CLINICAL RESEARCH: CLINICAL TRIAL
The Reno-Protective Effect of Hydration With Sodium Bicarbonate Plus N-Acetylcysteine in Patients Undergoing Emergency Percutaneous Coronary InterventionThe RENO Study
Alejandro Recio-Mayoral, MD*,*,
Marinela Chaparro, MD*,
Belén Prado, MD*,
Rocío Cózar, MD*,
Irene Méndez, MD*,
Debasish Banerjee, MD, MRCP ,
Juan C. Kaski, MD, DM, DSc ,
José Cubero, MD* and
Jose M. Cruz, MD*
* Department of Cardiology, Virgen Macarena University Hospital, Seville, Spain
Department of Renal and Transplantation, St. George’s Hospital, University of London, London, United Kingdom
Division of Cardiac and Vascular Sciences, St. George’s Hospital, University of London, London, United Kingdom.
Manuscript received August 16, 2006;
revised manuscript received November 1, 2006,
accepted November 16, 2006.
* Reprint requests and correspondence: Dr. Alejandro Recio-Mayoral, Division of Cardiac and Vascular Sciences, St. George’s Hospital, University of London, Cranmer Terrace, London SW17 0RE, United Kingdom. (Email: arecio{at}sgul.ac.uk).
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Abstract
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Objectives: This study was designed to determine the effectiveness of a protocol for rapid intravenous hydration to prevent contrast-induced nephropathy (CIN) in patients undergoing emergency percutaneous coronary intervention (PCI).
Background: Contrast-induced nephropathy frequently complicates PCI, resulting in prolonged hospitalization and increased in-hospital and long-term morbidity and mortality. Little is known regarding prevention of CIN in patients undergoing urgent PCI.
Methods: We conducted a prospective, controlled, randomized, single-center trial in 111 consecutive patients with acute coronary syndrome undergoing emergency PCI. As part of the hydration therapy, 56 patients (group A) received an infusion of sodium bicarbonate plus N-acetylcysteine (N-AC) started just before contrast injection and continued for 12 h after PCI. The remaining 55 patients (group B) received the standard hydration protocol consisting of intravenous isotonic saline for 12 h after PCI. In both groups, 2 doses of oral N-AC were administered the next day.
Results: The 2 groups were similar with respect to age, gender, diabetes mellitus, and baseline serum creatinine. A serum creatinine concentration >0.5 mg/dl from baseline after emergency PCI was observed in 1 patient in group A (1.8%) and in 12 patients in group B (21.8%; p < 0.001). Acute anuric renal failure was observed in 1 patient (1.8%) in group A and in 7 patients (12.7%) in group B (p = 0.032).
Conclusions: Rapid intravenous hydration with sodium bicarbonate plus N-AC before contrast injection is effective and safe in the prevention of CIN in patients undergoing emergency PCI.
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Abbreviations and Acronyms
| | ACS = acute coronary syndrome | | BUN = blood urea nitrogen | | CI = confidence interval | | CIN = contrast-induced nephropathy | | GFR = glomerular filtration rate | | N-AC = N-acetylcysteine | | OR = odds ratio | | PCI = percutaneous coronary intervention | | SCr = serum creatinine |
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 Iodinated contrast media are being used increasingly in the catheterization laboratory during diagnostic catheterization and percutaneous coronary intervention (PCI). Contrast-induced nephropathy (CIN) is a major cause of morbidity and mortality associated with PCI (1). The overall incidence of CIN after PCI has been reported between 3.3% and 16.5% (1,2), although this figure increases up to 50% in high-risk patients (3). In Europe, CIN is the third highest cause of acute renal failure, accounting for 10% of all causes of hospital-acquired renal failure (4). Several therapies for preventing CIN have been tested in patients undergoing elective PCI, with differing results. Only intravenous hydration with saline has been shown repeatedly to provide effective and safe prophylaxis for CIN in these patients (5). In the pathogenesis of CIN, renal ischemia and free radical formation induced by the contrast medium play an important role (6). Based on the hypothesis that alkalizing the renal tubule should confer protection against CIN in a prospective trial, Merten et al. (7) compared hydration with intravenous sodium bicarbonate and sodium chloride starting 1 h before contrast exposition. They showed that intravenous hydration with sodium bicarbonate provides greater benefits in the prevention of CIN (1.7% vs. 13.6%, p = 0.02). The results from the study by Merten et al. (7) with bicarbonate have not been replicated by others. N-acetylcysteine (N-AC), a potent antioxidant either directly as a free radical scavenger or indirectly through glutation production (8,9), may play an additional role in the prevention of CIN. Although several studies on the prophylactic effect of N-AC have given conflicting results, recent studies support a dose-dependent effect (10–12), suggesting that a higher dose could be needed in high-risk patients, in whom greater amounts of contrast could be administered.
