CLINICAL STUDY
The prognostic implications of further renal function deterioration within 48 h of interventional coronary procedures in patients with pre-existent chronic renal insufficiency
Luis Gruberg, MD*,
Gary S. Mintz, MD*,
Roxana Mehran, MD ,
George Dangas, MD, PhD,
Alexandra J. Lansky, MD,
Kenneth M. Kent, MD, PhD*,
Augusto D. Pichard, MD*,
Lowell F. Satler, MD* and
Martin B. Leon, MD
* Cardiac Catheterization Laboratory, Washington Hospital Center, Washington, DC, USA
Cardiovascular Research Foundation, New York, New York, USA
Manuscript received January 21, 2000;
revised manuscript received April 19, 2000,
accepted June 19, 2000.
Reprint requests and correspondence: Dr. Gary S. Mintz, Washington Hospital Center, 110 Irving Street NW, Suite 4B-1, Washington, DC 20010
gsm1{at}mhg.edu
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Abstract
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BACKGROUND
Acute deterioration in renal function is a recognized complication after coronary angiography and intervention.
OBJECTIVES
The goal of this study was to determine the impact on acute and long-term mortality and morbidity of contrast-induced deterioration in renal function after coronary intervention.
METHODS
We studied 439 consecutive patients who had a baseline serum creatinine  1.8 mg/dL (159.1 µmol/L) who were not on dialysis who underwent percutaneous coronary intervention in a tertiary referral center. All patients were hydrated before the procedure, and almost all received ioxaglate meglumine; 161 (37%) patients had an increase in serum creatinine 25% within 48 h or required dialysis and 278 (63%) did not. In-hospital and out-of-hospital clinical events (death, myocardial infarction, repeat revascularization) were assessed by source documentation.
RESULTS
Independent predictors of renal function deterioration were left ventricular ejection fraction (p = 0.02) and contrast volume (p = 0.01). In-hospital mortality was 14.9% for patients with further renal function deterioration versus 4.9% for patients with no creatinine increase (p = 0.001); other complications were also more frequent. Thirty-one patients required hemodialysis; their in-hospital mortality was 22.6%. Four patients were discharged on chronic dialysis. The cumulative one-year mortality was 45.2% for those who required dialysis, 35.4% for those who did not require dialysis and 19.4% for patients with no creatinine increase (p = 0.001). Independent predictors of one-year mortality were creatinine elevation (p = 0.0001), age (p = 0.03) and vein graft lesion location (p = 0.08).
CONCLUSIONS
For patients with pre-existing renal insufficiency, renal function deterioration after coronary intervention is a marker for poor outcomes. This is especially true for patients who require dialysis.
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Abbreviations and Acronyms
| | CI | = confidence interval | | CrCl | = creatinine clearance | | CRI | = chronic renal insufficiency | | MI | = myocardial infarction | | OR | = odds ratio |
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Acute deterioration in renal function is a recognized complication after coronary angiography, particularly for patients with pre-existing chronic renal insufficiency (CRI) (1–4). Previous studies have shown that 12 to 14% of patients who develop acute renal insufficiency during hospitalization do so after procedures involving radiographic contrast (5,6). For patients with abnormal baseline renal function, the incidence of progressive deterioration can be as high as 42% (1,7). For hospitalized, critically ill patients, this carries a poor prognosis, especially if dialysis becomes necessary (5–10).
The expanding use of diagnostic and therapeutic percutaneous interventions makes it important to understand the potential risks involved with these procedures. The purpose of this study was to review the in-hospital and long-term clinical outcomes of 439 consecutive patients with impaired baseline renal function who underwent percutaneous coronary intervention and had significant deterioration in renal function after the procedure.
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Methods
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Patient population.
The cohort is a consecutive series of 439 patients who had a baseline serum creatinine 1.8 mg/dL (159.1 µmol/L), but were not on dialysis, who underwent percutaneous coronary intervention. Patients were divided into two groups: 161 (37%) patients had an increase in serum creatinine 25% within 48 h or required dialysis (group 1) and 278 (63%) did not (group 2).
All patients underwent cardiac catheterization and intervention by standard techniques. All patients received intravenous hydration before the procedure. Hydration included 0.5 normal saline solution at 75 ml/h to 100 ml/h for 6 to 12 h before the intervention and for 6 h after the intervention. There was no formal protocol for use of periprocedural diuretics or other potentially renal-protective agents. The choice of radiocontrast material was left to the discretion of the operating physician; however, in over 95% of cases an ionic low osmolar contrast agent was used. Interventional treatment strategy (stents, rotational atherectomy, directional coronary atherectomy or excimer laser angioplasty) was performed by the operator based on vessel size, coronary anatomy and preprocedural lesion morphology. During the procedure heparin was administered to achieve an activated clotting time of approximately 300 s; heparin was not continued routinely after the procedure unless there were other indications for its use. Aspirin 325 mg was started at least 24 h before the procedure and continued indefinitely. After stent implantation patients received either ticlopidine (250 mg orally twice a day for two to four weeks) or clopidogrel (75 mg daily for two to four weeks). Other medications (that is, nitrates, calcium channel antagonists, etc.) were administered at the discretion of the operator.
