Abstract
Purpose
The purpose of the study was to compare creatinine clearance (CrCl), estimated glomerular filtration rate (eGFR) and serum creatinine (SCr) in predicting contrast-induced acute kidney injury (CI-AKI), dialysis and death following percutaneous coronary intervention (PCI).
Methods and Materials
Data were prospectively collected on 7759 consecutive patients within the Dartmouth Dynamic Registry undergoing PCI between January 1, 2000, and December 31, 2006. Renal function was measured at baseline and within 48 h after PCI using three methods: CrCl using the Cockcroft–Gault equation, eGFR using the abbreviated Modification of Diet in Renal Disease equation and SCr. We compared CrCl, eGFR and SCr in predicting CI-AKI, post-PCI dialysis-dependent renal failure and in-hospital mortality. Areas under the receiver operating characteristic curve (ROC) were calculated using logistic regression and tested for equality.
Results
On univariable analysis, CrCl [ROC: 0.69; 95% confidence interval (CI): 0.67–0.72] predicted CI-AKI better than eGFR (ROC: 0.67; 95% CI: 0.64–0.70) ( P =.013) and SCr (ROC: 0.64; 95% CI: 0.61–0.67) ( P <.001). Creatinine clearance (ROC: 0.73; 95% CI: 0.69–0.77) and eGFR (ROC: 0.70; 95% CI: 0.65–0.74) outperformed SCr for predicting in-hospital mortality. On multivariable analysis, CrCl (ROC: 0.77; 95% CI: 0.75–0.80), SCr (ROC: 0.78; 95% CI: 0.76–0.80) and eGFR (ROC: 0.77; 95% CI: 0.75–0.80) predicted CI-AKI well. Creatinine clearance (ROC: 0.88; 95% CI: 0.85–0.90) and eGFR (ROC: 0.87; 95% CI: 0.85–0.90) were strong independent predictors of in-hospital mortality.
Conclusions
Creatinine clearance, eGFR and SCr predict CI-AKI equally well. Creatinine clearance and eGFR are strong independent predictors of in-hospital mortality.
1
Introduction
Contrast-induced acute kidney injury (CI-AKI) has been reported as the third most common cause of hospital acquired renal failure . Nash et al. found that 11% of hospital-acquired renal insufficiency cases were due to contrast media, with coronary angiogram and angioplasty measuring as the most common causes. Contrast-induced AKI is a potentially serious adverse effect of percutaneous coronary intervention (PCI) and is often associated with significant morbidity and mortality . Three commonly used methods of assessing renal function are serum creatinine (SCr), creatinine clearance (CrCl) as measured by the Cockcroft–Gault equation and estimated glomerular filtration rate (eGFR) as measured by the Modification of Diet in Renal Disease (MDRD) equation. The Cockcroft–Gault and MDRD equations are frequently used in clinical practice, but there is no agreement over which measurement strategy is more accurate in assessing renal function or which measure provides the best insight into patient-specific procedural risk. Estimating renal function accurately is important because renal dysfunction is a major risk factor for developing CI-AKI . Therefore, identifying those patients at risk for developing CI-AKI post-PCI may be beneficial as these patients could receive protective therapies to potentially decrease their risk. The purpose of this investigation is to compare SCr, CrCl and eGFR in their ability to predict CI-AKI, need for post-PCI dialysis and in-hospital mortality.
2
Methods
2.1
Study population
We analyzed data from 7759 consecutive patients from the Dartmouth Dynamic registry who underwent PCI from January 1, 2000, to December 31, 2006. The Dartmouth Dynamic registry is a large prospective clinical registry of consecutive patients undergoing diagnostic or interventional cardiovascular catheterization procedures at Dartmouth-Hitchcock Medical Center . The registry was approved by the Institutional Review Board (Dartmouth Center for the Protection of Human Subjects).
