Skip Navigation


NDT Advance Access originally published online on November 4, 2007
Nephrology Dialysis Transplantation 2008 23(3):934-940; doi:10.1093/ndt/gfm689
This Article
Right arrow Abstract Freely available
Right arrow FREE Full Text (PDF) Freely available
Right arrow All Versions of this Article:
23/3/934    most recent
gfm689v1
Right arrow Alert me when this article is cited
Right arrow Alert me if a correction is posted
Services
Right arrow Email this article to a friend
Right arrow Similar articles in this journal
Right arrow Similar articles in ISI Web of Science
Right arrow Similar articles in PubMed
Right arrow Alert me to new issues of the journal
Right arrow Add to My Personal Archive
Right arrow Download to citation manager
Right arrow Search for citing articles in:
ISI Web of Science (4)
Right arrowRequest Permissions
Right arrow Disclaimer
Google Scholar
Right arrow Articles by Inrig, J. K.
Right arrow Articles by Szczech, L. A.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Inrig, J. K.
Right arrow Articles by Szczech, L. A.
Social Bookmarking
Add to CiteULike   Add to Connotea   Add to Del.icio.us  
What's this?

© The Author [2007]. Published by Oxford University Press on behalf of ERA-EDTA. All rights reserved. For Permissions, please e-mail: journals.permissions@oxfordjournals.org


Mortality, kidney disease and cardiac procedures following acute coronary syndrome

Jula K. Inrig1, Uptal D. Patel1, Libbie P. Briley2, Lilin She1, Barbara S. Gillespie2, J. Donald Easton3, Eric J. Topol4 and Lynda A. Szczech1

1 Duke Clinical Research Institute, Duke University Medical Center, Durham, NC, USA 2 Quintiles INC, Durham, NC, USA 3 Department of Clinical Neurosciences, Brown University School of Medicine, Providence, RI, USA 4 Scripps Translational Science Institute, La Jolla, CA, USA

Jula K. Inrig, Duke University Medical Center, Box 3646, Durham, NC 27710, USA. Tel: +1-919-6687516; Fax: +1-919-668-7128; E-mail: inrig001{at}mc.duke.edu



   Abstract
Top
 Abstract
Introduction
 Methods
 Results
 Discussion
 References
 
Background. Cardiac interventions are underutilized in patients with chronic kidney disease (CKD) following acute coronary syndrome (ACS) partly due to nephrotoxicity concerns.

Methods. We analyzed outcomes of 4631 subjects with ACS enrolled in the Blockade of the Glycoprotein IIb/IIIa Receptor to Avoid Vascular Occlusion trial, including time to death, time to reduced renal function (50% reduction in estimated glomerular filtration rate (eGFR) or development of end-stage renal disease (ESRD)) and percent change in eGFR from baseline.

Results. Subjects with a lower baseline eGFR were more likely to be older, female and have diabetes, hypertension, congestive heart failure or peripheral vascular disease (all P < 0.0001); they were less likely to be taking aspirin ≥162 mg or to have undergone a percutaneous coronary intervention (PCI) prior to enrollment (P < 0.0001). As eGFR declined, the proportion of subjects experiencing death versus reduced eGFR or ESRD qualitatively increased. In adjusted analyses, every 10 ml/min/1.73 m2 decrease in eGFR ≤ 90 was associated with a 15% increased hazard of death (HR 1.15, P = 0.01). In adjusted analyses of predictors of percent change in eGFR, catheterization (cath) with or without PCI compared to medical therapy during follow-up was not associated with significant differences in long-term eGFR (P = 0.09).

Conclusions. Among CKD subjects in this study, the risk of death greatly outweighed the risk of reduced eGFR or development of ESRD following ACS and the occurrence of cath ± PCI was not associated with significant differences in long-term renal function. The presence of CKD should not preclude potentially beneficial interventions and research should focus on reducing the high cardiovascular burden in this population.