Angiographic analysis.
Quantitative angiographic analysis was done at a dedicated Angiographic Core Laboratory by observers who were unaware of the clinical data and purpose of this study. Quantitative coronary angiographic analysis was performed using automated edge-detection algorithm (CMS, Medis Medical Imaging Systems, Ridgefield, Connecticut). Using the contrast filled catheter as the calibration standard, minimal lumen diameters, reference diameter and percent diameter stenosis before and after intervention were measured from multiple projections, and the results from the single "worst" and least foreshortened view were recorded. Standard qualitative morphologic criteria were tabulated (11,12). Left ventricular ejection fraction was determined by ventriculography or by echocardiography.
Clinical definitions.
Baseline laboratory values were obtained for all patients upon admission. Creatinine clearance (CrCl) was calculated by applying the Cockcroft-Gault formula to the baseline serum creatinine: CrCl = ([140 – age] x weight/serum creatinine x 72) with female gender adjustment (CrClfemale = CrCl x 0.85) (13).
Procedural success was defined as <50% residual diameter stenosis and Thrombolysis In Myocardial Infarction (TIMI) flow >grade 2 in the absence of major in-hospital complications: death, MI or urgent bypass surgery (within 24 h after procedure). Q-wave MI was identified by the presence of new Q-waves. Non-Q-wave MI was defined as the elevation of creatine kinase-MB fraction 5 x normal without the appearance of new Q-waves.
Follow-up clinical events were assessed by serial telephone interviews at 1, 3, 6, 12 months and yearly thereafter. All events were source-documented including death, MI and repeat intervention or bypass surgery as related to the treated lesion.
Statistical analysis.
Statistical analyses were performed using SAS 6.10 (SAS Institute). Continuous variables were presented as mean ± 1 standard deviation and were compared using Student t test. Categorical variables were presented as percentages and were compared using the chi-square statistics or the Fisher exact test. Kaplan-Meier survival curves were used to compare freedom from death and late events (death, MI or revascularization). Multivariate logistic regression analysis was used to determine predictors of renal function deterioration. Cox proportionate hazard model was used to determine predictors of late mortality. A p value <0.05 was considered statistically significant. Odds ratios (OR) and 95% confidence intervals (CI) are reported.
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Results
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Patient characteristics and procedural variables.
Patients with postprocedural renal function deterioration (group 1) were compared with patients with no increase in serum creatinine (group 2). The group with renal function deterioration included more diabetics and had worse left ventricular function. Other clinical characteristics were similar (Table 1).
Baseline serum creatinine was lower in group 1 (Table 2). However, CrCl (estimated by the Cockcroft-Gault formula) was similar for both groups, indicating no difference in baseline renal function when age and body weight were taken in account. The majority of the patients in both groups received ioxaglate meglumine, an ionic low osmolar contrast agent (Hexabrix, Mallinkrodt Medical Inc., St Louis, Missouri), 93% versus 90%, p = NS. There was a larger volume of contrast used in group 1 patients. Angiographic analysis is shown in Table 3. There was a higher frequency of saphenous vein graft lesions in group 1. This was reflected in larger reference vessel size and larger final minimal lumen diameter.
Predictors of renal function deterioration.
The following variables were entered into a multivariate model for predicting renal function deterioration: age, left ventricular ejection fraction, diabetes mellitus, hypertension, creatine kinase-MB >5x normal, baseline creatinine, CrCl, angiographic contrast volume, hematocrit drop and need for blood transfusion. The only independent predictors of renal function deterioration were blood transfusion (OR = 1.55, 95% CI = 1.27 to 1.91, p < 0.0001), contrast volume (OR = 1.003, 95% CI = 1.001 to 1.006, p = 0.01) and left ventricular ejection fraction (OR = 0.97, 95% CI = 0.95 to 0.99, p = 0.02).
Clinical outcome (Fig. 1).
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Figure 1 A flow diagram detailing the mortality of 439 patients with pre-existing renal insufficiency undergoing percutaneous coronary intervention.
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The combined (cardiac and noncardiac) in-hospital mortality in patients with further renal function deterioration was 14.9% compared with 4.9% in patients with no increase in creatinine (Table 4). The percentage of deaths from cardiac causes was also elevated in patients with renal function deterioration. Other complications (pulmonary edema, gastrointestinal bleeding and need for blood transfusions) were also more frequent for patients with renal function deterioration.
Thirty-one patients required hemodialysis during hospitalization. Their in-hospital mortality was 22.6%. Four patients were discharged on chronic dialysis. The cumulative one-year mortality was significantly higher in patients with renal function deterioration (37.7% vs. 19.4%, p = 0.001, Table 5 and Fig. 2) —35.4% for those who did not require dialysis and 45.2% for those who required dialysis. Of the 17 patients who required in-hospital dialysis and who were alive at one year, 3 required chronic dialysis.
