CLINICAL RESEARCH: INTERVENTIONAL CARDIOLOGY
Volume-to-Creatinine Clearance RatioA Pharmacokinetically Based Risk Factor for Prediction of Early Creatinine Increase After Percutaneous Coronary Intervention
Warren K. Laskey, MD, FACC*,*,
Charles Jenkins, MD*,
Faith Selzer, PhD ,
Oscar C. Marroquin, MD, FACC,
Robert L. Wilensky, MD, FACC ,
Ruchira Glaser, MD, FACC,
Howard A. Cohen, MD, FACC ,
David R. Holmes, Jr, MD, FACC|| for the NHLBI Dynamic Registry Investigators
* University of New Mexico School of Medicine, Albuquerque, New Mexico
University of Pittsburgh, Pittsburgh, Pennsylvania
University of Pennsylvania School of Medicine, Philadelphia, Pennsylvania
Lenox Hill Heart and Vascular Institute, New York, New York
|| Mayo Clinic, Rochester, Minnesota.
Manuscript received January 29, 2007;
revised manuscript received March 1, 2007,
accepted March 28, 2007.
* Reprint requests and correspondence: Dr. Warren K. Laskey, Division of Cardiology, Department of Internal Medicine, University of New Mexico School of Medicine, MSC10-5550 1, University of New Mexico, Albuquerque, New Mexico 87131-0001. (Email: wlaskey{at}salud.unm.edu).
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Abstract
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Objectives: This study sought to validate a pharmacokinetically derived measure of the risk of an early increase in serum creatinine after percutaneous coronary intervention (PCI).
Background: The ratio of the volume of contrast media to the creatinine clearance (V/CrCl) has been shown to correlate with the area under the curve of contrast media concentration over time.
Methods: We calculated V/CrCl in 3,179 consecutive patients undergoing PCI. An increase in serum creatinine of >0.5 mg/dl by 24 to 48 h was considered abnormal. Receiver-operator characteristic methods were used to identify the optimal sensitivity and specificity for the observed range of V/CrCl. The predictive value of V/CrCl for the risk of an early increase in creatinine was assessed using multivariable logistic regression.
Results: The overall incidence of an abnormal, early increase in creatinine was 1.5%. The mean and median values of V/CrCl for patients with (mean 5.2 ± 4.4, median 4.3, interquartile range 2.7 to 6.0) and without (mean 3.0 ± 2.0, median 2.5, interquartile range 1.7 to 3.8) an early creatinine increase were each significantly (p < 0.001) different between groups. Furthermore, there was a significant association between V/CrCl and an early increase in creatinine (overall and trend, p < 0.001). The receiver-operator characteristic curve analysis indicated that a V/CrCl ratio of 3.7 was a fair discriminator for the early creatinine increase (C-statistic 0.69). After adjusting for other known predictors of post-PCI creatinine increase, V/CrCl  3.7 remained significantly associated with an early abnormal increase in serum creatinine (odds ratio 3.84; 95% confidence interval 2.0 to 7.3, p < 0.001).
Conclusions: A V/CrCl ratio >3.7 was a significant and independent predictor of an early abnormal increase in serum creatinine after PCI in this unselected patient population.
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Abbreviations and Acronyms
| | CAN = contrast media-associated nephrotoxicity | | CrCl = creatinine clearance | | PCI = percutaneous coronary intervention |
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Radiographic contrast media-associated nephrotoxicity (CAN) is responsible for approximately 11% of all iatrogenic renal insufficiency and is the third most common cause of hospital-acquired renal failure (1). Contrast media-associated nephrotoxicity is traditionally defined as an increase in serum creatinine of either 0.5 mg/dl or 25% from baseline within 72 h of exposure (2,3). The association of the above-specified magnitude and time course of serum creatinine increase with short- and long-term adverse clinical outcomes is well established (4–6). Given that the majority of patients currently undergoing invasive cardiovascular procedures are either outpatients or are likely to be discharged within 24 h after the procedure (7), assessment of changes in serum creatinine beyond 24 h often is problematic. Therefore, a practical means of predicting an early postprocedural increase in creatinine would be of clinical benefit. Although underlying renal insufficiency and diabetes mellitus are known risk factors for the development of CAN (8,9), the precise role of the volume of contrast administered has yet to be established (9–14).
