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| Year : 2012 | Volume
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| Issue : 2 | Page : 280-285 |
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| A randomized trial of saline hydration to prevent contrast-induced nephropathy in patients on regular captopril or furosemide therapy undergoing percutaneous coronary intervention |
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Hassan Shemirani, Masood Pourrmoghaddas
Department of Cardiology, Faculty of Medicine, Isfahan University of Medical Sciences, Isfahan, Iran
Click here for correspondence address and email
| Date of Web Publication | 28-Feb-2012 |
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 Abstract | | |
Contrast-induced nephropathy (CIN) is characterized by acute deterioration of renal function that occurs after parenteral administration of contrast media in the absence of other causes. Although no definite proof has been obtained yet, the risk of diuretics or angiotensin-converting enzyme inhibitors (ACEI) to exacerbate CIN has been reported because of their effects on renal perfusion. This study was conducted to assess the protective effect of hydration alone in the prevention of CIN after percutaneous coronary intervention (PCI) in patients on diuretics or ACEI. This randomized clinical trial was conducted at the Chamran Hospital, Isfahan University of Medical Sciences, Iran, during the years 2006-2007. The study patients were divided into four groups, each group containing 60 patients. Patients in groups A and B were on regular treatment with ACEI (captopril) and patients in groups C and D were on regular diuretic (furosemide) therapy. About 36 h before PCI, captopril in group A and furosemide in group C were discontinued. The serum creatinine (Cr) levels were measured at the time of performing PCI and 24 h and 48 h after PCI in all patients. All patients received 1 mL/kg/h normal saline (0.9%) 12 h before and 24 h after PCI. The occurrence of CIN after PCI was diagnosed based on the following formula: Cr level after PCI - Cr level before PCI. If this value was greater than 0.5 mg/dL, it was coded as one and if the value was less than 0.5 mg/dL, it was coded as zero. The mean difference was analyzed and compared among the four groups by the ANOVA test. Three patients (5%) in group A, two patients (3.3%) in group B, two patients (3.3%) in group C and one patient (1.6%) in group D had a >0.5 mg/dL difference in serum Cr. The difference seen between these groups was not statistically significant (P > 0.05). This study shows that although furosemide and captopril can exacerbate CIN by impairment of renal perfusion, this can be prevented by hydration and discontinuation of furosemide and captopril may not be required.
How to cite this article:
Shemirani H, Pourrmoghaddas M. A randomized trial of saline hydration to prevent contrast-induced nephropathy in patients on regular captopril or furosemide therapy undergoing percutaneous coronary intervention. Saudi J Kidney Dis Transpl 2012;23:280-5 |
How to cite this URL:
Shemirani H, Pourrmoghaddas M. A randomized trial of saline hydration to prevent contrast-induced nephropathy in patients on regular captopril or furosemide therapy undergoing percutaneous coronary intervention. Saudi J Kidney Dis Transpl [serial online] 2012 [cited 2021 Feb 25];23:280-5. Available from: https://www.sjkdt.org/text.asp?2012/23/2/280/93153 |
| Introduction | |  |
Although drug treatment is the mainstay of therapy for patients with angina, [1] treating this entity by revascularizing the coronary arteries with percutaneous endovascular techniques is now at least five-times more common than it was 20 years ago. [2] In 2001, approximately one million patients underwent percutaneous coronary intervention (PCI) in the United States alone. [2]
Despite its known benefits, PCI has side-effects that may be related to time taken to perform PCI. They include vomiting, stroke, arrhythmia, hypotension, need for emergency surgery and contrast-induced nephropathy (CIN). [3],[4] Because angiographic procedures involving contrast media are scheduled beforehand, the best treatment for CIN is prevention. [5] Preventive measures include avoidance of volume depletion, administration of anti-oxidant agents such as N-acetylcysteine, [6] use of lower doses of contrast, avoidance of repetitive procedures and use of low or iso-osmolar contrast media. [7]