Patients undergoing emergency PCI represent a high-risk population for CIN, as opposed to those undergoing elective PCI (13). Various conditions may contribute to renal injury in this setting (i.e., hypotension and exposure to large volumes of contrast media), along with difficulties in establishing a prophylactic therapy in the acute setting.
A rapid hydration with saline sodium bicarbonate, in addition to causing intravascular volume expansion, could provide additional effects over the free radical scavenger properties of N-AC. To assess the effectiveness and safety of a CIN prevention protocol with sodium bicarbonate hydration plus N-AC, we carried out the RENO (Reno-Protective Effect of Hydration With Sodium Bicarbonate Plus N-Acetylcysteine in Patients Undergoing Emergency Percutaneous Coronary Intervention) study, a randomized, single-blind, single-center trial in patients undergoing emergency PCI.
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Methods
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Patients.
We prospectively studied 111 consecutive acute coronary syndrome (ACS) patients who were admitted to our coronary care unit between December 2004 and May 2005. All patients with myocardial infarction treated with primary PCI or rescue PCI, as well as patients with high-risk non–ST-segment elevation ACS needing urgent revascularization, were included. Urgent PCI was considered in high-risk non–ST-segment elevation ACS, defined by the following criteria: recurrent resting chest pain not responding to treatment, hemodynamic instability and cardiogenic shock, major arrhythmias, and early postinfarction unstable angina (14). In all cases, the coronary angiography was performed within the first 12 h from the onset of symptoms.
Cardiogenic shock was defined as prolonged hypotension (systolic blood pressure <90 mm Hg for at least 30 min) caused by severe left ventricular dysfunction or right ventricular infarction, requiring inotropic support medication and/or intra-aortic balloon pump to maintain a systolic blood pressure of  90 mm Hg (15).
There were no inclusion criteria based on glomerular filtration rate (GFR). Patients with end-stage renal failure on dialysis, uncontrolled hypertension (systolic blood pressure >160 mm Hg and/or diastolic blood pressure >100 mm Hg) and signs of cardiac failure not responding to medical treatment, known severe aortic valve stenosis (area <1.0 cm2), allergy to iodated contrast or N-AC, and pregnancy were excluded from the study. The study protocol was reviewed and approved by the local ethics committee, and all patients gave written informed consent before the study entry.
Study protocol.
Patients were randomly assigned to an active prophylactic treatment before PCI (group A) or to standard hydration after the procedure (group B). The patients allocated to group A received an initial intravenous bolus of 5 ml/kg/h of alkaline saline solution with 154 mEq/l of sodium bicarbonate in 5% glucose and H2O (adding 77 ml of 1,000 mEq/l sodium bicarbonate to 433 ml of 5% glucose in H2O) plus 2,400 mg of N-AC in the same solution over 1 h. In all patients, the bolus was administered in the 60 min preceding contrast injection. Afterward, patients received fluid therapy, without N-AC, at 1.5 ml/kg/h perfusion rate in the 12 h after the procedure plus 2 doses of 600 mg N-AC orally the next day. Patients in group B were treated according to our institution protocol with perfusion of isotonic saline (0.9%) at rate of 1 ml/kg/h for 12 h after PCI plus 2 doses of 600 mg N-AC orally the next day. In both groups, the maximum dose administered was that administered for patients weighing 100 kg.
