellitus | 165 (68.2%) | 44 (80.0%) | 0.10 |
| Duration (years) | 16.2 ± 10.7 | 16.5 ± 11.2 | 0.89 |
| Treatment with insulin | 31 (18.8%) | 13 (29.5%) | 0.15 |
| Hypertension | 210 (86.8%) | 43 (78.2%) | 0.14 |
| Dyslipidemia | 66 (27.3%) | 20 (36.4%) | 0.19 |
| Prior myocardial infarction | 71 (29.3%) | 22 (40.0%) | 0.15 |
| Prior coronary bypass | 14 (5.8%) | 2 (3.6%) | 0.75 |
| Prior percutaneous coronary intervention | 52 (21.5%) | 12 (21.8%) | 1.00 |
| Prior cerebrovascular accident | 22 (9.1%) | 9 (16.4%) | 0.14 |
| Hydration before procedure | 151 (62.4%) | 32 (58.2%) | 0.65 |
| Amount of hydration (mL) | 1,028 ± 580 | 1,020 ± 570 | 0.95 |
| Duration of hydration | 0.76 | ||
| 0 to 12 hours | 27 (17.9%) | 4 (12.5%) | |
| 12 to 24 hours | 83 (55.0%) | 19 (59.4%) | |
| Over 24 hours | 41 (27.2%) | 9 (28.1%) | |
| Contrast media | 0.46 | ||
| Iso-osmolar | 109 (45.0%) | 28 (50.9%) | |
| Low osmolar | 133 (55.0%) | 27 (49.1%) | |
| Contrast volume (mL) | 194 ± 80 | 197 ± 64 | 0.73 |
| V/CrCl | 5.8 ± 4.4 | 9.1 ± 9.3 | 0.01 |
| Shock | 15 (6.2%) | 8 (14.5%) | 0.05 |
| Hemoglobin (g/dL) | 11.8 ± 2.1 | 10.8 ± 2.1 | 0.001 |
| Peak serum creatinine (mg/dl) | 1.83 ± 0.97 | 2.41 ± 1.63 | 0.02 |
| 24 to 48 hours | 208 (86.0%) | 46 (83.6%) | 0.67 |
| 48 to 72 hours | 34 (14.0%) | 9 (16.4%) | |
| eGFR (mL/min) | 40.0 ± 13.3 | 33.1 ± 15.7 | 0.003 |
| LV ejection fraction (%) | 53.3 ± 14.4 | 45.1 ± 16.6 | <0.001 |
| LV systolic dysfunction | 98 (40.5%) | 35 (63.6%) | 0.002 |
| Multivessel coronary artery disease | 176 (72.7%) | 47 (85.5%) | 0.06 |
| Involved | |||
| Left main | 17 (7.0%) | 9 (16.4%) | 0.04 |
| Left anterior descending | 197 (81.4%) | 47 (85.5%) | 0.56 |
| Left circumflex | 156 (64.5%) | 40 (72.7%) | 0.27 |
| Right | 148 (61.2%) | 32 (58.2%) | 0.76 |
| Number of stent | 1.00 | ||
| 1 | 142 (58.7%) | 32 (58.2%) | |
| 2 or more | 100 (41.3%) | 23 (41.8%) | |
| Type of stent | 1.00 | ||
| 1 st generation DES | 64 (26.4%) | 14 (25.5%) | |
| 2 nd generation DES | 178 (73.6%) | 41 (74.0%) | |
Receiver-operator characteristics curve analysis showed fair discrimination between patients with CKD with and without the development of CI-AKI after revascularization at a contrast V/CrCl of 6.0 (C-statistic of 0.62). At this cutoff value, the sensitivity and specificity were 53% and 72%, respectively (p <0.001). Binary logistic regression was performed to recognize predictors of CI-AKI in patients with CKD undergoing PCI ( Table 2 ). The significant univariate predictors of CI-AKI were LV systolic dysfunction, AMI, V/CrCl >6.0, serum hemoglobin level, shock, and PCI for LM disease. In the multivariate regression model, the independent predictors for the occurrence of CI-AKI were female gender, LV systolic dysfunction, AMI, V/CrCl >6.0, serum hemoglobin level, and PCI for LM disease.
| Univariate analysis | Multivariate analysis | |||
|---|---|---|---|---|
| p value | HR | 95% CI | p value | |
| Age ≥70 | 0.23 | 0.57 | 0.28-1.20 | 0.14 |
| Female gender | 0.06 | 2.42 | 1.04-5.64 | 0.04 |
| Body surface area (m 2 ) | 0.75 | 3.23 | 0.34-30.90 | 0.31 |
| LV systolic dysfunction | 0.002 | 2.25 | 1.09-4.66 | 0.03 |
| Acute myocardial infarction | 0.002 | 2.36 | 1.07-5.17 | 0.03 |
| Diabetes mellitus | 0.10 | 1.22 | 0.55-2.68 | 0.63 |
| Type of contrast | 0.46 | 1.21 | 0.60-2.43 | 0.59 |
| V/CrCl > 6.0 | 0.002 | 2.99 | 1.18-7.60 | 0.02 |
| eGFR | 0.003 | 1.00 | 0.97-1.04 | 0.82 |
| Hemoglobin (g/dL) | 0.001 | 0.82 | 0.67-1.01 | 0.05 |
| Number of inserted stent (≥2) | 1.00 | 0.88 | 0.43-1.80 | 0.72 |
| Shock | 0.05 | 1.24 | 0.39-3.97 | 0.72 |
| PCI for LM disease | 0.02 | 3.86 | 1.35-11.07 | 0.01 |
| Hydration before procedure | 0.32 | 1.19 | 0.54-2.65 | 0.66 |
Stay updated, free articles. Join our Telegram channel
Full access? Get Clinical Tree