2.2
Data collection
Patient, disease and procedure characteristics were collected prospectively on all patients in the study, and we report them by baseline renal function as determined by SCr, eGFR and CrCl standard thresholds ( Tables 1 and 2 ). Patient characteristics included age, gender, body mass index (BMI), morbid obesity, hypertension, hypercholesterolemia, diabetes mellitus, peripheral vascular disease and chronic obstructive pulmonary disease. Cardiac disease characteristics included history of congestive heart failure, chest pain, stable angina, acute coronary syndrome, prior myocardial infarction, cardiogenic shock, ejection fraction (estimated and/or calculated), prior thrombolysis, prior coronary artery bypass graft (CABG) and acuity of current case (elective, urgent, emergent). Laboratory measures included baseline hematocrit and baseline SCr (mg/dl); baseline CrCl was calculated using the Cockcroft–Gault equation adjusted per 1.73 m 2 (ml/min/1.73 m 2 ): [(140−age in years)×body weight in kg×0.85 (if female)]/(72×SCr in mg/dl); baseline eGFR was calculated using the abbreviated MDRD equation (ml/min/1.73 m 2 ): 186×(SCr in mg/dl) −1.154 ×(age in years) −0.203 ×(0.742 if female)×(1.210 if African American) . Cardiovascular procedure characteristics recorded were type of procedure (diagnostic and interventional, staged interventional), mean dose and type of contrast agent used, coronary disease classification (single-vessel, double-vessel or triple-vessel disease; critical left main disease; significant left main disease; indeterminant) and intraaortic balloon pump use. Pre-PCI prophylactic treatment such as hydration, use of sodium bicarbonate, or use of N -acetylcysteine was not available as it was not captured in the data collection for the Dartmouth Dynamic Registry. Clinical outcomes measured in the post-PCI hospitalization period were CI-AKI, new-onset dialysis-dependent renal failure, in-hospital mortality from all causes, cardiac events (new myocardial infarction, cardiac arrest, stent thrombosis), stroke and postprocedure length of stay measured in days ( Table 3 ). Baseline SCr was defined as the last SCr prior to PCI. We defined AKI according to the Acute Kidney Injury Network criteria as an increase in SCr by at least ≥0.3 mg/dl or ≥50% from baseline to peak SCr that was measured within 48 h post-PCI . Vital status was assessed at discharge, and all-cause mortality was confirmed by comparing the data from the Dartmouth Dynamic Registry with the data from the Social Security Administration Death Master File using birth dates and social security numbers. We report in-hospital mortality in Table 3 as an outcome of the index hospitalization.
| Variables | SCr<1.5 N (%) | SCr≥1.5 N (%) | P | eGFR≥60 N (%) | eGFR<60 N (%) | P | CrCl≥60 N (%) | CrCl<60 N (%) | P |
|---|---|---|---|---|---|---|---|---|---|
| Mean±S.D. | Mean±S.D. | Mean±S.D. | Mean±S.D. | Mean±S.D. | Mean±S.D. | ||||
| N | 7013 (90.39) | 746 (9.61) | 5824 (75.06) | 1935 (24.94) | 5584 (71.97) | 2175 (28.03) | |||
| Age (years) | 63.8±12.3 | 72.1±11.3 | <.001 | 60.7±11.0 | 76.3±9.1 | <.001 | 62.1±12.0 | 71.0±11.3 | <.001 |