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Figure 2 Kaplan-Meier estimates of survival for group 1 (renal function deterioration, solid line) versus group 2 (no increase in serum creatinine, dashed line, p < 0.001).
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When the one-year mortality was compared with regard to the percent increase in creatinine, there was a noticeable difference in patients with a 25% increase or greater (Fig. 3). Myocardial infarction and revascularization events were similar in both groups.
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Figure 3 Relation of the percentage increase in serum creatinine to 1-year mortality. There was a significant increase in mortality when the increase in creatinine was greater than 25% (p < 0.0001).
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Predictors of mortality.
We separated the two groups into those patients with and those patients without diabetes (Fig. 4). There was no difference in long-term survival between diabetic patients versus patients who were not diabetic with no increase in creatinine or between diabetic patients versus patients who were not diabetic with a further deterioration in renal function.
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Figure 4 Kaplan-Meier estimates of survival comparing diabetic patients versus patients who were not diabetic in group 1 (renal function deterioration, p = NS) and diabetic patients versus patients who were not diabetic in group 2 (no increase in serum creatine, p = NS). DM = diabetes mellitus.
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The following variables were entered into a multivariate model predicting death during the follow-up period: age, male gender, diabetes mellitus, baseline CrCl, left ventricular ejection fraction, left main and vein graft lesion location, stent deployment, final minimum lumen diameter, creatine kinase-MB release, in-hospital dialysis, contrast volume, creatinine elevation, hematocrit drop and blood transfusion. Independent predictors of death were creatinine elevation (OR = 3.86, 95% CI = 1.96 to 7.58, p = 0.0001), age (OR = 1.05, 95% CI = 1.05 to 1.09, p = 0.03) and vein graft lesion location (OR = 1.55, 95% CI = 0.95 to 2.52, p = 0.08).
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Discussion
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Patients with baseline azotemia and postangioplasty deterioration in renal function had worse short-term and long-term outcomes compared with patients who did not. These patients had significant comorbidities (Table 1) and a significant increase in most in-hospital adverse events: death, non-Q-wave MI, pulmonary edema and bleeding. At one-year follow-up, mortality rates were high for both groups, but especially for patients with deterioration in renal function (47.7%). Using multivariate analysis, creatinine elevation, advanced patient age and vein graft lesion location were independent predictors of death in these patients.
Renal function deterioration postcontrast.
Renal function deterioration after exposure to radiographic contrast agents is common in patients with impaired renal function (1,2). Diabetes mellitus is one of the strongest predictors of acute renal failure after coronary intervention (6). In a study of patients with diabetic nephropathy and azotemia who underwent prerenal transplant coronary angiography, 50% had a serum creatinine increase >25%, and 12% required dialysis within a week (4). This was not substantiated in this study. Other reported risk factors include chronic renal insufficiency; dehydration; ionic, high osmolar contrast agents and congestive heart failure (14–17).
The renal function deterioration is an important predictor of in-hospital mortality. Rich et al. (2) reported 183 patients 70 years of age undergoing cardiac catheterization—including patients with prior renal insufficiency (mean serum creatinine 1.3 ± 0.7 mg/dL); 21/183 patients (11.5%) developed progressive renal dysfunction (serum creatinine elevation >0.5 mg/dL), which persisted in five of them (24%). The overall in-hospital mortality was 7.1% to 14.3% for those who developed progressive renal dysfunction and 6.2% for those who did not. Levy et al. (10) reported 183 patients who developed contrast-mediated renal dysfunction and compared these index patients against 174 "controls" matched for age and baseline serum creatinine. The in-hospital mortality was 34% in the index cases versus 7% in the control population.
A 25% increase in creatinine was the typical definition of renal function deterioration used in the preceding studies. The use of this "cutoff" as a predictor of cumulative mortality was substantiated in this study (Fig. 3).
Patients with azotemia were at a higher risk for bleeding complications and required blood transfusions more often. Bleeding, hypovolemia and hypotension may lead to further deterioration in renal function. In this study blood transfusion, but not bleeding, was an independent predictor of creatinine elevation, nor was it a predictor of mortality.
Dialysis.
The risk of emergency dialysis after radiographic contrast ranges up to 12% in patients with baseline serum creatinine levels above 1.4 mg/dL (18). In-hospital mortality rates for patients who require emergency dialysis have been reported to be as high as 62%; conversely, in patients who developed renal failure but did not require dialysis, the mortality rate was lower (31%) (18). In one report of 132 critically ill patients in the intensive care unit who developed acute renal failure and required dialysis, the in-hospital mortality rate was 70%; of those who were discharged, 33% were dialysis dependent (19).
Using a definition similar to the current study (a 25% increase in creatinine), McCullough et al. (6) reported an incidence of acute renal failure after coronary interventions of 14.5%. The in-hospital mortality rate for these patients was 7.1 but increased to 35.7% for patients who required dialysis.