Keywords: acute coronary syndrome; cardiac catheterization; cardiac interventions; chronic kidney disease; mortality; outcomes



   Introduction
Top
 Abstract
 Introduction
Methods
 Results
 Discussion
 References
 
Cardiovascular disease affects ~71 million Americans; in 2003 alone, more than 850 000 individuals were hospitalized for acute coronary syndrome (ACS) [1]. Nearly 40% of patients who present with ACS have some degree of renal dysfunction [2]. Chronic kidney disease (CKD) is a known independent risk factor for cardiovascular disease [3] and is associated with detrimental outcomes among ACS patients [4,5]. Two reasons may explain why CKD is associated with adverse outcomes after cardiovascular events: beneficial therapies appear less likely to be used among patients with CKD as renal function declines [6–10] and percutaneous cardiac procedures may lead to excess toxicity among patients with baseline renal dysfunction [11].

Unfortunately, due to the epidemics of diabetes mellitus and obesity, the prevalence of CKD is expected to exceed 20 million people by 2010, resulting in a large population at risk for cardiovascular events [12]. Appropriate evidence-based therapies for this burgeoning population remain unclear because patients with renal impairment have been systematically excluded from large cardiovascular trials [13]. Thus, treatment decisions for this chronically ill population are difficult and can be affected by a variety of clinical parameters. Further, physicians must often balance the decision to perform diagnostic and therapeutic cardiovascular procedures among CKD patients with the possibility of losing viable renal function.

While it has been clearly demonstrated that the presence of CKD is a risk factor for radiocontrast-associated nephrotoxicity that can result in decreased short- and long-term survival [14–18], the relationship between kidney function, cardiac procedures and long-term renal outcomes is yet to be defined. Herein, we compared renal and patient survival among subjects with and without CKD who were admitted to the hospital with an ACS. Secondly, we compared renal outcomes among subjects who did or did not receive percutaneous cardiac procedures following ACS.



   Methods
Top
 Abstract
 Introduction
 Methods
Results
 Discussion
 References
 
Selection of subjects
A total of 9190 subjects who completed the Blockade of the Glycoprotein IIb/IIIa Receptor to Avoid Vascular Occlusion (BRAVO) trial were potentially available for this analysis. The methods and results of BRAVO have previously been described [19,20]. Briefly, BRAVO was a randomized double-blind trial comparing lotrafiban (an oral glycoprotein IIb/IIIa inhibitor) or matching placebo plus aspirin in patients with documented acute cardiovascular or cerebrovascular disease. Subjects enrolled in BRAVO were followed for 1 year (median follow-up 366 days). Subjects qualified for the BRAVO study if they had (1) a myocardial infarction (MI) within 14 days of baseline evaluation; (2) a diagnosis of unstable angina within 14 days of baseline evaluation; (3) an ischemic stroke confirmed by history, physical examination and computed tomographic (CT) or magnetic resonance (MR) imaging scan to be entered into the study no sooner than 5 days before and no later than 30 days after the acute event; (4) a transient ischemic attack (TIA) within 30 days of baseline evaluation, confirmed through positive history and/or physical examination in the absence of any significant findings on CT or MR imaging scan or (5) evidence of peripheral vascular disease combined with evidence of either cardiovascular or cerebrovascular disease. Subjects were excluded from the original trial if they had severe CKD (creatinine clearance <30 ml/min by Cockcroft–Gault formula) or concomitant severe disease, such as neoplasm that was likely to limit life expectancy or study participation to <2 years.

Study measurements and definitions
At enrollment, the following parameters were obtained and were available for our analyses: age; gender; race; body mass index (BMI); baseline heart rate; tobacco use; history of diabetes mellitus, hypertension, congestive heart disease, peripheral vascular disease and stroke; history of cardiac catheterization (cath) ± percutaneous coronary intervention (PCI); aspirin dose ≥162 mg/day and treatment arm (lotrafiban versus placebo). Serum creatinine was measured at baseline, at 72 h or hospital discharge, at 7, 10, and 14 days; at month 3 and every 3 months subsequent to completion of the trial.