There was no limitation in concomitant treatment, including diuretics and angiotensin-converting enzyme inhibitors, which were left to the discretion of the interventional and coronary care unit cardiologists. Only the patients were blinded and not told to which group they were randomized.
Coronary angiography was performed according to standard clinical practice using the femoral approach. The low-osmolality nonionic contrast medium Iomeprol (Iomeron, Bracco s.p.a, Milan, Italy) with 350 mg/ml of iodine content was used in all cases. All decisions regarding procedural hemodynamics, including contrast doses, were left to the discretion of the interventional cardiologist.
Serum creatinine (SCr) and blood urea nitrogen (BUN) concentrations were measured at admission, daily for the next 3 days, and on day 7 after the procedure. The GFR was calculated using the Modification of Diet in Renal Disease Study group equation (16). Likewise, arterial blood pH was assessed immediately before the procedure and 2 h thereafter. Diuresis was collected for 24 h after the procedure.
The primary end point was the development of acute CIN, defined as an absolute increase in SCr concentration of 0.5 mg/dl or more from baseline value in the 3 days after PCI (17–19). The following secondary end points were assessed: 1) other conventional definitions of CIN: an increase in SCr >25% over the baseline value and >50% over the baseline value, both within the first 3 days (6,19); and 2) adverse clinical events, including acute pulmonary edema during and after the procedure, acute anuric renal failure that did or did not result in temporary renal replacement therapy, and death in the 7 days after the procedure. Renal replacement therapy (hemodialysis or hemofiltration) was undertaken in patients with anuria (urine output <20 ml/h) despite the administration of more than 1 g intravenous furosemide and presence of volume overload and/or BUN >200 mg/dl.
Statistical analysis.
We calculated the sample size of our study assuming a CIN rate of 20% in group B based on the rate previously reported by Marenzy et al. (13) in patients undergoing primary PCI. For group A, patients treated with sodium bicarbonate and a high dose of N-AC, we assumed a CIN rate of 3%, similar to that reported by Briguori et al. (11) using high doses of N-AC (3.5%) and by Merten et al. (7) using sodium bicarbonate (1.7%). Analysis indicated that a sample size of 55 patients would be necessary in each arm to detect a statistically significant different with a power of 80%, with a type I error of 0.05.
Analysis was conducted on an intention-to-treat basis. Categorical variables were expressed as percentages and analyzed by chi-square or Fisher exact test as appropriate. Continuous variables were expressed as mean ± SD and compared with the t test, except levels of SCr and BUN, which were compared with the nonparametric Wilcoxon-Mann-Whitney U test. We used Spearman correlation coefficients to evaluate the relationship between volumes of contrast medium administered during procedure and maximum change in SCr from the baseline value in the first 3 days after PCI. A repeated-measures analysis of variance was used to test the interaction of treatment in the evolution of GFR during follow-up. Multivariate logistic regression analysis was performed to examine the effects of different possible confounding variables on the incidence of CIN. All statistical analyses were performed with the Statistical Package for the Social Sciences version 13.0 (SPSS Inc., Chicago, Illinois). A 2-sided p value of <0.05 was considered to be significant.
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Results
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Baseline characteristics.
Of the 120 patients randomized, 111 (34 women, ages 65 ± 10 years) had SCr measurements completed and were included in the study. The baseline characteristics of the patients are shown in Table 1.
Treatment compliance.
In group A, the therapy was discontinued prematurely in 2 patients; in 1 diabetic patient with severe left ventricular dysfunction, the protocol was stopped after bolus perfusion as a result of a pulmonary edema clinic just after a left ventriculography was performed. This patient required intravenous nitrates and furosemide and CIN developed afterward, with a maximum SCr of 1.7 mg/dl. The other case was a high-risk non–ST-segment elevation ACS patient with PCI on the right coronary artery, in whom perfusion was stopped 4 h after PCI subsequent to the development of a right ventricular infarction. Bolus administration of sodium saline was given before a new procedure was carried out because of an acute in-stent thrombosis that was treated with a new bare-metal stent; CIN did not develop in this patient.