Whether these patients, especially patients who require dialysis, die from renal failure itself or from the underlying conditions is an unresolved issue (18). Analysis of our data and data from other studies suggests that comorbidities alone do not account for the increased mortality. When the effect of comorbidity was controlled in a multivariate model in this study, renal deterioration still predicted increased mortality.
Potential mechanisms.
At least four mechanisms have been implicated in contrast-induced nephropathy. After radiographic contrast exposure, there is a brief period of vasodilation followed by renal vasoconstriction leading to intense, but transient, reduction in renal blood flow, direct toxicity to renal tubular epithelium, tubular obstruction by protein precipitates and complement activation (14).
Recent works have suggested that endothelin, a potent endogenous vasoconstrictor, may be an important contributor to ischemic damage to the kidneys in certain circumstances and has been proposed as one of the potential mediators of renal vascular vasoconstriction. The exposure to large volumes of contrast material is associated with increased levels of circulating endothelin both in animal models and in humans. This is even more exaggerated in diabetic patients or patients with CRI (20,21). The simultaneous release of various endogenous renal vasodilators—such as atrial natriuretic peptide, nitric oxide and prostaglandins E2 and I2—may play an important role in counterbalancing the vasoconstrictive effects of endothelin by enhancing the glomerular filtration rate and urinary output (22).
Prevention.
Several measures have been tried in an attempt to prevent or reduce further renal function deterioration after contrast exposure: hydration, furosemide, mannitol, calcium channel-blockers, dopamine, atrial natriuretic peptide, endothelin inhibitors and theophylline (23–25). Hydration with 0.45% saline and the use of low osmolality contrast media have been shown to provide some protection (24,26). Recent reports have also suggested that forced diuresis with furosemide, mannitol and intravenous 0.45% saline may have a beneficial effect (27).
Study limitations.
The current report is a retrospective analysis, and, therefore, the results and conclusions are subject to the limitations inherent in all such reports. location and poor left ventricular ejection fraction. In addition, this was a high-risk patient population with a majority of the patients having had previous bypass surgery. The use of glycoprotein IIb/IIIa inhibitors in this patient population was <2%. Serum creatinine was only measured for 48 h; we may have missed a later increase in creatinine in some of the 63% of the patients who did not have renal function deterioration within 48 h of their procedure.
Clinical implications.
These data show that in patients with pre-existing renal insufficiency, renal function deterioration (elevation of serum creatinine above 25% baseline levels or need for dialysis) after coronary intervention is a marker for poor in-hospital and long-term outcomes. Patients who require dialysis after the procedure are especially prone to a poor clinical outcome, and every measure should be taken to avoid such an end point. Even in the era of modern interventional cardiology and new contrast agents, the risk of renal injury remains high with important long-term consequences.
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WRITING COMMITTEE MEMBERS, D. B. Mark, D. S. Berman, M. J. Budoff, J. J. Carr, T. C. Gerber, H. S. Hecht, M. A. Hlatky, J. M. Hodgson, M. S. Lauer, et al.
ACCF/ACR/AHA/NASCI/SAIP/SCAI/SCCT 2010 Expert Consensus Document on Coronary Computed Tomographic Angiography: A Report of the American College of Cardiology Foundation Task Force on Expert Consensus Documents
Circulation,
June 8, 2010;
121(22):
2509 - 2543.
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F. O. Lima, M. H. Lev, R. A. Levy, G. S. Silva, M. Ebril, E. C. de Camargo, S. Pomerantz, A. B. Singhal, D. M. Greer, H. Ay, et al.
Functional Contrast-Enhanced CT for Evaluation of Acute Ischemic Stroke Does Not Increase the Risk of Contrast-Induced Nephropathy
AJNR Am. J. Neuroradiol.,
May 1, 2010;
31(5):
817 - 821.
[Abstract]
[Full Text]
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S. M. Bagshaw, D. N. Cruz, N. Aspromonte, L. Daliento, F. Ronco, G. Sheinfeld, S. D. Anker, I. Anand, R. Bellomo, T. Berl, et al.
Epidemiology of cardio-renal syndromes: workgroup statements from the 7th ADQI Consensus Conference
Nephrol. Dial. Transplant.,
May 1, 2010;
25(5):
1406 - 1416.
[Full Text]
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J. M. Stolker, P. A. McCullough, S. Rao, S. E. Inzucchi, J. A. Spertus, T. M. Maddox, F. A. Masoudi, L. Xiao, and M. Kosiborod
Pre-Procedural Glucose Levels and the Risk for Contrast-Induced Acute Kidney Injury in Patients Undergoing Coronary Angiography
J. Am. Coll. Cardiol.,
April 6, 2010;
55(14):
1433 - 1440.