For this analysis, estimated glomerular filtration rate (eGFR) was calculated using the abbreviated MDRD equation [21]:


Formula

while the Cockcroft–Gault equation [22] was used in the primary trial:


Formula

For descriptive purposes, subjects were stratified into groups adapted from stages of CKD delineated by the National Kidney Foundation (i.e. each stage was divided into two groups). However, eGFR was analyzed as a continuous variable wherever possible.

The following definitions were used in this analysis:

  • •  Reduced renal function was defined as a decrement in eGFR of 50% from baseline or the development of end-stage renal disease (ESRD) (defined as a reduction in eGFR to <15 ml/min/1.73 m2).
  • Percent change in eGFR = [(precatheterization eGFR – postcatheterization follow-up eGFR)/precatheterization eGFR]*100.
  • Subjects were coded as receiving a cardiac catheterization or PCI during the course of the study if they underwent either of these procedures after enrollment.

Primary outcome
The primary outcomes of interest included reduced renal function (50% decrement in eGFR or development of ESRD) and the occurrence of death. Secondary outcome measurements included percent change in eGFR during follow-up.

Statistical methods
Our analysis was restricted to subjects enrolled in BRAVO with the diagnosis of unstable angina or acute MI within 14 days of baseline evaluation (N = 4634). Demographic and clinical factors were summarized and compared between groups of subjects stratified on the basis of renal function. Continuous variables were compared using the Spearman correlation test and binary categorical variables were compared using the Wilcoxon rank sum test.

Univariate survival probabilities were compared among groups of subjects based on the category of eGFR using Kaplan–Meier methodology with the log-rank test.

Cox proportional hazards regression was used to model the association between eGFR, cardiac procedures (cath ± PCI) and the hazard of reduced renal function or the hazard of death while controlling for other predictors. Proportional hazards assumptions and linearity assumptions for continuous variables were assessed by restricted cubic splines. When the relationship was found to be nonlinear, appropriate transformations were applied. Due to a nonlinear association between eGFR and log hazards ratio, a two-piece-wise linear spline was used to represent the eGFR effect. Cardiac procedures and eGFR were both treated as time-dependent covariates in the model predicting death. Baseline eGFR was used in models predicting the hazard of reduced renal function. Due to presumed non-proportional hazards following coronary artery bypass grafting (CABG), subjects who underwent CABG after enrollment were censored in the time-to-event analyses at the time of CABG and were excluded in other event rate analyses. The aforementioned baseline variables that were candidates for risk factor adjustment were first included in the model and retained using P = 0.05 as the inclusion criterion. Interactions between clinically relevant variables such as eGFR and the occurrence of cath ± PCI were tested in separate models.

To assess for changes in eGFR that may have occurred in association with undergoing cath ± PCI, percent changes in eGFR following these procedures were compared between groups undergoing and not undergoing these procedures. Subjects who had undergone cath ± PCI were included in the analyses only if they had an eGFR measured both before and after the procedures (N = 406): the post-cath ± PCI eGFR must have been taken within 7–180 days after the procedure(s), while the pre-cath ± PCI eGFR was the last eGFR measure taken before the procedure(s). Subjects were excluded from the analysis if the only available pre-cath ± PCI GFR for a subject was taken at baseline and the procedure(s) did not occur within 30 days after baseline. For each subject undergoing cardiac catheterization or PCI, three subjects were selected randomly from subjects who did not undergo cath ± PCI (i.e., the medication-only subjects) and who had serum creatinine measured within a 30-day window of both the pre- and the postprocedure eGFR of the cath ± PCI patient. Percent changes in eGFR were compared using the ANOVA test, adjusting for the timing of the first eGFR taken. In multivariable analyses, a general linear model was used that controlled for baseline eGFR, timing of eGFR and the above-mentioned baseline variables.