In pharmacokinetic terms, systemic exposure to a drug (and, therefore, its safety and efficacy profile) is best quantified by the area under the drug’s blood concentration versus time curve (15). Recently, the derivation and validation of V/CrCl as a surrogate for the area under the curve has been reported in normal volunteers (16). We hypothesized that this index would be useful in the prediction of an abnormal increase in post-percutaneous coronary intervention (PCI) creatinine and that this index would show better predictive performance over considerations of volume or underlying renal function alone (6,8,9,11,12). We tested this hypothesis prospectively in an unselected population of patients undergoing PCI.
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Methods
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Theoretical background.
Systemic exposure to a drug is best assessed by quantifying the area under the blood concentration versus time curve. Contrast media are distributed and eliminated consistent with a linear model (17,18). Systemic clearance of a drug is equal to the ratio of the following time-dependent variables: the rate of elimination, dX/dt(t), and the blood drug concentration, C(t). Thus,
 | (1) |
Integrating numerator and denominator in Equation 1 yields:
 | (2) |
Rearranging Equation 2 yields:
 | (3) |
Therefore, systemic exposure (area under the curve) is directly related to dose and inversely related to systemic clearance. For contrast media exposure, the volume of contrast injected is equal to the total dose. Because contrast media are renally excreted in an unmetabolized state (19), their systemic clearance can be approximated by the creatinine clearance. Thus, the area under the blood concentration versus time curve can be approximated by the total volume of contrast given divided by creatinine clearance (CrCl):
 | (4) |
Patient population.
The present study population is composed of consecutive patients enrolled in the National Heart, Lung, and Blood Institute Dynamic Registry undergoing PCI in recruitment waves 4 (February 2004 to May 2004) and 5 (February 2006 to August 2006). The Dynamic Registry is a multicenter registry (25 clinical centers in the U.S. and Canada) whose purpose, structure, and function have been previously reported (20,21). Data collected include patient history, demographics, and procedural details including the total volume of contrast administered and in-hospital adverse events. In combined waves 4 and 5 (n = 4,093), after excluding patients with no recorded contrast volume (n = 107), those on dialysis (n = 125), those without paired creatinine determinations (n = 649), and those without recorded weight or age (n = 33), data from 3,179 patients were available for the present analysis. An increase in creatinine from baseline of >0.5 mg/dl after PCI was considered abnormal. The volume (V) to creatinine clearance (CrCl) ratio, an estimate of contrast media area under the curve, was calculated by dividing the volume of contrast received by the patient’s CrCl. The CrCl was estimated using the Cockcroft-Gault method (22): CrCl (ml/min) = 140 – age (years) x weight (kg)/72 x serum creatinine (mg/dl) {x 0.85 for female subjects}.
Statistical analysis.
Crude incidence rates for in-hospital adverse events and abnormal post-PCI creatinine increases were calculated. Continuous explanatory variables were categorized into either accepted cut points (e.g., decades for age) or into tertiles (e.g., contrast volume). Odds ratios and 95% confidence intervals were calculated using logistic regression. Additionally, continuous variables are summarized as mean ± SD or medians and interquartile ranges and compared using the Wilcoxon rank sum test. Receiver-operator characteristics analysis was used to determine the optimal cut point for V/CrCl in this population using SPSS (version 14.0, SPSS Inc., Chicago, Illinois). Logistic regression was used to model the association between the V/CrCl cut point (identified by the receiver-operator characteristics analysis) and an abnormal increase in creatinine. Risk factors were initially screened for univariate association with an abnormal increase in creatinine at p < 0.20, and identified variables were then assessed in a forward stepwise manner using a p value criterion of  0.05. The final model includes the volume/clearance ratio and other important baseline characteristics and is also adjusted for age and diabetes mellitus. The goodness-of-fit assumption was assessed using the Hosmer-Lemeshow method and satisfied when p > 0.05. Statistical significance for all comparisons was defined when p < 0.05.
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Results
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The mean age for the entire population was 64 ± 12 years; the mean body mass index was 29.5 ± 6.4 kg/m2; the mean creatinine clearance was 86.9 ± 38.2 ml/min; and the mean estimated glomerular filtration rate (using the Modification of Diet in Renal Disease method) was 74.8 ± 25.1 ml/min.