[Abstract]
[Full Text]
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M. A. Alpert and C. Carlino
Pre-Procedural Blood Glucose Levels: A New Risk Marker for Contrast-Induced Acute Kidney Injury in Patients Without Diabetes With Acute Myocardial Infarction
J. Am. Coll. Cardiol.,
April 6, 2010;
55(14):
1441 - 1443.
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E. A. J. Hoste, J. J. De Waele, S. A. Gevaert, S. Uchino, and J. A. Kellum
Sodium bicarbonate for prevention of contrast-induced acute kidney injury: a systematic review and meta-analysis
Nephrol. Dial. Transplant.,
March 1, 2010;
25(3):
747 - 758.
[Abstract]
[Full Text]
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D. Kiski, W. Stepper, E. Brand, G. Breithardt, and H. Reinecke
Impact of renin-angiotensin-aldosterone blockade by angiotensin-converting enzyme inhibitors or AT-1 blockers on frequency of contrast medium-induced nephropathy: a post-hoc analysis from the Dialysis-versus-Diuresis (DVD) trial
Nephrol. Dial. Transplant.,
March 1, 2010;
25(3):
759 - 764.
[Abstract]
[Full Text]
[PDF]
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S. K. Goergen, G. Rumbold, G. Compton, and C. Harris
Systematic Review of Current Guidelines, and Their Evidence Base, on Risk of Lactic Acidosis after Administration of Contrast Medium for Patients Receiving Metformin
Radiology,
January 1, 2010;
254(1):
261 - 269.
[Abstract]
[Full Text]
[PDF]
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N. Kumar, L. Dahri, W. Brown, N. Duncan, S. Singh, C. Baker, I. Malik, A. Palmer, M. Griffith, T. Cairns, et al.
Effect of Elective Coronary Angiography on Glomerular Filtration Rate in Patients with Advanced Chronic Kidney Disease
Clin. J. Am. Soc. Nephrol.,
December 1, 2009;
4(12):
1907 - 1913.
[Abstract]
[Full Text]
[PDF]
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K. Spargias, E. Adreanides, E. Demerouti, A. Gkouziouta, A. Manginas, G. Pavlides, V. Voudris, and D. V. Cokkinos
Iloprost Prevents Contrast-Induced Nephropathy in Patients With Renal Dysfunction Undergoing Coronary Angiography or Intervention
Circulation,
November 3, 2009;
120(18):
1793 - 1799.
[Abstract]
[Full Text]
[PDF]
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J. R. Brown, C. A. Block, D. J. Malenka, G. T. O'Connor, A. C. Schoolwerth, and C. A. Thompson
Sodium Bicarbonate Plus N-Acetylcysteine Prophylaxis: A Meta-Analysis
J. Am. Coll. Cardiol. Intv.,
November 1, 2009;
2(11):
1116 - 1124.
[Abstract]
[Full Text]
[PDF]
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P. M. Palevsky
Defining Contrast-Induced Nephropathy
Clin. J. Am. Soc. Nephrol.,
July 1, 2009;
4(7):
1151 - 1153.
[Full Text]
[PDF]
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R. J. Solomon, R. Mehran, M. K. Natarajan, S. Doucet, R. E. Katholi, C. S. Staniloae, S. K. Sharma, M. Labinaz, J. L. Gelormini, and B. J. Barrett
Contrast-Induced Nephropathy and Long-Term Adverse Events: Cause and Effect?
Clin. J. Am. Soc. Nephrol.,
July 1, 2009;
4(7):
1162 - 1169.
[Abstract]
[Full Text]
[PDF]
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M. Elahi, S. Asopa, A. Pflueger, N. Hakim, and B. Matata
Acute kidney injury following cardiac surgery: impact of early versus late haemofiltration on morbidity and mortality
Eur J Cardiothorac Surg,
May 1, 2009;
35(5):
854 - 863.
[Abstract]
[Full Text]
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S. Morikawa, T. Sone, H. Tsuboi, H. Mukawa, I. Morishima, M. Uesugi, Y. Morita, Y. Numaguchi, K. Okumura, and T. Murohara
Renal Protective Effects and the Prevention of Contrast-Induced Nephropathy by Atrial Natriuretic Peptide
J. Am. Coll. Cardiol.,
March 24, 2009;
53(12):
1040 - 1046.
[Abstract]
[Full Text]
[PDF]
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S. Goldfarb, P. A. McCullough, J. McDermott, and S. B. Gay
Contrast-Induced Acute Kidney Injury: Specialty-Specific Protocols for Interventional Radiology, Diagnostic Computed Tomography Radiology, and Interventional Cardiology
Mayo Clin. Proc.,
February 1, 2009;
84(2):
170 - 179.
[Abstract]
[Full Text]
[PDF]
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J. C. Weinreb
Which Study When? Is Gadolinium-enhanced MR Imaging Safer than Iodine-enhanced CT?
Radiology,
October 1, 2008;
249(1):
3 - 8.