All P-values reported are two-sided, and all confidence intervals (CI) reported are 95% intervals. All analyses were performed using SAS (version 8.2, SAS Institute Inc., Cary, NC, USA).



   Results
Top
 Abstract
 Introduction
 Methods
 Results
Discussion
 References
 
Study population
A total of 4634 subjects with unstable angina or acute MI were enrolled in BRAVO and were included in this analysis (baseline characteristics based on eGFR can be seen in Table 1). In general, subjects with a lower baseline eGFR were significantly more likely to be older, white, female and have a history of diabetes mellitus, hypertension, congestive heart failure or peripheral vascular disease. Subjects with a lower baseline eGFR were also significantly less likely to have undergone a cath ± PCI previously or at baseline, to have smoked tobacco or to be taking daily aspirin therapy ≥162 mg at baseline.


View this table:
[in this window]
[in a new window]

  		Table 1 Baseline characteristics among subjects characterized by eGFR (ml/min/1.73 m2) categories

 
Outcomes based on stage of kidney disease
In univariate analysis, subjects with a lower baseline eGFR had a shorter time to a composite endpoint of a 50% reduction in eGFR, development of ESRD or death (P = 0.007). However, the relative number of subjects who developed reduced eGFR, progressed to ESRD or died varied based on baseline kidney function (Table 2). Among all categories of subjects based on eGFR, with the exception of subjects whose eGFR ≥ 90 ml/min/1.73 m2 at baseline, death accounted for a greater proportion of the events than did reduction of eGFR or progression to ESRD. Additionally, the relative proportion of subjects experiencing death as compared to those experiencing a 50% reduction of eGFR or progression to ESRD qualitatively increased as the categories of kidney function declined.


View this table:
[in this window]
[in a new window]

  		Table 2 Number (No.) of subjects experiencing each event of 50% reduction in eGFR, development of ESRD or death grouped by baseline eGFR (ml/min/1.73 m2)a,b

 
In adjusted analyses predicting the hazard of reduced renal function, subjects with a higher baseline eGFR were more likely to experience reduced renal function during follow-up (Table 3). Other variables associated with an increased hazard of reduced renal function included increasing age, congestive heart failure and higher BMI.


View this table:
[in this window]
[in a new window]

  		Table 3 Multivariable model of predictors of time to 50% decrease in eGFR or development of end-stage renal disease

 
In multivariable models predicting death, every 10 ml/ min/1.73 m2 decrease in time-varying eGFR <90 was associated with a 15% increase in hazard of death (HR = 1.15, P = 0.01) (Table 4). Other significant predictors of increased mortality included increasing age, the presence of diabetes mellitus, the occurrence of cardiac cath ± PCI during the period of study and history of congestive heart failure. A history of cath ± PCI prior to enrollment and use of aspirin ≥162 mg were associated with decreased mortality.


View this table:
[in this window]
[in a new window]

  		Table 4 Multivariable model of predictors of time to death

 
There was no interaction between eGFR and occurrence of cardiac cath ± PCI during the course of the study as a significant predictor of renal outcomes (P > 0.10 for eGFR ≤90 and for eGFR >90). Thus, subjects with a lower eGFR were not more likely to develop reduced renal function or ESRD with the occurrence of cardiac procedures. There was also no interaction between eGFR and the occurrence of cardiac cath ± PCI as a significant predictor of mortality (P > 0.10 for eGFR ≤90 and for eGFR >90). Thus, poorer outcomes associated with the occurrence of a cath ± PCI during follow-up did not vary based on underlying renal function.

Renal outcomes among subjects undergoing cath ± PCI versus medical therapy
Change in eGFR over time was compared among a subset of the entire cohort to include all subjects who underwent a cath ± PCI and subjects not undergoing these procedures but having serum creatinine measurements available during similar time periods (Table 5, Figure 1). Subjects who underwent a cath ± PCI during the study were younger, were less likely to be taking ≥162 mg of aspirin and were less likely to have a history of congestive heart failure or peripheral vascular disease. Subjects who underwent cath ± PCI were more likely to have had a prior cath ± PCI and have a history of stroke. Subjects who underwent cath ± PCI during the study also had higher eGFR compared to subjects treated with medical therapy.