Postprocedural creatinine values were available in 92.8% of patients at 24 h and in an additional 6.8% from 24 h and 48 h. The overall incidence of an abnormal increase in creatinine, as previously defined, was 1.5%.
As seen in Table 1, older patients (70 to 79 years and 80 years) were significantly more likely to develop an early increase in creatinine compared with patients <60 years. The mean age for those without an increase in creatinine was 63.9 ± 12 years and 69.9 ± 12 years for those with a creatinine increase (p < 0.001). There was no association between this early increase in creatinine and gender. Patients with a creatinine increase were more likely to have a lower body mass index (mean 27.5 ± 4.8) compared with those without an increase in creatinine (mean 29.5 ± 6.4; p = 0.02). Compared with white patients, black patients were 2.3 times more likely to develop an early increase in creatinine. Patients with a history of concomitant disease, (e.g., congestive heart failure, chronic kidney disease [defined historically in the Dynamic Registry], cerebrovascular disease, or diabetes mellitus) all had a significant or near significant higher risk of early creatinine increase. The mean baseline creatinine in those patients with a history of chronic kidney disease was significantly higher than those without a history of chronic kidney disease (1.85 ± 0.87 vs. 1.05 ± 0.28, respectively; p < 0.001). Lower values for CrCl were associated with a higher risk for post-PCI creatinine increase. The mean CrCl in patients with an early increase in creatinine was significantly lower (67.6 ± 41.5 ml/min) compared with patients without an increase in creatinine (87.2 ± 38.1 ml/min; p < 0.001) as was the estimated glomerular filtration rate (69.5 ± 42.9 ml/min vs. 74.9 ± 24.7 ml/min; p = 0.006).
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Table 1 Univariate Association of Patient Demographics and Cardiac Risk Factors With an Early Abnormal Creatinine Increase After Percutaneous Coronary Intervention
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Procedural characteristics are shown in Table 2. There was no association between the total volume or type of contrast media (nonionic low osmolar, nonionic iso-osmolar, ionic high osmolar, ionic low osmolar) and an early creatinine increase. The significant association between an abnormal creatinine increase and periprocedural hydration likely reflects the use of the latter more often in subjects at risk of CAN. There was a borderline significant difference in the total volume of contrast administered to those with (255 ± 124 ml) and without (224 ± 112 ml; p = 0.06) the early increase in creatinine.
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Table 2 Univariate Association of Procedural Characteristics With an Early Abnormal Creatinine Increase After PCI
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As seen in Table 3, patients with an early creatinine increase had lower rates of angiographic and procedural success and a significantly higher incidence of postprocedural complications; specifically, bleeding requiring transfusion, death, and death or myocardial infarction. The overall incidence of any major adverse clinical event (defined as death, myocardial infarction, or coronary bypass surgery) was significantly higher in the patients with an early abnormal creatinine increase.
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Table 3 Univariate Association of In-Hospital Outcomes With an Early Abnormal Creatinine Increase After Percutaneous Coronary Intervention
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The mean V/CrCl ratio was 3.0 ± 2.0 in patients without a creatinine increase and 5.2 ± 4.4 in patients with an increase in creatinine (p < 0.001), whereas the median V/CrCl ratios for those without and with CAN were 2.5 (interquartile range 1.7 to 3.8) and 4.3 (interquartile range 2.7 to 6.0), respectively (p < 0.001). There was a significant association between higher V/CrCl ratio values and the risk of an early increase in creatinine (Fig. 1). The distribution of values for V/CrCl in patients with and without an early, abnormal increase in creatinine is shown in Figure 2.
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Figure 1 Relationship Between V/CrCl Ratio and Early Creatinine Increase
The association between ratio of the volume of contrast media to the creatinine clearance (V/CrCl) and the percentage of patients with an early abnormal increase in creatinine after percutaneous coronary intervention (PCI) was highly significant (p < 0.001 overall and for trend).
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Figure 2 Distribution of V/CrCl Ratio in Current Study
The distributions of ratio of the volume of contrast media to the creatinine clearance (V/CrCl) values in patients with and without an early abnormal increase in creatinine were significantly different (p < 0.001). CAN = contrast media-associated nephrotoxicity.
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Receiver-operator characteristic curve analysis showed fair discrimination between patients with and without an early increase in creatinine (C-statistic of 0.69) at a V/CrCl ratio of 3.7 (Fig. 3). At this value, the sensitivity and specificity for detection of an early, abnormal post-PCI creatinine increase were 65% and 75%, respectively.