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A. M. From, B. J. Bartholmai, A. W. Williams, S. S. Cha, and F. S. McDonald
Mortality Associated With Nephropathy After Radiographic Contrast Exposure
Mayo Clin. Proc.,
October 1, 2008;
83(10):
1095 - 1100.
[Abstract]
[Full Text]
[PDF]
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S. Langner, S. Stumpe, M. Kirsch, M. Petrik, and N. Hosten
No Increased Risk for Contrast-Induced Nephropathy after Multiple CT Perfusion Studies of the Brain with a Nonionic, Dimeric, Iso-Osmolal Contrast Medium
AJNR Am. J. Neuroradiol.,
September 1, 2008;
29(8):
1525 - 1529.
[Abstract]
[Full Text]
[PDF]
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R. Solomon
Contrast-Induced Acute Kidney Injury: Is There a Risk after Intravenous Contrast?
Clin. J. Am. Soc. Nephrol.,
September 1, 2008;
3(5):
1242 - 1243.
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X. Fei, X. Du, Q. Yang, Y. Shen, P. Li, J. Liao, and K. Li
64-MDCT Coronary Angiography: Phantom Study of Effects of Vascular Attenuation on Detection of Coronary Stenosis
Am. J. Roentgenol.,
July 1, 2008;
191(1):
43 - 49.
[Abstract]
[Full Text]
[PDF]
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M. Mockel, M. Radovic, Y. Kuhnle, V. Combe, J. Waigand, S. Schroder, R. Dietz, U. Frei, and K.-U. Eckardt
Acute renal haemodynamic effects of radiocontrast media in patients undergoing left ventricular and coronary angiography
Nephrol. Dial. Transplant.,
May 1, 2008;
23(5):
1588 - 1594.
[Abstract]
[Full Text]
[PDF]
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P. A. McCullough
Contrast-Induced Acute Kidney Injury
J. Am. Coll. Cardiol.,
April 15, 2008;
51(15):
1419 - 1428.
[Abstract]
[Full Text]
[PDF]
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A. Nusca, R. Melfi, and G. Di Sciascio
Review: Percutaneous coronary interventions and statins therapy
Therapeutic Advances in Cardiovascular Disease,
April 1, 2008;
2(2):
101 - 107.
[Abstract]
[PDF]
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J. K. Inrig, U. D. Patel, L. P. Briley, L. She, B. S. Gillespie, J. D. Easton, E. J. Topol, and L. A. Szczech
Mortality, kidney disease and cardiac procedures following acute coronary syndrome
Nephrol. Dial. Transplant.,
March 1, 2008;
23(3):
934 - 940.
[Abstract]
[Full Text]
[PDF]
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M. Rudnick and H. Feldman
Contrast-Induced Nephropathy: What Are the True Clinical Consequences?
Clin. J. Am. Soc. Nephrol.,
January 1, 2008;
3(1):
263 - 272.
[Abstract]
[Full Text]
[PDF]
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G. T. C. Wong and M. G. Irwin
Contrast-induced nephropathy
Br. J. Anaesth.,
October 1, 2007;
99(4):
474 - 483.
[Abstract]
[Full Text]
[PDF]
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A. O Onbasili, Y. Yeniceriglu, P. Agaoglu, A. Karul, T. Tekten, H. Akar, and G. Discigil
Trimetazidine in the prevention of contrast-induced nephropathy after coronary procedures
Heart,
June 1, 2007;
93(6):
698 - 702.
[Abstract]
[Full Text]
[PDF]
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A. Deo, M. Fogel, and S. E. Cowper
Nephrogenic Systemic Fibrosis: A Population Study Examining the Relationship of Disease Development to Gadolinium Exposure
Clin. J. Am. Soc. Nephrol.,
March 1, 2007;
2(2):
264 - 267.
[Abstract]
[Full Text]
[PDF]
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S.-H. Jo, T.-J. Youn, B.-K. Koo, J.-S. Park, H.-J. Kang, Y.-S. Cho, W.-Y. Chung, G.-W. Joo, I.-H. Chae, D.-J. Choi, et al.
Renal Toxicity Evaluation and Comparison Between Visipaque (Iodixanol) and Hexabrix (Ioxaglate) in Patients With Renal Insufficiency Undergoing Coronary Angiography: The RECOVER Study: A Randomized Controlled Trial
J. Am. Coll. Cardiol.,
September 5, 2006;
48(5):
924 - 930.
[Abstract]
[Full Text]
[PDF]
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N. Pannu, N. Wiebe, M. Tonelli, and for the Alberta Kidney Disease Network
Prophylaxis Strategies for Contrast-Induced Nephropathy
JAMA,
June 21, 2006;
295(23):
2765 - 2779.
[Abstract]
[Full Text]
[PDF]
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I. Michishita and Z. Fujii
A Novel Contrast Removal System From the Coronary Sinus Using an Adsorbing Column During Coronary Angiography in a Porcine Model
J. Am. Coll. Cardiol.,
May 2, 2006;
47(9):
1866 - 1870.