CIN has gained increased attention in clinical practice, particularly during cardiac intervention, and also in many other radiological procedures in which iodinated contrast media are used. There is, at present, good clinical evidence from well-controlled randomized studies that CIN is a common cause of acute renal dysfunction. [8],[9] CIN is the acute deterioration of renal function seen after parenteral administration of radiocontrast media in the absence of other causes. CIN is generally defined as an increase in serum creatinine concentration of at least 0.5 mg/dL (44 mol/L) or 25% above the baseline within 48 h after contrast administration. [10],[11],[12],[13],[14] Contrast agents also have direct toxic effects on renal tubular cells, causing vacuolization, altered mitochondrial function and apoptosis. [15]
Atopy does not play a role in the pathogenesis of CIN. The incidence of CIN in the general population has been calculated to be 2%. In high-risk patients, i.e. patients with chronic renal impairment, diabetes mellitus, congestive heart failure and older age, the incidence has been calculated to be 20-30%. [10],[11],[12],[13],[14] CIN has been associated with increased morbidity, extended length of hospital stay and increased costs. [16] Several risk factors have been described for CIN. [17],[18],[19]
A risk score for prediction of CIN after PCI has been reported by Mehran et al. [19] It should be emphasized that higher contrast volume is an important risk factor for CIN. [17],[18],[19] Patients who are hospitalized for PCI have some predisposing factors for CIN. These factors include fasting, vomiting during contrast media injection and diuresis after the procedure. Drugs such as angiotensin-converting enzyme inhibitors (ACEI) and diuretics by their effects on renal perfusion exacerbate CIN. Although no definite proof has been obtained yet, the risk of diuretics or ACEI to exacerbate CIN has been reported because of their effects on renal perfusion. [20],[21] It is thus clear that CIN is a potentially harmful condition. The reason that the problem of CIN seems to be increasing is because the number of angiographies and PCI examinations in clinical practice is increasing and, today, higher doses of contrast are administered to sicker and older patients. [10],[11],[12],[13],[14],[22] Therefore, this study was conducted to assess the protective effect of hydration alone in the prevention of adverse effects of diuretics or ACEI in CIN after PCI.
| Materials and Methods | | |
This single-center, randomized controlled clinical trial was conducted at the Chamran Hospital, Isfahan University of Medical Sciences, Iran during the years 2006-2007. Patients were among those referred for PCI and were on captopril or furosemide. Exclusion criteria included patients with serum Cr >1.5 mg/dL or glomerular filtration rate <60 mL/min, consumption of both captopril and furosemide, PCI during acute myocardial infarction, heart failure of class III-IV New York Heart Association (NYHA), previous exposure to contrast media in the 14 days before randomization and need for emergency coronary artery bypass graft (CABG) during PCI. Age and sex were not considered as exclusion criteria.
All patients gave written informed consent. Eligible patients were divided into four groups, and each group contained 60 patients. Patients in groups A and B were on regular use of captopril and patients in groups C and D were on daily furosemide. They were on these drugs before the study.
For washout effect of the drugs, about 36 h before PCI, captopril in group A and furosemide in group C were discontinued. The serum Cr levels were recorded at the time of PCI and 24 h and 48 h after the PCI.
After appropriate nursing evaluation and initial measurement of blood pressure and weight, all patients received normal saline (0/9%) in a dose of 1 mL/kg/h 12 h before and 24 h after PCI. The type of contrast media used was meglumine from Darou Pakhch Company. According to the definition of CIN, the formula used for diagnosis was: Actual Cr = Cr level after PCI ─ Cr level before PCI
If the difference was greater than 0.5 mg/dL, it was taken as code one and if the difference was less than 0.5 mg/dL, it was taken as code zero. Post-contrast Cr was assessed on the mornings of days one and two and the highest value on these days was used to calculate the change in serum Cr that was the primary end-point.