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Figure 3 Receiver-Operator Characteristics Curve
Receiver-operator characteristics analysis indicated an optimum cutoff value for ratio of the volume of contrast media to the creatinine clearance (V/CrCl) of 3.7 (*). The C-statistic was 0.69.
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Univariate logistic regression indicated that V/CrCl was a highly significant predictor of an early abnormal creatinine increase (odds ratio 5.06; 95% confidence interval 2.79 to 9.20). Multivariable analysis indicated that a V/CrCl 3.7 was significantly and independently related to the risk of an early abnormal increase in creatinine (Table 4). Notably, the total volume of contrast was not retained in the final model.
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Table 4 Multivariable Association Between an Early Abnormal Increase in Creatinine Level After PCI and V/CrCl Ratio
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Discussion
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In this report we show the predictive utility of the ratio of the volume of contrast media administered to the estimated creatinine clearance in assessing the risk of an abnormal early post-PCI increase in serum creatinine. Because V/CrCl corresponds closely to the area under the blood contrast media concentration versus time curve, this index should more closely predict the safety profile of contrast media, particularly with respect to the risk of CAN, than the absolute volume of contrast alone.
The literature on the subject of CAN is extensive and has been the subject of numerous recent comprehensive reviews (3,23–27). Several studies have sought to establish a relationship between the total volume of contrast media administered, baseline renal function, and risk of CAN after angiography. Contrast volume/CrCl was used in a retrospective analysis of 152 patients with chronic kidney disease (defined as a baseline creatinine >2.0 mg/dl) and was found to be predictive of CAN (defined as an increase in creatinine of 1.0 mg/dl) at a cutoff value of 6.0 (28). This cutoff was then used prospectively in 250 consecutive patients (creatinine of 0.3 to 5.8 mg/dl) and found to have a sensitivity of 79% and specificity of 97% for predicting CAN (28). These data are not strictly comparable with those reported herein because of differences in the number of patients studied, the number with chronic kidney disease, and the definition and overall incidence of CAN.
A contrast volume limit of 5 ml/kg divided by serum creatinine has been proposed as a way to predict CAN in patients receiving contrast media (29). This was validated in 115 patients with chronic kidney disease (Cr >1.8 mg/dl) undergoing angiography. Patients who received >5 ml/kg/ serum creatinine had a higher incidence of CAN. This formula was applied retrospectively in 16,592 patients undergoing cardiac catheterization to determine its utility in predicting the risk of postprocedural dialysis. Patients who received a volume of contrast in excess of 5 ml/kg/serum creatinine were 6-fold more likely to develop nephropathy requiring dialysis (30).
In our study of 3,179 consecutive unselected patients undergoing PCI, we found that a V/CrCl >3.7 predicted the patient at risk for an abnormal early postprocedural increase in creatinine. In contrast to the aforementioned studies, we included a broader spectrum of patients and used a more practical criterion for CAN—an early, abnormal increase in creatinine. Although the true incidence of the traditionally defined CAN (2,3) is likely underestimated in our study because of the failure to obtain sufficient samples beyond 24 h, our results are relevant to those patients for whom the detection of an early increase in postprocedural creatinine may be meaningful (31). Such evidence of renal vulnerability to the effects of contrast media are useful for risk stratification. Furthermore, real-world clinical practice often precludes observing the majority of patients beyond 24 h. Despite the likely underestimation of the incidence of CAN without systematic 48- and 72-h sampling, our data regarding the value of V/CrCl as a predictor of an early postprocedural increase in creatinine remain valid. In this sample we were also able to confirm the previously described association between an abnormal post-PCI creatinine increase and adverse in-hospital outcomes (9) despite the overall low risk of the present population. Additional studies of the utility of this ratio in populations with more prevalent underlying kidney disease undergoing angiography and/or PCI and with more extended creatinine determinations would be informative.
The relationship posited herein between contrast volume, renal exposure, and the risk of CAN does not take into account the many unpredictable hemodynamic and rheologic disturbances during PCI. Previous studies, as well as the present study, have identified numerous clinical, demographic, and procedural factors that are significantly associated with CAN after PCI (32,33). That V/CrCl remained independently associated with the risk of an early postprocedural creatinine increase after adjustment for these important confounders (Table 4) is supportive of our original hypothesis.