View this table:
[in this window]
[in a new window]

  		Table 5 Baseline characteristics of subjects undergoing cath ± PCI versus medical therapya

 

Figure 1
View larger version (34K):
[in this window]
[in a new window]
[Download PowerPoint slide]
  		Fig. 1 Change in eGFR percentage among subjects undergoing cath/PCI as compared to subjects receiving medical therapy.

 
In unadjusted analyses, subjects who underwent cath ± PCI had a mean percent change in eGFR of 0.4% (± 22.4) compared to 2.5% (± 24.0) among subjects treated medically (P = 0.13).

In adjusted analyses of predictors of percent change in eGFR, the occurrence of cath ± PCI compared to medical therapy was not associated with a significant difference in eGFR in the long-term follow-up (P = 0.09). Factors associated with greater percent reductions in eGFR over the course of follow-up included higher eGFR at baseline (P < 0.001), increasing age (P < 0.0001), increased heart rate (0.04), baseline aspirin ≥162 mg/day (P = 0.03) and treatment arm (P = 0.0002).

No interaction was observed between percutaneous cardiac procedures and eGFR (P = 0.17) as a predictor of percent change in eGFR among this subcohort. Thus, various levels of eGFR did not alter the association between cardiac procedures and change in eGFR over time (i.e. neither subjects with higher nor with lower eGFR were likely to have a change in renal function with the occurrence of a cardiac procedure).



   Discussion
Top
 Abstract
 Introduction
 Methods
 Results
 Discussion
References
 
Epidemiologic and natural history studies have demonstrated that CKD is a prevalent, independent risk factor for all-cause and cardiovascular mortality. Yet, prior analyses suggest that reduced eGFR is associated with decreased utilization of diagnostic and therapeutic interventions such as cardiac catheterization and PCI [7,8,10,23] likely due to concern about radiocontrast-associated nephrotoxicity and long-term renal dysfunction. However, we have demonstrated that among subjects with CKD, there was no increased risk of a long-term decrease in renal function following cath ± PCI. Further, our study confirms that the presence of CKD is strongly associated with an increased risk of death following ACS [10,24–32].

Prior studies have shown that following cardiac procedures, patients with CKD have an increased risk of acute renal failure [7,17,33], but long-term renal outcomes have not been fully elucidated. In an observational study of 439 CKD patients (serum creatinine > 1.8 mg/dl) who underwent cardiac interventions, <1% required renal replacement therapy on discharge; however, long-term renal outcomes following discharge were not assessed [16]. In our investigation, we found no increased risk of progressive renal failure among patients undergoing a cardiac procedure as compared to medical therapy during follow-up.

Patients with CKD have high mortality rates irrespective of treatments following ACS. In our analysis, there was an ~6% rate of mortality in 1 year among subjects with eGFR < 60, which significantly overshadowed reductions in eGFR or development of ESRD. In similar analyses, 1-year mortality among CKD patients following ACS has been reported to range from ~5% to 25% [26,31,34], emphasizing the need for research aimed at reducing this high cardiovascular burden.

Our study also demonstrates that subjects with CKD are less likely to receive beneficial treatments that may improve cardiovascular outcomes. In our multivariable analyses, subjects treated with ASA ≥ 162 mg, as well as subjects who underwent cath ± PCI upon presentation with ACS prior to enrollment, had improved survival. Unfortunately, subjects with CKD at enrollment were significantly less likely to be treated with these therapies.

