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Prophylactic management of contrast-induced acute kidney injury in high-risk patients.

The administration of iodinated contrast has been documented to be one of the most common iatrogenic causes of acute kidney injury (AKI). The reported worldwide incidence is estimated to be 21.6% in adults, with AKI-associated mortality rates to be 23.9% in adults, though these rates vary across different nations (Susantitaphong et al., 2013). The variance in the reported incidence occurs because contrast-induced AKI (CI-AKI) depends on the type of contrast and definition of CI-AKI used. Despite the variance, it is known that the incidence of CIAKI is greater in both high-risk patients as well as with the amount of contrast media given (Morabito et al., 2012). High-risk patients are patients who have chronic or acute conditions that may compromise their kidneys, such as chronic kidney disease (CKD), diabetes mellitus, congestive heart failure (CHF), acute hypotension or conditions that cause volume depletion, and ST-elevation myocardial infarctions. These medical conditions cause the filtration function of the kidneys to be diminished. When the body's compensatory mechanisms are not working to maintain kidney function, it increases the risk for AKI from iodinated contrast. Iodinated contrast is filtered through the kidneys, and when compensatory mechanisms are not working to maintain filtration function, the contrast dye accumulates in the filtration system of the kidneys, thereby causing CI-AKI (Solomon & Dauerman, 2010). Another contributor to CI-AKI is when large amounts of contrast media are injected into a patient's blood vessel. Large amounts of contrast media are especially used in angiograms because it requires the healthcare provider to inject several dyes to see the blood vessels to perform an efficient coronary intervention (James et al., 2013). Hence, patients who are at the highest risk for developing CI-AKI are those with compromised kidney function who need to undergo a coronary interventional procedure.

While AKI used to be seen as quick, generally reversible damage to the kidneys, studies have shown that there are short- and long-term deleterious effects that may increase patient morbidity and mortality, especially in patients at high-risk for developing AKI. Some short-term prospective studies have shown that high-risk patients carry the risk of undergoing problems related to worsening comorbidities if renal function is compromised, such as worsening heart failure (Meinel, De Cecco, Schoepf, & Katzberg, 2014). Long-term prospective studies have also found deleterious effects. One study showed that CIAKI resulted in an increased risk for dialysis, death, and permanent renal insufficiency (Meinel et al., 2014). Because of the short- and long-term effects, the high incidence of CI-AKI in high-risk patients, and no specific treatment for CI-AKI, it is crucial in identifying and adopting a standardized procedure to prevent CI-AKI.

Definition

The definition that is widely used in institutions or prior literature for any type of AKI is an increase of serum creatinine greater than or equal to 0.5 mg/dL from the baseline serum creatinine within a short time span, such as 24 to 72 hours (McDonald et al., 2013). Similarly, CI-AkI is defined as an injury to the kidneys in a narrow timeframe shortly after the administration of iodinated contrast. CI-AKI is commonly defined as a "rise in blood urea nitrogen (BUN), serum creatinine, or a decline in estimated glomerular filtration rate (eGFR) occurring in a narrow time window typically 24 to 72 hours--after administration of iodinated contrast material" (Meinel et al., 2014, p. 2). The American College of Radiology (2013) has defined CI-AKI with the Acute Kidney Injury Network (AKIN) criteria along with AKI occurring within 48 hours after the injection of the iodinated contrast material. AKIN criteria require at least one of three conditions to be met for the condition to be considered an AKI event: a) an absolute increase in serum creatinine levels by greater than or equal to 0.3 mg/dL from baseline, b) a relative increase in serum creatinine by greater than or equal to 50% from baseline, or c) a urine output decreased to less than or equal to 0.5 mL/kg/hour for at least six hours (Lakhal et al., 2011). Because many facilities do not measure urine output in non-critically ill adults, many studies often used the first two AKIN criteria. Other definitions of CI-AKI exist and are used in various studies. This demonstrates the need for a standardized definition of CI-AKI for the results of studies to be comparable.

Pathophysiology

The pathophysiology that contributes to CI-AKI is complex. When the filtration system of the kidneys is compromised, the contrast material builds up. This not only causes direct tubular toxicity and intraluminal obstruction, but also renal hypoxia and subsequent release of reactive oxygen species (ROS) (Susantitaphong & Eiam-Ong, 2014). Renal hypoxia occurs when oxygen supply does not meet oxygen demand, which results from the reduction of effective blood flow to the kidneys. To further complicate this, when the contrast dye is not readily filtered, the body increases reabsorption of it, which may increase metabolism, and therefore, result in increased oxygen consumption in the kidneys (Susantitaphong & Eiam-Ong, 2014). The process leads to further microvascular damage and renal hypoxia.

When intrarenal hypoxia occurs, the imbalance of oxygen supply and demand to the kidneys produces ROS by polymorphonuclear neutrophils at the site of the inflammation (Mittal, Siddiqui, Tran, Reddy, & Malik, 2014). Under the inflammatory pathway, ROS opens the interendothelial junctions, which allow the inflammatory cells to cross the endothelial barrier. These inflammatory cells not only clear out foreign particles, but may also cause tissue injury at the site of inflammation (Mittal et al., 2014). Therefore, many aspects of the pathophysiological process can cause CI-AKI, which suggests that more than one pharmacological agent may be helpful in preventing CI-AKI from occurring.