This study was not intended to examine the relationship between the type of contrast media and the risk of CAN. The inability to identify an association between these variables is the result of a combination of factors: nonrandom assignment of contrast media, operator bias in the choice of contrast media, and type II error attribuable to the low overall event rate.
Although V/CrCl is useful in retrospective analyses of the relationship between contrast volume and subsequent renal injury, the cut point of 3.7 may be a useful tool in determining the amount of contrast volume that is likely to result in an early abnormal increase in creatinine. Thus, multiplying a patient’s estimated CrCl by 3.7 would give an estimate of the maximum amount of contrast for a given procedure, above which the likelihood of developing renal injury would be concerning.
In summary, we have shown that V/CrCl is a useful and independent predictor of an early increase in postprocedural serum creatinine in unselected patients undergoing PCI. This index may be applied prospectively to calculate the maximum volume of contrast media that can be given without significantly increasing the risk of CAN.
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Footnotes
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This study was supported in part by grant HL 33292-14 from the National Heart, Lung, and Blood Institute, Bethesda, Maryland, and the Robert S. Flinn Endowment for Cardiovascular Medicine (University of New Mexico School of Medicine).
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References
|
|---|
1. Nash K, Hafeez A, Hou S. Hospital-acquired renal insufficiency Am J Kidney Dis 2002;39:930-936.[CrossRef][Web of Science][Medline]2. Gleeson TG, Bulugahapitiya S. Contrast-induced nephropathy Am J Roentgenol 2004;183:1673-1689.[Free Full Text] 3. Murphy SW, Barrett BJ, Parfrey PS. Contrast nephropathy J Am Soc Nephrol 2000;11:177-182.[Free Full Text] 4. Levy EM, Viscoli CM, Horwitz RI. The effect of acute renal failure on mortalityA cohort analysis. JAMA 1996;275:1489-1494.[Abstract/Free Full Text] 5. Lindsay J, Canos DA, Apple S, Pinnow E, Aggrey GK, Pichard AD. Causes of acute renal dysfunction after percutaneous coronary intervention and comparison of late mortality rates with postprocedure rise of creatine kinase-MB versus rise of serum creatinine Am J Cardiol 2004;94:786-789.[CrossRef][Web of Science][Medline] 6. Rihal CS, Textor SC, Grill DE, et al. Incidence and prognostic importance of acute renal failure after percutaneous coronary intervention Circulation 2002;105:2259-2264.[Abstract/Free Full Text] 7. American College of Cardiology National Cardiovascular Data Registry Catheter PCI RegistryAmerican College of Cardiology Foundation Institutional Outcomes Report 2005 Y4. 2006. 8. Lautin EM, Freeman NJ, Schoenfeld AH, et al. Radiocontrast-associated renal dysfunction: incidence and risk factors Am J Roentgenol 1991;157:49-58.[Abstract/Free Full Text] 9. McCullough PA, Wolyn R, Rocher LL, Levin RN, O’Neill WW. Acute renal failure after coronary intervention: incidence, risk factors, and relationship to mortality Am J Med 1997;103:368-375.[CrossRef][Web of Science][Medline] 10. Manske CL, Sprafka JM, Strony JT, Wang Y. Contrast nephropathy in azotemic diabetic patients undergoing coronary angiography Am J Med 1990;89:615-620.[CrossRef][Web of Science][Medline] 11. Dangas G, Iakovou I, Nikolsky E, et al. Contrast-induced nephropathy after percutaneous coronary interventions in relation to chronic kidney disease and hemodynamic variables Am J Cardiol 2005;95:13-19.[CrossRef][Web of Science][Medline] 12. Marenzi G, Lauri G, Assanelli E, et al. Contrast-induced nephropathy in patients undergoing primary angioplasty for acute myocardial infarction J Am Coll Cardiol 2004;44:1780-1785.[Abstract/Free Full Text] 13. Nikonoff T, Skau T, Berglund J, Nyberg P, Spangberg-Viklund B, Larsson R. Effects of femoral arteriography and low osmolar contrast agents on renal function Acta Radiol 1993;34:88-91.