The SAS package was used for statistical analysis. Data were analyzed by using the ANOVA procedure for continuous variables. Differences were considered statistically significant at a P-level of 0.05.
| Results | | |
A total of 256 patients were enrolled but, during and after PCI, 16 patients were excluded because they needed emergency CABG or were on combined drugs or had incomplete laboratory data. Thus, 240 patients completed the study and were included in the final analysis.
Their mean age was 60 ± 14 years (40-75 years), and they included 116 males (48.3%). The baseline characteristics of the study patients in the four groups are depicted in [Table 1].
In group A patients in whom captopril was discontinued, the mean change of serum Cr was 0.22 ± 0.07 mg/dL and in group B in whom captopril was continued, it was 0.13 ± 0.06 mg/dL (P = 0.7). In group C patients in whom furosemide was discontinued, the mean change of serum Cr was 0.17 ± 0.08 mg/dL and in group D in whom furosemide was continued, it was 0.14 ± 0.05 mg/dL (P = 0.2). The mean difference was analyzed among the four groups by the ANOVA test.
Three patients (5%) in group A, two patients (3.3%) in group B, two patients (3.3%) in group C and one patient (1.6%) in group D had a >0.5 mg/dL difference in serum Cr; no meaningful difference was seen among these groups (P > 0.05) [Figure 1]. | Figure 1: Mean serum creatinine before and after percutaneous coronary intervention in the four study groups (P > 0.05).
Groups A and B: Consumption of captopril
Groups C and D: Consumption of furosemide
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| Discussion | | |
Previous studies have recommended that for prevention of CIN, use of drugs such as N-acetylcysteine and theophyline could be effective. [6],[11] The major finding of this study is that despite consumption of furosemide and captopril, which by their effects on renal perfusion can exacerbate CIN, hydration of patients alone before and after PCI without use of other drugs has a protective effect in the prevention of CIN.
Early studies evaluating the renal effects of radiocontrast administration in dogs demonstrated a reduction in renal perfusion lasting up to 20 h after radiocontrast administration. [23] It seems plausible that adequate hydration may counteract some of the putative hemodynamic effects that may lead to CIN. We identified several studies that evaluated the effects of various hydration protocols and use of diuretics in the incidence of CIN. Four studies [24],[25],[26],[27] compared forced diuresis (furosemide and/or mannitol) with hydration, of which three showed a significant increase in the rate of CIN in the groups receiving diuretics. Two studies [28],[29] evaluated bolus intravenous infusions of 0.9% saline (250-300 mL) immediately before or during cardiac catheterization versus slow intravenous hydration 12 h prior to the procedure. Neither found a significant difference between treatment groups; however, both studies had small sample sizes (n = 39 and n = 37, respectively) and the event rates were low. Two additional studies [30],[31] compared oral hydration with prolonged intravenous hydration (12 h before and after), and found contradictory results. Taylor et al [31] (n = 36) found no difference between treatment groups; however, the oral hydration group in this study received 6 h of intravenous hydration in addition to oral intake. Trivedi et al [30] (n = 53) found that oral hydration alone appeared to be inferior to intravenous hydration in the prevention of CIN (34.6% vs 3.7%; P = 0.005) in patients with normal renal function undergoing cardiac catheterization. Interestingly, the incidence of CIN in the oral hydration group was much higher than expected in this patient population.
In addition to timing and route of hydration, other factors, such as fluid tonicity and fluid composition, may also play a role. Single studies supporting the use of isotonic versus half isotonic saline [32] suggest that isotonic fluids may be superior to hypotonic fluids, probably because of their enhanced ability to expand intravascular volume. Therefore, our patients received intravenous normal saline continuously.