Pharmacological Management

The pharmacological management of CI-AKI is based on the pathophysiological principles of this condition. Though there are multiple preventative modalities currently being researched for CI-AKI, only the most promising or historical therapies will be presented in this article, including intravenous normal saline, N-acetylcysteine, and statins. An analysis of the current research on these therapies will be included to assess its safety and efficacy.

Intravenous Normal Saline

Intravenous hydration with 0.9% sodium chloride (NaCl) is the most proven method in preventing CI-AKI (Weisbord & Palevsky, 2008). There are two mechanisms in which hydration plays a role in preventing CIAKI. One mechanism involves the expansion of the intravascular space in the kidneys, which suppresses vasopressin secretion, inhibits the renin-angiotensin pathway, and increases the production of renal prostaglandins (Susantitaphong & Eiam-Ong, 2014). All cause vasodilatory effects, which blunt the vasoconstrictive effect of the contrast media on the renal medulla. The second mechanism of intravenous hydration is hypothesized to be involved in attenuating the direct toxic effect of contrast media on tubular cells. This happens by decreasing the concentration of the contrast in the tubular lumen as the increased volume decreases reabsorption of the contrast medium (Susantitaphong & EiamOng, 2014).

It is recommended to administer intravenous normal saline in patients at a rate of 1 mL/kg/hour 12 hours pre-procedure and 12 hours post-procedure (Mueller et al., 2002). In a classical study, a large number of participants (1,620) undergoing coronary angioplasty participated in a randomized controlled trial that assessed whether isotonic or hypotonic fluids would be better in preventing CIAKI (Mueller et al., 2002). Baseline characteristics, such as age, sex, diabetes mellitus, hypertension, and chronic renal insufficiency, were well-matched between the two groups. The primary endpoint was to measure CI-AKI based on an increase in serum creatinine of at least 0.5 mg/dL within 48 hours. Overall, the normal saline group had a significantly reduced occurrence of CI-AKI at 0.7% compared to 2.0% in the 0.45% NaCl group (Mueller et al., 2002). Therefore, it is apparent that normal saline is a better alternative for preventative therapy with CI-AKI development in high-risk patients than 0.45% NaCl. However, patients with severe left-ventricular dysfunction have an increased risk for fluid overload, and caution should be used with hydration therapy with 0.45% NaCl (Brar et al., 2014). This would reduce the risk of secondary problems, such as pulmonary edema.

Recently, research has focused on finding cost-effective methods for the prevention of CI-AKI. Researchers are trying to determine whether oral hydration or intravenous hydration is superior in preventing CI-AKI in high-risk patients undergoing a coronary intervention. A small study of 102 patients with diabetes who were undergoing a coronary angiography or angioplasty were either hydrated with intravenous normal saline of 1 mL/kg/h or oral mineral water of 1 mL/kg/h (Wrobel, Sinkiewicz, Gordon, & Wozniak-Wisniewska, 2010). The creatinine clearance was very similar in both groups after 72 hours of the procedure, with 65.3 +/- 23.39 mL/minute in the oral therapy and 73.5 +/- 21.94 mL/minute in the intravenous group (Wrobel et al., 2010). The intravenous group had a larger mean volume of contrast medium injected into the patients, thereby possibly affecting the serum creatinine clearance, yet it was still lower than the creatinine clearance for the oral therapy group. The difference between the two groups was minimal, and the power of the study was limited by its small sample size. Another randomized controlled trial with 225 high-risk patients undergoing coronary angiography and/or percutaneous coronary intervention compared the effectiveness of oral hydration and intravenous hydration for prevention of CI-AKI (Akyuz et al., 2014). The study found that the incidence of CI-AKl was 6.9% with the oral therapy versus 73% with the intravenous therapy, indicating that oral hydration is as effective as intravenous hydration in preventing CIAKI in high-risk patients. However, the study had several shortcomings, including a small sample size along with a statistically insignificant outcome (p = 0.89).

Other studies have been conducted that have been included in meta-analyses. One meta-analysis assessed the results of six prospective randomized controlled trials (Cheungpasitporn et al., 2014). The sample size was large, with 513 patients whose kidney function ranged from normal to CKD Stage 3. Within the intravenous fluid regimen group, 8.1% developed CIAKI. Of the oral hydration group, 9.5% developed CI-AKI. Because it was a meta-analysis, the two groups could have had heterogeneities due to differences in the study population, which could have affected the results. Despite this, there was no significant difference between the two groups, and it was concluded that oral hydration therapy does not pose more risk in patients with normal to moderately reduced kidney function, with a suggestion of possibly considering it as an outpatient treatment option when giving contrast. While oral hydration may be a more cost-effective option in an outpatient setting with low-risk patients, the safety and efficacy of oral hydration over intravenous hydration for high-risk patients in preventing CI-AKI are inconclusive and should not be used as a current therapy in acute care settings until further research shows more supporting evidence for the use of oral hydration.