[Abstract]
[Full Text]
[PDF]
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D. G., I. I., N. E., A. E.D., M. G.S., K. N.N., L. A.J., M. I., S. G.W., M. J.W., et al.
Radiocontrast-Induced Acute Renal Failure--Impact beyond the Acute Phase: Contrast-Induced Nephropathy after Percutaneous Coronary Interventions in Relation to Chronic Kidney Disease and Hemodynamic Variables. Am J Cardiol 95: 13-19, 2005
J. Am. Soc. Nephrol.,
March 1, 2006;
17(3):
595 - 599.
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S. M. Bagshaw, F. A. McAlister, B. J. Manns, and W. A. Ghali
Acetylcysteine in the Prevention of Contrast-Induced Nephropathy: A Case Study of the Pitfalls in the Evolution of Evidence
Arch Intern Med,
January 23, 2006;
166(2):
161 - 166.
[Abstract]
[Full Text]
[PDF]
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P. J. Cowburn, H. Patel, R. R. Pipes, and J. D. Parker
Contrast nephropathy post cardiac resynchronization therapy: An under-recognized complication with important morbidity
Eur J Heart Fail,
August 1, 2005;
7(5):
899 - 903.
[Abstract]
[Full Text]
[PDF]
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M. C. Heinrich, M. K. Kuhlmann, A. Grgic, M. Heckmann, B. Kramann, and M. Uder
Cytotoxic Effects of Ionic High-osmolar, Nonionic Monomeric, and Nonionic Iso-osmolar Dimeric Iodinated Contrast Media on Renal Tubular Cells in Vitro
Radiology,
June 1, 2005;
235(3):
843 - 849.
[Abstract]
[Full Text]
[PDF]
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S. M. Bagshaw and W. A. Ghali
Theophylline for Prevention of Contrast-Induced Nephropathy: A Systematic Review and Meta-analysis
Arch Intern Med,
May 23, 2005;
165(10):
1087 - 1093.
[Abstract]
[Full Text]
[PDF]
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I. Iakovou, T. Schmidt, E. Bonizzoni, L. Ge, G. M. Sangiorgi, G. Stankovic, F. Airoldi, A. Chieffo, M. Montorfano, M. Carlino, et al.
Incidence, Predictors, and Outcome of Thrombosis After Successful Implantation of Drug-Eluting Stents
JAMA,
May 4, 2005;
293(17):
2126 - 2130.
[Abstract]
[Full Text]
[PDF]
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R. L. Mehta
Acute Renal Failure and Cardiac Surgery: Marching in Place or Moving Ahead?
J. Am. Soc. Nephrol.,
January 1, 2005;
16(1):
12 - 14.
[Full Text]
[PDF]
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G. Marenzi, G. Lauri, E. Assanelli, J. Campodonico, M. De Metrio, I. Marana, M. Grazi, F. Veglia, and A. L. Bartorelli
Contrast-induced nephropathy in patients undergoing primary angioplasty for acute myocardial infarction
J. Am. Coll. Cardiol.,
November 2, 2004;
44(9):
1780 - 1785.
[Abstract]
[Full Text]
[PDF]
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K. Spargias, E. Alexopoulos, S. Kyrzopoulos, P. Iacovis, D. C. Greenwood, A. Manginas, V. Voudris, G. Pavlides, C. E. Buller, D. Kremastinos, et al.
Ascorbic Acid Prevents Contrast-Mediated Nephropathy in Patients With Renal Dysfunction Undergoing Coronary Angiography or Intervention
Circulation,
November 2, 2004;
110(18):
2837 - 2842.
[Abstract]
[Full Text]
[PDF]
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R. Gupta, Y. Birnbaum, and B. F. Uretsky
The renal patient with coronary artery disease: Current concepts and dilemmas
J. Am. Coll. Cardiol.,
October 6, 2004;
44(7):
1343 - 1353.
[Abstract]
[Full Text]
[PDF]
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R. Mehran, E. D. Aymong, E. Nikolsky, Z. Lasic, I. Iakovou, M. Fahy, G. S. Mintz, A. J. Lansky, J. W. Moses, G. W. Stone, et al.
A simple risk score for prediction of contrast-induced nephropathy after percutaneous coronary intervention: Development and initial validation
J. Am. Coll. Cardiol.,
October 6, 2004;
44(7):
1393 - 1399.
[Abstract]
[Full Text]
[PDF]
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A. V. Kshirsagar, C. Poole, A. Mottl, D. Shoham, N. Franceschini, G. Tudor, M. Agrawal, C. Denu-Ciocca, E. Magnus Ohman, and W. F. Finn
N-Acetylcysteine for the Prevention of Radiocontrast Induced Nephropathy: A Meta-Analysis of Prospective Controlled Trials
J. Am. Soc. Nephrol.,
March 1, 2004;
15(3):
761 - 769.