Intervention data and analyses.
There were no significant differences in SCr and BUN values measured immediately before the procedure (baseline) (Table 2). Arterial blood pH before the catheterization was similar in both groups (7.37 ± 0.04 in group A vs. 7.37 ± 0.04 in group B, p = 0.84). Two hours after contrast administration, patients in group A showed a serum alkalinization, whereas patients in group B experienced a decrease in serum pH (7.41 ± 0.03 vs. 7.36 ± 0.03 respectively, p < 0.0001) (Table 2).
The diuresis measured in the 24 h after contrast infusion was significantly lower in group B than group A (1,955 ± 529 ml/24 h vs. 3,098 ± 693 ml/24 h, p < 0.0001). The mean contrast volume administered was not significantly different in group A versus group B (Table 2). However, when the response of individuals patients was assessed in each group, we found that in group B patients there was a higher change in SCr in patients who received a large volume of contrast medium (r = 0.45; p < 0.0006) (Fig. 1). In group A patients, however, no relationship was found between contrast volume administered and change in SCr levels (r = 0.034; p = 0.80).
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Figure 1 Volumes of Contrast Medium (ml) Correlated With Maximum Change in SCr 72 h After PCI
The solid lines represent the point estimated, and the upper and lower lines represent 2 SD. PCI = percutaneous coronary intervention; SCr = serum creatinine.
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CIN incidence and clinical outcomes.
In a total of 13 patients CIN developed: 12 in group B (21.8%) and 1 (1.8%) in group A (difference 20%, 95% confidence interval [CI] 8% to 31%, p = 0.0009) with an odds ratio (OR) of 0.065 (95% CI 0.008 to 0.521, p = 0.01) for patients in group A. The absolute risk reduction of CIN in group A compared with group B was 20%, resulting in a number required to treat of 5 patients to prevent 1 case of CIN. In the multivariate analysis adjusted for age, baseline SCr, left ventricular function, and volume of contrast medium, the OR in patients allocated to group A was 0.002 (95% CI 0.0004 to 0.102, p = 0.002). The incidences of CIN using different criteria are shown in Figure 2.
The difference found in CIN rates between groups was not related to depressed left ventricular function nor on baseline reduced renal function. No significant interactions were found between protocol and left ventricular function (p = 0.17) or GFR (p = 0.29).
The GFR measured at baseline was comparable in the 2 groups (74 ± 20 ml/min in the control group vs. 75 ± 21 ml/min in the treatment group, p = 0.82). As shown in Figure 3, in group B there was a significant deterioration of GFR that reached a trough at day 3 after the procedure, and there was a significant improvement in GFR in group A, evident from the first day (p < 0.009 for the trend).
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Figure 3 Evolution of GFR at Baseline (Before PCI) and Days 1, 2, 3, and 7
Data are mean ± 2 SD. GFR = glomerular filtration rate, estimated using the Levey formula (16); PCI = percutaneous coronary intervention.
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There was a significant difference between groups in the rate of acute anuric renal failure, 7 patients (12.7%) and 1 patient (1.8 %) in groups B and A, respectively (p = 0.032, 95% CI 0.2 to 0.13). Four patients required renal replacement therapy, 3 in group B and 1 in group A. Acute renal failure developed in this latter patient more than 72 h after admission, and therefore did not meet criteria for CIN (Table 3).
Acute heart failure during the catheterization developed in 2 patients in group B and 1 in group A (3.6% vs. 1.8%, p = 0.62). The CIN developed during the monitoring in these 3 patients.
In our study, the global mortality was 4.5%, but we did not find a significant difference in global mortality during the 7 days of monitoring between groups, 1 patient in group A (died of cardiogenic shock) and 4 patients in group B (2 patients died of cardiogenic shock and 2 patients died of multiorgan failure) (Table 3).