| Gender (female) | 2149 (30.64) | 209 (28.02) | .138 | 1359 (23.33) | 999 (51.63) | <.001 | 1390 (24.89) | 968 (44.51) | <.001 |
| BMI | 29.1±5.9 | 29.1±6.1 | .854 | 30.2±5.8 | 26.0±5.2 | <.001 | 29.2±5.9 | 28.9±6.1 | .067 |
| Morbid obesity | 561 (8.35) | 75 (10.43) | .147 | 573 (10.28) | 63 (3.39) | <.001 | 451 (8.39) | 185 (8.97) | .404 |
| Hypertension | 4317 (62.49) | 568 (76.45) | <.001 | 3480 (60.64) | 1405 (73.48) | <.001 | 3317 (60.16) | 1568 (73.37) | <.001 |
| Hypercholesterolemia | 4331 (62.71) | 442 (59.89) | .073 | 3662 (63.81) | 1111 (58.32) | <.001 | 3478 (63.05) | 1295 (60.86) | .065 |
| Diabetes mellitus | 1773 (25.83) | 308 (41.85) | <.001 | 1530 (26.82) | 551 (29.06) | .156 | 1324 (24.16) | 757 (35.72) | <.001 |
| PVD | 549 (8.20) | 106 (14.64) | <.001 | 386 (6.93) | 269 (14.50) | <.001 | 389 (7.25) | 266 (12.93) | <.001 |
| COPD | 581 (8.71) | 116 (16.04) | <.001 | 420 (7.57) | 277 (14.97) | <.001 | 430 (8.05) | 267 (13.00) | <.001 |
| Cardiac disease | |||||||||
| Congestive heart failure | 635 (9.41) | 196 (26.89) | <.001 | 408 (7.29) | 423 (22.52) | <.001 | 399 (7.40) | 432 (20.71) | <.001 |
| Chest pain | 4279 (65.65) | 412 (59.71) | .005 | 3623 (66.85) | 1068 (59.73) | <.001 | 3442 (66.09) | 1249 (62.45) | .013 |
| Stable angina | 1052 (17.08) | 103 (15.65) | .312 | 889 (17.34) | 266 (15.74) | .316 | 863 (17.48) | 292 (15.52) | .022 |
| Acute coronary syndromes | 2031 (32.48) | 227 (33.68) | .029 | 1678 (32.19) | 580 (33.82) | .456 | 1623 (32.45) | 635 (32.97) | .888 |
| Prior myocardial infarction | 3523 (52.57) | 444 (62.18) | <.001 | 2893 (52.02) | 1074 (57.90) | <.001 | 2736 (51.24) | 1231 (59.30) | <.001 |
| Cardiogenic shock | 84 (1.20) | 33 (4.42) | <.001 | 59 (1.01) | 58 (3.00) | <.001 | 46 (0.82) | 71 (3.26) | <.001 |
| Ejection fraction | |||||||||
| ≥70 | 383 (14.69) | 12 (14.63) | .057 | 328 (14.62) | 67 (15.02) | <.001 | 324 (14.84) | 71 (14.06) | <.001 |
| 60–69 | 988 (37.90) | 22 (26.83) | 874 (38.97) | 136 (30.49) | 845 (38.69) | 165 (32.67) | |||
| 50–59 | 669 (25.66) | 25 (30.49) | 585 (26.08) | 109 (24.44) | 571 (26.14) | 123 (24.36) | |||
| 40–49 | 333 (12.77) | 9 (10.98) | 279 (12.44) | 63 (14.13) | 272 (12.45) | 70 (13.86) | |||
| <40 | 234 (8.98) | 14 (17.07) | 177 (7.89) | 71 (15.92) | 172 (7.88) | 76 (15.05) | |||
| Prior therapy | |||||||||
| Prior thrombolysis | 528 (8.19) | 46 (6.73) | .350 | 454 (8.47) | 120 (6.80) | .049 | 398 (7.72) | 176 (8.92) | .144 |
| Prior CABG | 937 (13.79) | 179 (24.55) | <.001 | 740 (13.10) | 376 (20.04) | <.001 | 697 (12.82) | 419 (20.09) | <.001 |
| Laboratory measures | |||||||||
| Baseline hematocrit | 39.0±4.8 | 35.5±5.6 | <.001 | 39.6±4.6 | 35.9±4.9 | <.001 | 39.5±4.6 | 36.6±5.3 | <.001 |
| Baseline SCr (mg/dl) | 1.0±0.2 | 2.0±1.0 | <.001 | 1.0±0.2 | 1.4±0.7 | <.001 | 0.9±0.2 | 1.5±0.7 | <.001 |
| Baseline CrCl (ml/min/1.73 m 2 ) | 93.6±38.6 | 42.8±17.5 | <.001 | 103.7±34.4 | 43.6±11.8 | <.001 | 101.3±36.8 | 56.5±28.1 | <.001 |
| Baseline eGFR (ml/min/1.73 m 2 ) | 76.4±25.7 | 35.8±10.5 | <.001 | 80.3±25.6 | 49.1±17.5 | <.001 | 85.0±19.0 | 40.4±18.0 | <.001 |
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