[Abstract]
[Full Text]
[PDF]
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A. S. Gami and V. D. Garovic
Contrast Nephropathy After Coronary Angiography
Mayo Clin. Proc.,
February 1, 2004;
79(2):
211 - 219.
[Abstract]
[PDF]
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H. M. Sadeghi, G. W. Stone, C. L. Grines, R. Mehran, S. R. Dixon, A. J. Lansky, M. Fahy, D. A. Cox, E. Garcia, J. E. Tcheng, et al.
Impact of Renal Insufficiency in Patients Undergoing Primary Angioplasty for Acute Myocardial Infarction
Circulation,
December 2, 2003;
108(22):
2769 - 2775.
[Abstract]
[Full Text]
[PDF]
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G. W. Stone, P. A. McCullough, J. A. Tumlin, N. E. Lepor, H. Madyoon, P. Murray, A. Wang, A. A. Chu, G. L. Schaer, M. Stevens, et al.
Fenoldopam Mesylate for the Prevention of Contrast-Induced Nephropathy: A Randomized Controlled Trial
JAMA,
November 5, 2003;
290(17):
2284 - 2291.
[Abstract]
[Full Text]
[PDF]
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C. A. Herzog
How to Manage the Renal Patient with Coronary Heart Disease: The Agony and the Ecstasy of Opinion-Based Medicine
J. Am. Soc. Nephrol.,
October 1, 2003;
14(10):
2556 - 2572.
[Full Text]
[PDF]
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G. N. Levine, M. J. Kern, P. B. Berger, D. L. Brown, L. W. Klein, D. J. Kereiakes, T. A. Sanborn, A. K. Jacobs, and for the American Heart Association Diagnostic and
Management of Patients Undergoing Percutaneous Coronary Revascularization
Ann Intern Med,
July 15, 2003;
139(2):
123 - 136.
[Abstract]
[Full Text]
[PDF]
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E. J. Thompson and S. L. King
Acetylcysteine and Fenoldopam: Promising New Approaches for Preventing Effects of Contrast Nephrotoxicity
Crit. Care Nurse,
June 1, 2003;
23(3):
39 - 46.
[Full Text]
[PDF]
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S. Provenchere, G. Plantefeve, G. Hufnagel, E. Vicaut, C. de Vaumas, J.-B. Lecharny, J.-P. Depoix, F. Vrtovsnik, J.-M. Desmonts, and I. Philip
Renal Dysfunction After Cardiac Surgery with Normothermic Cardiopulmonary Bypass: Incidence, Risk Factors, and Effect on Clinical Outcome
Anesth. Analg.,
May 1, 2003;
96(5):
1258 - 1264.
[Abstract]
[Full Text]
[PDF]
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R. V. Freeman, R. H. Mehta, W. Al Badr, J. V. Cooper, E. Kline-Rogers, and K. A. Eagle
Influence of concurrent renal dysfunction on outcomes of patients with acute coronary syndromes and implications of the use of glycoprotein IIb/IIIa inhibitors
J. Am. Coll. Cardiol.,
March 5, 2003;
41(5):
718 - 724.
[Abstract]
[Full Text]
[PDF]
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J. Kay, W. H. Chow, T. M. Chan, S. K. Lo, O. H. Kwok, A. Yip, K. Fan, C. H. Lee, and W. F. Lam
Acetylcysteine for Prevention of Acute Deterioration of Renal Function Following Elective Coronary Angiography and Intervention: A Randomized Controlled Trial
JAMA,
February 5, 2003;
289(5):
553 - 558.
[Abstract]
[Full Text]
[PDF]
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K.-G. i Shyu, J.-J. Cheng, and P. Kuan
Acetylcysteine protects against acute renal damage in patients with abnormal renal function undergoing a coronary procedure
J. Am. Coll. Cardiol.,
October 16, 2002;
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[Abstract]
[Full Text]
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C. S. Rihal, S. C. Textor, D. E. Grill, P. B. Berger, H. H. Ting, P. J. Best, M. Singh, M. R. Bell, G. W. Barsness, V. Mathew, et al.
Incidence and Prognostic Importance of Acute Renal Failure After Percutaneous Coronary Intervention
Circulation,
May 14, 2002;
105(19):
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[Abstract]
[Full Text]
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C. Mueller, G. Buerkle, H. J. Buettner, J. Petersen, A. P. Perruchoud, U. Eriksson, S. Marsch, and H. Roskamm
Prevention of Contrast Media-Associated Nephropathy: Randomized Comparison of 2 Hydration Regimens in 1620 Patients Undergoing Coronary Angioplasty
Arch Intern Med,
February 11, 2002;
162(3):
329 - 336.
[Abstract]
[Full Text]
[PDF]
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L. M. Ruilope, D. J. van Veldhuisen, E. Ritz, and T. F. Luscher
Renal function: the Cinderella of cardiovascular risk profile
J. Am. Coll. Cardiol.,
December 1, 2001;
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[Abstract]
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Top
Abstract
Methods