Understanding the mechanism that results in poorer prognosis for patients with CKD after ACS is a critical first step in preventing morbidity and mortality in this high-risk population. We have demonstrated that subjects with eGFR ≤ 90 ml/min/1.73 m2, subjects undergoing cardiac cath ± PCI during follow-up, older subjects and those with DM or CHF all experienced hastened mortality following ACS. The severity of heart disease, indicated by the need for interventional procedures or marked by the presence of symptoms or comorbid states, is the most likely mechanism determining the prognosis of this population. Patients in this population experience increased rates of vascular calcification as well as the comorbid effects of DM and obesity [35]. In addition, the uremic effects of advanced renal disease provide an increase in oxidative stress that has been proposed as a nontraditional cardiovascular risk factor in this patient population [36].

While this study demonstrates that patients with CKD and ACS are at a greater risk for mortality than reduction in eGFR, its conclusions should be interpreted in the setting of certain limitations. This cohort was recruited for a clinical trial and may therefore not be representative of the general population. Selection biases for subject inclusion may affect our findings and should be considered when generalizing these results to all patients with CKD, particularly with respect to race and to patients with advanced kidney disease, as subjects with an eGFR < 30 ml/min were excluded from the original trial. Indication bias may affect the results of any observational study in that the indication for treatment may affect the likelihood of the outcome. In particular, we are unable to control for unmeasured confounders that may have directed the occurrence of a cardiac catheterization or PCI. Finally, it should be acknowledged that due to the timing and frequency of creatinine measurement, acute renal failure cannot be discerned from progression of underlying kidney disease. Because of the possibility that a subject may have experienced acute renal failure as a preterminal event, no effort was made to differentiate between acute and reversible versus chronic and irreversible kidney disease. Rather, all loss of kidney function was referred to as a reduction in eGFR.

Among subjects with CKD in this study, the risk of death greatly outweighed the risk of further reduction in eGFR or development of ESRD. While it remains unclear whether more accurate assessment of coronary disease by cardiac catheterization or management of existing disease by PCI improves outcomes among CKD patients, our study suggests that cardiac interventions do not significantly worsen long-term renal function. In summary, more aggressive management of the increased cardiovascular risk in CKD patients is clearly needed and the presence of CKD should not preclude the use of potentially beneficial diagnostic and therapeutic interventions.



   Acknowledgments
 
J.K.I. was supported by NIH grant K12 RR17630 and 1KL2 RR024127–01. U.D.P. was supported by NIH grant 1K23DK075929–01. This manuscript was presented in poster format at the American Society of Nephrology Annual Meeting in San Diego, California on 17 November 2006.

Conflict of interest statement. None declared.