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Discussion
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The results of our study suggest that in patients undergoing emergency PCI, rapid hydration with saline sodium bicarbonate and high doses of N-AC just before contrast injection reduce renal dysfunction and the rate of CIN as a result of reduced oxidative stress.
The overall incidence of acute pulmonary edema (2.7%) was similar to that reported in previous studies (7,10,13). It is worth noting that the incidence of acute pulmonary edema did not differ between groups.
We used SCr for assessment of renal function. However, it is conceivable that cystatin C levels, a marker of GFR that is not affected by tubular transport, could have been a better indicator of kidney function (20).
Several studies have shown that CIN after an interventional procedure is a frequent complication associated with poor outcome (1,2,21). A standardized saline hydration strategy has been shown to be effective in decreasing the risk of CIN (17,22). Most studies have evaluated intravenous hydration regimens with saline at a rate of 1 ml/kg/h, 6 to 12 h before and after contrast exposure in patients undergoing elective procedures (11,23,24). Actually, international guidelines such as those of the European Society of Urogenital Radiology recommend the routine use of a hydration protocol before contrast exposition (18). Given the fact that an acidic environment promotes free radical formation, hydration with bicarbonate theoretically should be more effective, as proven by Merten et al. (7).
In patients at high risk of developing CIN, the addition of high-dose N-AC (1,200 mg twice both on the day before and the day after the procedure) could play an important role in CIN prevention (11,25,26). In this setting, Ochoa et al. (27) assessed that administration of high doses of N-AC with a shortened hydration protocol results in a notably lower incidence of CIN.
Critical patients, especially those with an ACS undergoing primary PCI or urgent procedures, constitute a group at high risk of developing CIN (28,29). This also holds true for patients with normal renal function, in whom higher morbidity and mortality rates are found (13). In our study, the incidence of CIN was significantly higher in patients in group B, allocated to standard hydration after PCI, as compared with group A, in which patients received high doses of N-AC plus an infusion of sodium bicarbonate just before contrast injection. This fact was related to a higher, although not significant, incidence of acute renal failure requiring renal replacement therapy and mortality, and both were similar to previously reported data (12,30–32).
Several conditions contribute to renal damage: hemodynamic instability and hypotension with reduced cardiac output, metabolic acidosis secondary to myocardial infarction (33), the use of large volumes of contrast media, and difficulties in establishing a prophylactic therapy in the acute setting. In patients undergoing emergency PCI, hypotension and reduced cardiac output, as well certain degree of dehydration secondary to vomiting and diaphoresis, could contribute to prerenal azotemia. We found a relatively high BUN level at baseline in both groups, with levels toward the upper limit of normal, but with normal SCr levels. This prerenal azotemia seems to play an important role in the activation of tubuloglomerular feedback and the renin-angiotensin system. The rapid bicarbonate infusion, with the subsequent volume expansion, could stimulate diuresis, diluting circulating contrast medium and vasoconstriction mediator concentrations and preventing activation of tubuloglomerular feedback (34).
The generation of reactive oxygen species formed as a result of postischemic oxidative stress, a pH-dependent reaction, is known to play a pathogenic role in CIN. In patients undergoing emergency PCI, this oxidative stress could be increased because of metabolic acidosis secondary to myocardial ischemia (6).
Recently Marenzi et al. (12) have shown a dose-dependent effect of N-AC for the prevention of CIN in patients undergoing primary angioplasty. In this study, patients allocated to receive high doses of N-AC (1,200-mg intravenous bolus of N-AC just before contrast medium injection plus 1,200 mg orally twice daily for the 48 h after PCI) showed a CIN rate of 8% in contrast to 33% of the patients in the control group (p < 0.001). As CIN criteria, they used a SCr increase of 25% or more from baseline.
For the same CIN criteria, our study shows a similar incidence of CIN in group B, but with an interesting reduction of CIN in group A. We are aware that our relatively small sample size calls for caution in the interpretation of the results, and that our findings need to be confirmed in large multicenter studies.