Our study shows that although furosemide and captopril by impairment of renal perfusion can exacerbate CIN, diuretics and ACEI do not cause CIN in all patients. CIN might occur in susceptible patients, but this condition can be prevented by adequate hydration, and discontinuation of furosemide and captopril is not required. Although there are some recommendations that for prevention of CIN consumption of N-acetylcysteine is needed, good hydration alone is enough. [11],[30]
| References | | |
| 1. | Dzavik V. New Frontiers and unresolved controversies in percutaneous coronary intervention. Am J Cardiol 2003;91:27A-33A. 
[PUBMED] |
| 2. | American Heart Association. Heart Disease and stroke statistics: 2004 update. www.American heart. Ony (12 August 2004)
|
| 3. | Sidney C. Smith JR, James T, et al. ACC/AHA guidelines for Percutaneous coronary intervention (Revision of the 1993 PTCA guidelines)-Executive summary : A report of the American college of cardiology / American Heart Association Task Force on practice guidelines (committee to Revise the 1993 guidelines for Percutaneous Transluminal coronary angioplasty) Endorsed by the Society for Cardiac Angioplasty and Interventions. Circulation 2001;103:3019-41.
|
| 4. | Brinker JA, Davidson CJ, laskey W. Preventing in-hospital cardiac and renal complication in high- risk PCI patients. European Heart J Suppl 2005;7:G13-24 .
|
| 5. | Asif A, Epstein M. Prevention of radiocontrast-induced nephropathy. Am J Kidney Dis 2004; 44:12-24.
[PUBMED] [FULLTEXT] |
| 6. | Pannu N, Manns B, Lee H, Tonelli M. Systematic review of the impact of N-acetylcysteine on contrast nephropathy. Kidney Int 2004;65: 1366-74
|
| 7. | Aspelin P, Aubry P, Fransson SG, et al. Nephrotoxic effects in high-risk patients undergoing angiography. N Engl J Med 2003; 348:491-9.
[PUBMED] [FULLTEXT] |
| 8. | Lameire N, Van Biesen W, Vanholder R. Acute renal failure. Lancet 2005;365:417- 30.
[PUBMED] [FULLTEXT] |
| 9. | Singri N, Ahya SN, Levin ML. Acute renal failure. JAMA 2003;289:747-51.
[PUBMED] [FULLTEXT] |
| 10. | Murphy SW, Barrett BJ, Parfrey PS. Contrast nephropathy. J Am Soc Nephrol 2000;11:177- 82.
[PUBMED] [FULLTEXT] |
| 11. | Fishbane S, Durham JH, Marzo K, Rudnick M. N-Acetylcysteine in the prevention of radio-contrast-induced nephropathy. J Am Soc Nephrol 2004;15:251-60.
[PUBMED] [FULLTEXT] |
| 12. | Gleeson TG, Bulugahapitiya S. Contrast-induced nephropathy. AJR Am J Roentgenol 2004;183:1673-89.
[PUBMED] [FULLTEXT] |
| 13. | Maeder M, Klein M, Fehr T, Rickli H. Contrast nephropathy: review focusing on prevention. J Am Coll Cardiol 2004;44:1763-71.
[PUBMED] [FULLTEXT] |
| 14. | Goldenberg I, Matetzky S. Nephropathy induced by contrast media: pathogenesis, risk factors and preventive strategies. CMAJ 2005; 172:1461-71.
[PUBMED] [FULLTEXT] |
| 15. | Persson PB, Hansell P, Liss P. Pathophysiology of contrast medium induced nephropathy. Kidney Int 2005;68:14-22.
[PUBMED] [FULLTEXT] |
| 16. | McCullough PA, Wolyn R, Rocher LL, Levin RN, O'Neill WW. Acute renal failure after coronary intervention: incidence, risk factors, and relationship to mortality. Am J Med 1997;103:368-75.
[PUBMED] [FULLTEXT] |
| 17. | Rihal CS, Textor SC, Grill DE, et al. Incidence and prognostic importance of acute renal failure after percutaneous coronary intervention. Circulation 2002;105:2259-64.