   References
Top
 Abstract
 Introduction
 Methods
 Results
 Discussion
 References
 

  1. Thom T, Haase N, Rosamond W, et al. Heart disease and stroke statistics—2006 update: a report from the American Heart Association Statistics Committee and Stroke Statistics Subcommittee. Circulation (2006) 113:e85–151.[Free Full Text]
  2. Reddan DN, Szczech LA, Tuttle RH, et al. Chronic kidney disease, mortality, and treatment strategies among patients with clinically significant coronary artery disease. J Am Soc Nephrol (2003) 14:2373–2380.[Abstract/Free Full Text]
  3. Go AS, Chertow GM, Fan D, et al. Chronic kidney disease and the risks of death, cardiovascular events, and hospitalization. N Engl J Med (2004) 351:1296–1305.[Abstract/Free Full Text]
  4. Krumholz HM, Chen J, Wang Y, et al. Comparing AMI mortality among hospitals in patients 65 years of age and older: evaluating methods of risk adjustment. Circulation (1999) 99:2986–2992.[Abstract/Free Full Text]
  5. Shlipak MG, Heidenreich PA, Noguchi H, et al. Association of renal insufficiency with treatment and outcomes after myocardial infarction in elderly patients. Ann Intern Med (2002) 137:555–562.[Abstract/Free Full Text]
  6. Beattie JN, Soman SS, Sandberg KR, et al. Determinants of mortality after myocardial infarction in patients with advanced renal dysfunction. Am J Kidney Dis (2001) 37:1191–1200.[Web of Science][Medline]
  7. Freeman RV, Mehta RH, Al Badr W, et al. 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 (2003) 41:718–724.[Abstract/Free Full Text]
  8. Chertow GM, Normand SL, McNeil BJ. "Renalism": inappropriately low rates of coronary angiography in elderly individuals with renal insufficiency. J Am Soc Nephrol (2004) 15:2462–2468.[Abstract/Free Full Text]
  9. Winkelmayer WC, Charytan DM, Levin R, et al. Poor short-term survival and low use of cardiovascular medications in elderly dialysis patients after acute myocardial infarction. Am J Kidney Dis (2006) 47:301–308.[CrossRef][Web of Science][Medline]
  10. Keough-Ryan TM, Kiberd BA, Dipchand CS, et al. Outcomes of acute coronary syndrome in a large Canadian cohort: impact of chronic renal insufficiency, cardiac interventions, and anemia. Am J Kidney Dis (2005) 46:845–855.[CrossRef][Web of Science][Medline]
  11. McCullough PA. Why is chronic kidney disease the "spoiler" for cardiovascular outcomes? J Am Coll Cardiol (2003) 41:725–728.[Free Full Text]
  12. US Renal Data Systems (USRDS). Annual Data Report: Atlas of End-Stage Renal Disease in the United States. National Institutes of Health, National Institute of Diabetes and Digestive and Kidney Diseases, Bethesda, MD 2005.
  13. Coca SG, Krumholz HM, Garg AX, et al. Under-representation of renal disease in randomized controlled trials of cardiovascular disease. JAMA (2006) 296:1377–1384.[Abstract/Free Full Text]
  14. McCullough PA, Wolyn R, Rocher LL, et al. 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]
  15. Manske CL, Sprafka JM, Strony JT, et al. Contrast nephropathy in azotemic diabetic patients undergoing coronary angiography. Am J Med (1990) 89:615–620.[CrossRef][Web of Science][Medline]
  16. Gruberg L, Mintz GS, Mehran R, et al. The prognostic implications of further renal function deterioration within 48 h of interventional coronary procedures in patients with pre-existent chronic renal insufficiency. J Am Coll Cardiol (2000) 36:1542–1548.[Abstract/Free Full Text]
  17. 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]
  18. Gruberg L, Mehran R, Dangas G, et al. Acute renal failure requiring dialysis after percutaneous coronary interventions. Catheter Cardiovasc Interv (2001) 52:409–416.[CrossRef][Web of Science][Medline]
  19. Topol EJ, Easton JD, Amarenco P, et al. Design of the blockade of the glycoprotein IIb/IIIa receptor to avoid vascular occlusion (BRAVO) trial. Am Heart J (2000) 139:927–933.[CrossRef][Web of Science][Medline]
  20. Topol EJ, Easton D, Harrington RA, et al. Randomized, double-blind, placebo-controlled, international trial of the oral IIb/IIIa antagonist lotrafiban in coronary and cerebrovascular disease. Circulation (2003) 108:399–406.[Abstract/Free Full Text]
  21. Levey AS, Bosch JP, Lewis JB, et al. A more accurate method to estimate glomerular filtration rte from serum creatinine: a new prediction equation. Ann Intern Med (1999) 130:461–470.[Abstract/Free Full Text]