Our study suggests that a rapid hydration with saline sodium bicarbonate provides a cumulative effect over reactive oxygen species scavenging properties of N-AC, reducing the formation of these reactive oxygen species.
Study limitations.
The relative limitations of our study are those inherent in a single-blind, single-center study with a small sample size. Thus, these findings should be confirmed in a larger multicenter trial.
Conclusions.
In conclusion, this study shows that a systematic protocol of a rapid intravenous hydration with sodium bicarbonate plus high doses of N-AC is an effective and safe approach in preventing CIN in patients undergoing urgent PCI.
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Acknowledgments
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The authors acknowledge assistance of the staff of the catheterization and coronary care unit, and Maria Dolores Mellado and Mireia Bastante for their contributions.
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References
|
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1. 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]2. Iakovou I, Dangas G, Mehran R, et al. Impact of gender on the incidence and outcome of contrast-induced nephropathy after percutaneous coronary intervention J Invasive Cardiol 2003;15:18-22.[Medline] 3. Sanaei-Ardekani M, Movahed MR, Movafagh S, Ghahramani N. Contrast-induced nephropathy: a review Cardiovasc Revasc Med 2005;6:82-88.[CrossRef][Medline] 4. Briguori C, Tavano D, Colombo A. Contrast agent–associated nephrotoxicity Prog Cardiovasc Dis 2003;45:493-503.[CrossRef][Web of Science][Medline] 5. Goldenberg I, Matetzky S. Nephropathy induced by contrast media: pathogenesis, risk factors and preventive strategies Can Med Assoc J 2005;172:1461-1471.[Abstract/Free Full Text] 6. Detrenis S, Meschi M, Musini S, Savazzi G. Lights and shadows on the pathogenesis of contrast-induced nephropathy: state of the art Nephrol Dial Transplant 2005;20:1542-1550.[Free Full Text] 7. Merten GJ, Burgess WP, Gray LV, et al. Prevention of contrast-induced nephropathy with sodium bicarbonate: a randomized controlled trial JAMA 2004;291:2328-2334.[Abstract/Free Full Text] 8. Fishbane S, Durham JH, Marzo K, Rudnick M. N-acetylcysteine in the prevention of radiocontrast-induced nephropathy J Am Soc Nephrol 2004;15:251-260.[Abstract/Free Full Text] 9. Tepel M, van der Giet M, Schwarzfeld C, Laufer U, Liermann D, Zidek W. Prevention of radiographic-contrast-agent-induced reductions in renal function by acetylcysteine N Engl J Med 2000;343:180-184.[Abstract/Free Full Text] 10. Baker CS, Wragg A, Kumar S, De Palma R, Baker LR, Knight CJ. A rapid protocol for the prevention of contrast-induced renal dysfunction: the RAPPID study J Am Coll Cardiol 2003;41:2114-2118.[Abstract/Free Full Text] 11. Briguori C, Colombo A, Violante A, et al. Standard vs. double dose of N-acetylcysteine to prevent contrast agent associated nephrotoxicity Eur Heart J 2004;25:206-211.[Abstract/Free Full Text] 12. Marenzi G, Assanelli E, Marana I, et al. N-acetylcysteine and contrast-induced nephropathy in primary angioplasty N Engl J Med 2006;354:2773-2782.[Abstract/Free Full Text] 13. 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] 14. Bertrand ME, Simoons ML, Fox KA, et al. Management of acute coronary syndromes in patients presenting without persistent ST-segment elevation Eur Heart J 2002;23:1809-1840.[Free Full Text] 15. Hochman JS, Sleeper LA, Webb JG, et al. SHOCK Investigators Early revascularization in acute myocardial infarction complicated by cardiogenic shockShould We Emergently Revascularize Occluded Coronaries for Cardiogenic Shock. N Engl J Med 1999;341:625-634.[Abstract/Free Full Text] 16. Levey AS, Bosch JP, Lewis JB, Greene T, Rogers N, Roth D, Modification of Diet in Renal Disease Study Group A more accurate method to estimate glomerular filtration rate from serum creatinine: a new prediction equation Ann Intern Med 1999;130:461-470.