[PUBMED] [FULLTEXT] |
| 18. | Cochran ST, Wong WS, Roe DJ. Predicting angiography-induced acute renal function impairment: clinical risk model. AJR Am J Roentgenol 1983;141:1027-33.
[PUBMED] [FULLTEXT] |
| 19. | Mehran R, Aymong ED, Nikolsky E, et al. A simple risk score for prediction of contrast-induced nephropathy after percutaneous coronary intervention: development and initial validation. J Am Coll Cardiol 2004;44:1393-9.
[PUBMED] [FULLTEXT] |
| 20. | Gambaro G, Perazella MA. Adverse renal effects of anti-inflammatory agents: evaluation of selective and nonselective cyclooxygenase inhibitors. J Intern Med 2003;253:643-52.
[PUBMED] [FULLTEXT] |
| 21. | Toprak O, Cirit M, Bayata S, Yesil M, Aslan SL. The effect of preprocedural captopril on contrast-induced nephropathy in patients who underwent coronary angiography. Anadolu Kardiyol Derg 2003;3:98-103.
|
| 22. | Toms AP, Cash CJ, Linton SJ, Dixon AK. Requests for body computed tomography: increasing workload, increasing indications and increasing age. Eur Radiol 2001;11:2633- 7.
[PUBMED] [FULLTEXT] |
| 23. | Katzberg RW, Morris TW, Schulman G, et al. Reactions to intravenous contrast media, part II: acute renal response in euvolemic and dehydrated dogs. Radiology 1983;147:331-4.
[PUBMED] [FULLTEXT] |
| 24. | Solomon R, Werner C, Mann D, D'Elia J, Silva P. Effects of saline, mannitol, and furosemide to prevent acute decreases in renal function induced by radiocontrast agents. N Engl J Med 1994;331:1416-20
|
| 25. | Stevens MA, McCullough PA, Tobin KJ, et al. A prospective randomized trial of prevention measures in patients at high risk for contrast nephropathy: results of the P.R.I.N.C.E. Study. J Am Coll Cardiol 1999;33:403-11.
|
| 26. | Weinstein JM, Heyman S, Brezis M. Potential deleterious effect of furosemide in radiocontrast nephropathy. Nephron. 1992;62:413-5.
[PUBMED] |
| 27. | Weisberg LS, Kurnik PB, Kurnik BR. Risk of radiocontrast nephropathy in patients with and without diabetes mellitus. Kidney Int 1994;45: 259-65.
[PUBMED] |
| 28. | Bader BD, Berger ED, Heede MB. What is the best hydration regimen to prevent contrast media induced nephrotoxicity? Clin Nephrol 2004;62:1-7.
|
| 29. | Krasuski RA, Beard BM, Geoghagan JD, Thompson CM, Guidera SA. Optimal timing of hydration to erase contrast-associated nephropathy: the OTHER CAN study. J Invasive Cardiol 2003;15:699-702.
[PUBMED] |
| 30. | Trivedi HS, Moore H, Nasr S, et al. A randomized prospective trial to assess the role of saline hydration on the development of contrast nephrotoxicity. Nephron Clin Pract 2003; 93:C29-34.
[PUBMED] |
| 31. | Taylor AJ, Hotchkiss D, Morse RW, McCabe J. PREPARED: Preparation for Angiography in Renal Dysfunction: a randomized trial of inpatient vs outpatient hydration protocols for cardiac catheterization in mild-to-moderate renal dysfunction. Chest 1998;114:1570-4.
[PUBMED] [FULLTEXT] |
| 32. | Mueller C, Buerkle G, Buettner HJ, et al. Prevention of contrast media-associated nephrpathy: randomized comparison of 2 hydration regimens in 1620 patients undergoing coronary angioplasty. Arch Intern Med 2002;162:329-36.
[PUBMED] [FULLTEXT] |
Correspondence Address:
Hassan Shemirani
Noor Hospital, Isfahan
Iran
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PMID: 22382219 
[Figure 1]
[Table 1] |
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