[Web of Science][Medline] 14. Parfrey PS, Griffiths SM, Barrett BJ, et al. Contrast material-induced renal failure in patients with diabetes mellitus, renal insufficiency, or bothA prospective controlled study. N Engl J Med 1989;320:143-149.[Abstract] 15. U.S. Food and Drug Administration. Toxicokinetics: the assessment of systemic exposure in toxicity studies. Guideline 1995. Available at: http://www.fda.gov/cder/guidance/ichs3a.pdf. Accessed July 30, 2006. 16. Sherwin PF, Cambron R, Johnson JA, Pierro JA. Contrast dose-to-creatinine clearance ratio as a potential indicator of risk for radiocontrast-induced nephropathy: correlation of D/CrCL with area under the contrast concentration-time curve using iodixanol Invest Radiol 2005;40:598-603.[CrossRef][Web of Science][Medline] 17. Bourin M, Jolliet P, Ballereau F. An overview of the clinical pharmacokinetics of X-ray contrast media Clin Pharmacokinet 1997;32:180-193.[Web of Science][Medline] 18. Dean PB, Kivisaari L, Kormano M. Contrast enhancement pharmacokinetics of six ionic and nonionic contrast media Invest Radiol 1983;18:368-374.[Web of Science][Medline] 19. Frennby B, Sterner G. Contrast media as markers of GFR Eur Radiol 2002;12:475-484.[CrossRef][Web of Science][Medline] 20. Williams DO, Holubkov R, Yeh W, et al. The National Heart, Lung and Blood Institute Registries Percutaneous coronary intervention in the current era compared with 1985–86 Circulation 2000;102:2945-2951.[Abstract/Free Full Text] 21. Laskey WK, Williams DO, Vlachos HA, et al. Changes in the practice of percutaneous coronary intervention: a comparison of enrollment waves of the NHLBI Dynamic Registry Am J Cardiol 2001;87:964-969.[CrossRef][Web of Science][Medline] 22. Cockcroft DW, Gault MH. Prediction of creatinine clearance from serum creatinine Nephron 1976;16:31-41.[Web of Science][Medline] 23. Rudnick MR, Berns JS, Cohen RM, et al. Contrast media-associated nephrotoxicity Semin Nephrol 1997;17:15-26.[Web of Science][Medline] 24. Andrew E, Berg KJ. Nephrotoxic effects of X-ray contrast media J Toxicol Clin Toxicol 2004;93:1515-1519. 25. Morcos SK, Thomsen HS, Webb JA, Contrast Media Safety Committee, European Society of Urogenital Radiology (ESUR) Contrast media-induced nephrotoxicity: a consensus report Eur Radiol 1999;9:1602-1613.[CrossRef][Web of Science][Medline] 26. Tepel M, Aspelin P, Lameire N. Contrast-induced nephrotoxicityA clinical and evidence-based approach. Circulation 2006;113:1799-1806.[Free Full Text] 27. Maeder M, Klein H, Fehr T, Rickli H. Contrast nephropathy: review focused on prevention J Am Coll Cardiol 2004;44:1763-1771.[Abstract/Free Full Text] 28. Altmann DB, Zwas D. Use of contrast volume to estimated creatinine clearance ratio to predict renal failure after angiography J Intervent Cardiol 1997;10:113-119.[CrossRef][Web of Science] 29. Cigarroa RG, Lange RA, Williams RH, Hillis LD. Dosing of contrast material to prevent contrast nephropathy in patients with renal disease Am J Med 1989;86:649-652.[CrossRef][Web of Science][Medline] 30. Freeman R. Nephropathy requiring dialysis after percutaneous coronary intervention and the critical role of an adjusted contrast dose Am J Cardiol 2002;90:1068-1073.[CrossRef][Web of Science][Medline] 31. McCullough PA, Bertrand ME, Brinker JA, Stacul F. A meta-analysis of the renal safety of iodixanol compared with low osmolar contrast media J Am Coll Cardiol 2006;48:692-699.[Abstract/Free Full Text] 32. Mehran R, Aymong ED, Nikolsky E, et al. A simple risk score for prediction of contrast-induced nephropathy after percutaneous coronary intervention J Am Coll Cardiol 2004;44:1393-1399.[Abstract/Free Full Text] 33. McCullough PA, Adam A, Becker CR, et al. Risk prediction of contrast-induced nephropathy Am J Cardiol 2006;98(Suppl):27K-36K.[Web of Science][Medline]
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Abstract
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