  22. Cockcroft DW, Gault MH. Prediction of creatinine clearance from serum creatinine. Nephron (1976) 16:31–41.[Web of Science][Medline]
  23. Szczech LA, Best PJ, Crowley E, et al. Outcomes of patients with chronic renal insufficiency in the bypass angioplasty revascularization investigation. Circulation (2002) 105:2253–2258.[Abstract/Free Full Text]
  24. Lemos PA, Arampatzis CA, Hoye A, et al. Impact of baseline renal function on mortality after percutaneous coronary intervention with sirolimus-eluting stents or bare metal stents. Am J Cardiol (2005) 95:167–172.[CrossRef][Web of Science][Medline]
  25. Fathi RB, Gurm HS, Chew DP, et al. The interaction of vascular inflammation and chronic kidney disease for the prediction of long-term death after percutaneous coronary intervention. Am Heart J (2005) 150:1190–1197.[CrossRef][Web of Science][Medline]
  26. Sadeghi HM, Stone GW, Grines CL, et al. Impact of renal insufficiency in patients undergoing primary angioplasty for acute myocardial infarction. Circulation (2003) 108:2769–2775.[Abstract/Free Full Text]
  27. Naidu SS, Selzer F, Jacobs A, et al. Renal insufficiency is an independent predictor of mortality after percutaneous coronary intervention. Am J Cardiol (2003) 92:1160–1164.[CrossRef][Web of Science][Medline]
  28. Reinecke H, Regetmeier A, Matzkies F, et al. Even moderate chronic renal failure is associated with impaired acute and long-term outcome after coronary angioplasty. Nephrology (2003) 8:110–115.[CrossRef][Medline]
  29. Reinecke H, Trey T, Matzkies F, et al. Grade of chronic renal failure, and acute and long-term outcome after percutaneous coronary interventions. Kidney Int (2003) 63:696–701.[CrossRef][Web of Science][Medline]
  30. Han JH, Chandra A, Mulgund J, et al. Chronic kidney disease in patients with non-ST-segment elevation acute coronary syndromes. Am J Med (2006) 119:248–254.[CrossRef][Web of Science][Medline]
  31. Ix JH, Mercado N, Shlipak MG, et al. Association of chronic kidney disease with clinical outcomes after coronary revascularization: the arterial revascularization therapies study (ARTS). Am Heart J (2005) 149:512–519.[CrossRef][Web of Science][Medline]
  32. Yamaguchi J, Kasanuki H, Ishii Y, et al. Prognostic significance of serum creatinine concentration for in-hospital mortality in patients with acute myocardial infarction who underwent successful primary percutaneous coronary intervention (from the Heart Institute of Japan Acute Myocardial Infarction [HIJAMI] Registry). Am J Cardiol (2004) 93:1526–1528.[CrossRef][Web of Science][Medline]
  33. 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]
  34. 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]
  35. Dellegrottaglie S, Saran R, Rajagopalan S. Vascular calcification in patients with renal failure: culprit or innocent bystander? Cardiol Clin (2005) 23:373–384.[CrossRef][Web of Science][Medline]
  36. Himmelfarb J. Relevance of oxidative pathways in the pathophysiology of chronic kidney disease. Cardiol Clin (2005) 23:319–330.[CrossRef][Web of Science][Medline]
Received for publication: 2. 4.07
Accepted in revised form: 6. 9.07


Add to CiteULike CiteULike   Add to Connotea Connotea   Add to Del.icio.us Del.icio.us    What's this?



This Article
Right arrow Abstract Freely available
Right arrow FREE Full Text (PDF) Freely available
Right arrow All Versions of this Article:
23/3/934    most recent
gfm689v1
Right arrow Alert me when this article is cited
Right arrow Alert me if a correction is posted
Services
Right arrow Email this article to a friend
Right arrow Similar articles in this journal
Right arrow Similar articles in ISI Web of Science
Right arrow Similar articles in PubMed
Right arrow Alert me to new issues of the journal
Right arrow Add to My Personal Archive
Right arrow Download to citation manager
Right arrow Search for citing articles in:
ISI Web of Science (4)
Right arrowRequest Permissions
Right arrow Disclaimer
Google Scholar
Right arrow Articles by Inrig, J. K.
Right arrow Articles by Szczech, L. A.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Inrig, J. K.
Right arrow Articles by Szczech, L. A.
Social Bookmarking
Add to CiteULike   Add to Connotea   Add to Del.icio.us  
What's this?