[Abstract/Free Full Text] 17. Itoh Y, Yano T, Sendo T, Oishi R. Clinical and experimental evidence for prevention of acute renal failure induced by radiographic contrast media J Pharmacol Sci 2005;97:473-488.[CrossRef][Web of Science][Medline] 18. Morcos SK, Thomsen HS. European Society of Urogenital Radiology guidelines on administering contrast media Abdom Imaging 2003;28:187-190.[CrossRef][Web of Science][Medline] 19. Maeder M, Klein M, Fehr T, Rickli H. Contrast nephropathy: review focusing on prevention J Am Coll Cardiol 2004;44:1763-1771.[Abstract/Free Full Text] 20. Hoffmann U, Fischereder M, Kruger B, Drobnik W, Kramer BK. The value of N-acetylcysteine in the prevention of radiocontrast agent-induced nephropathy seems questionable J Am Soc Nephrol 2004;15:407-410.[Abstract/Free Full Text] 21. Bagshaw SM, Culleton BF. Contrast-induced nephropathy: epidemiology and prevention Minerva Cardioangiol 2006;54:109-129.[Medline] 22. Gami AS, Garovic VD. Contrast nephropathy after coronary angiography Mayo Clin Proc 2004;79:211-219.[Abstract/Free Full Text] 23. Goldenberg I, Shechter M, Matetzky S, et al. Oral acetylcysteine as an adjunct to saline hydration for the prevention of contrast-induced nephropathy following coronary angiographyA randomized controlled trial and review of the current literature. Eur Heart J 2004;25:212-218.[Abstract/Free Full Text] 24. Shyu KG, Cheng JJ, Kuan P. Acetylcysteine protects against acute renal damage in patients with abnormal renal function undergoing a coronary procedure J Am Coll Cardiol 2002;40:1383-1388.[Abstract/Free Full Text] 25. Billinger M, Hess OM, Meier B. Prevention of contrast-induced renal dysfunction by N-acetylcysteineTruth or myth?. Eur Heart J 2004;25:188-189.[Free Full Text] 26. Maeder M, Klein M, Fehr T, Rickli H. Contrast nephropathy: review focusing on prevention J Am Coll Cardiol 2004;44:1763-1771.[Abstract/Free Full Text] 27. Ochoa A, Pellizzon G, Addala S, et al. Abbreviated dosing of N-acetylcysteine prevents contrast-induced nephropathy after elective and urgent coronary angiography and intervention J Interv Cardiol 2004;17:159-165.[CrossRef][Medline] 28. Polena S, Yang S, Alam R, et al. Nephropathy in critically ill patients without preexisting renal disease Proc West Pharmacol Soc 2005;48:134-135.[Medline] 29. van den Berk G, Tonino S, de Fijter C, Smit W, Schultz MJ. Bench-to-bedside review: preventive measures for contrast-induced nephropathy in critically ill patients Crit Care 2005;9:361-370.[CrossRef][Web of Science][Medline] 30. Zahn R, Vogt A, Zeymer U, et al. In-hospital time to treatment of patients with acute ST elevation myocardial infarction treated with primary angioplasty: determinants and outcomeResults from the registry of percutaneous coronary interventions in acute myocardial infarction of the Arbeitsgemeinschaft Leitender Kardiologischer Krankenhausarzte. Heart 2005;91:1041-1046.[Abstract/Free Full Text] 31. Carrabba N, Santoro GM, Balzi D, et al. In-hospital management and outcome in women with acute myocardial infarction (data from the AMI-Florence Registry) Am J Cardiol 2004;94:1118-1123.[CrossRef][Web of Science][Medline] 32. Cannon CP, Gibson CM, Lambrew CT, et al. Relationship of symptom-onset-to-balloon time and door-to-balloon time with mortality in patients undergoing angioplasty for acute myocardial infarction JAMA 2000;283:2941-2947.[Abstract/Free Full Text] 33. Makino J, Uchino S, Morimatsu H, Bellomo R. A quantitative analysis of the acidosis of cardiac arrest: a prospective observational study Crit Care 2005;9:R357-R362.[CrossRef][Web of Science][Medline] 34. Rudnick MR, Kesselheim A, Goldfarb S. Contrast-induced nephropathy: how it develops, how to prevent it Cleve Clin J Med 2006;73:75-77.[Abstract/Free Full Text]
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January 28, 2009;
301(4):
378 - 379.
[Full Text]
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C. A. Herzog
Kidney disease in cardiology
Nephrol. Dial. Transplant.,
January 1, 2009;
24(1):
34 - 37.
[Full Text]
[PDF]
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N. Lameire, W. Van Biesen, E. Hoste, and R. Vanholder
The prevention of acute kidney injury: an in-depth narrative review Part 1: volume resuscitation and avoidance of drug- and nephrotoxin-induced AKI
NDT Plus,
December 1, 2008;
1(6):
392 - 402.
[Abstract]
[Full Text]
[PDF]
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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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M. Maioli, A. Toso, M. Leoncini, M. Gallopin, D. Tedeschi, C. Micheletti, and F. Bellandi
Sodium Bicarbonate Versus Saline for the Prevention of Contrast-Induced Nephropathy in Patients With Renal Dysfunction Undergoing Coronary Angiography or Intervention
J. Am. Coll. Cardiol.,
August 19, 2008;
52(8):
599 - 604.
[Abstract]
[Full Text]
[PDF]
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D. A. Baumgarten and J. H. Ellis
Contrast-Induced Nephropathy: Contrast Material Not Required?
Am. J. Roentgenol.,
August 1, 2008;
191(2):
383 - 386.
[Abstract]
[Full Text]
[PDF]
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S. D. Weisbord, M. K. Mor, A. L. Resnick, K. C. Hartwig, A. F. Sonel, M. J. Fine, and P. M. Palevsky
Prevention, Incidence, and Outcomes of Contrast-Induced Acute Kidney Injury
Arch Intern Med,
June 23, 2008;
168(12):
1325 - 1332.
[Abstract]
[Full Text]
[PDF]
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S. R. Dixon, C. L. Grines, and W. W. O'Neill
The year in interventional cardiology.
J. Am. Coll. Cardiol.,
June 17, 2008;
51(24):
2355 - 2369.
[Full Text]
[PDF]
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A. N. DeMaria, J. J. Bax, O. Ben-Yehuda, P. Clopton, G. K. Feld, G. S. Ginsburg, B. H. Greenberg, J. D. Knoke, W. Y.W. Lew, J. A.C. Lima, et al.
Highlights of the year in JACC 2007.
J. Am. Coll. Cardiol.,
January 29, 2008;
51(4):
490 - 512.
[Full Text]
[PDF]
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A. X. Garg, T. Greene, and N. W. Levin
A well-conducted randomized trial that establishes no benefit of therapy is an important medical advance
Nephrol. Dial. Transplant.,
January 1, 2008;
23(1):
52 - 55.
[Full Text]
[PDF]
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A. M. From, B. J. Bartholmai, A. W. Williams, S. S. Cha, A. Pflueger, and F. S. McDonald
Sodium Bicarbonate is Associated with an Increased Incidence of Contrast Nephropathy: A Retrospective Cohort Study of 7977 Patients at Mayo Clinic
Clin. J. Am. Soc. Nephrol.,
January 1, 2008;
3(1):
10 - 18.
[Abstract]
[Full Text]
[PDF]
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S. D. Weisbord and P. M. Palevsky
Prevention of Contrast-Induced Nephropathy with Volume Expansion
Clin. J. Am. Soc. Nephrol.,
January 1, 2008;
3(1):
273 - 280.
[Abstract]
[Full Text]
[PDF]
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