N-acetylcysteine

N-acetylcysteine (NAC) is an antioxidant that has vasodilatory effects. Its mechanism is not fully understood, but it is thought to be involved in minimizing ROS and vasoconstriction after contrast injection, thereby preventing CI-AKI. In healthy patients with a normal renal function or any comorbidities that may compromise renal function, NAC has not shown to have a preventative benefit (Kshirsagar et al., 2004). Previous research by Tepel et al. (2000) was an eye-catching study because it showed a significant difference in the incidence of CI-AKI with NAC. The study had 83 patients with chronic renal insufficiency who had to undergo a computed tomography (CT) with an iodinated contrast agent. The intervention group took a 600 mg antioxidant acetylcysteine (NAC) twice daily with 0.45% NaCl before and after administration of the contrast agent, while the control group received a placebo with 0.45% NaCl. In the intervention group, 2% of the patients had an increase in the serum creatinine concentration 48 hours after administration, compared to 21% in the control group. Though there was a difference between the two groups, the study had shortcomings, including a small sample size and a non-significant p-value. However, this study fueled further research on NAC.

Current research shows a wide array of conflicting results for the use of NAC in high-risk patients to prevent CI-AKI. A study intervention involving 2,308 high-risk patients undergoing angiography received either NAC 1,200 mg orally twice a day or a placebo before and after the angiogram (Berwanger et al., 2011). The high-risk patients were included in the study if they had at least one risk factor for CIAKI, including age of greater than 70 years old, chronic renal failure, diabetes mellitus, hypotension, or heart failure. There was no significant difference between the intervention and the control groups in the development of CI-AKI within the 48 to 96 hours after angiography (Berwanger et al., 2011). This was a strong, double-blinded, randomized controlled trial with a large sample size, a very similar baseline characteristics among the two groups, and an adequate statistical power of 84%, with a strong methodological quality. One limitation of this study was that providers were able to use other interventions besides hydration to prevent CI-AKI based on their discretion. However, these interventions were minimal and well-balanced between the groups.

In another study, 487 patients with renal dysfunction undergoing cardiac catheterization were randomly assigned to intravenous NAC 500 mg immediately before the procedure or to another group that received 200 mL of normal saline (Webb et al., 2004). Though the study was terminated early because the Data Safety Monitoring Committee deemed it to be futile, it found that the primary endpoint of CI-AKI occurred at 23.3% for the NAC group and 20.7% for the placebo group, with a p-value of 0.57 indicating no statistical difference (Webb et al., 2004). This large, randomized controlled trial found that intravenous NAC is ineffective in preventing CI-AKI for high-risk patients. Though some small studies have shown the efficacy of NAC in preventing CI-AKI in high-risk patients, many others with large-scale studies have not (Berwanger et al., 2011; Webb et al., 2004). Therefore, NAC is not a recommended standardized prophylaxis treatment for high-risk patients undergoing a coronary intervention.

Statins

Statin therapy is a newly investigated topic regarding CI-AKI prevention. Statins are known to have an inhibitory effect on hydroxymethylglutaryl coenzyme A reductase, which lowers serum low-density lipoprotein cholesterol concentrations, and therefore, the risk for heart disease (Han et al., 2014). Patients undergoing angiography are normally those who have coronary artery disease and who have been placed on statin therapy already or will be placed on it after the angiography (Han et al., 2014). Some researchers are currently investigating the effect of statin therapy prior to the injection of contrast material with high-risk patients undergoing coronary interventional procedures as a prophylactic management for CI-AKI (Han et al., 2014). While the mechanism may not be fully understood, it is known that statins have a pleiotropic effect (Han et al., 2014). This effect is an anti-inflammatory, antioxidant, and antithrombotic action because it reduces high-sensitivity C-reactive protein levels and oxidative stress, which prevents direct contrast toxicity, such as nephron cell death (Han et al., 2014).

A randomized controlled trial was conducted with 504 statin-naive patients who were assigned to either 40 mg of rosuvastatin therapy followed by 20 mg/day until discharge versus no therapy until the day of discharge (Leoncini et al., 2014). CIAKI, defined in this study as an increase in serum creatinine of 0.5 or more within 72 hours after contrast administration, was the primary endpoint analyzed. CI-AKI occurred in 6.7% of the patients in the statin therapy group and 15.1% in the control group with a statistically significant difference (p = 0.003) (Leoncini et al., 2014). The study also used intravenous normal saline and oral NAC therapy as a standardized prophylactic regimen for both groups. Though a strong study, NAC and statin therapy may have had a synergistic effect in reducing CI-AKI incidence, there fore contributing to the significantly decreased incidence in the statin therapy group. Another randomized control trial was performed with 410 patients who were either assigned to the atorvastatin group (80 mg within 24 hours before contrast administration and 40 mg right before the procedure) or the control group (no intervention or had standard therapy) (Patti et al., 2011). Patients who had moderate to severe renal dysfunction were hydrated with normal saline, while the others were not. The primary endpoint assessed for CI-AKI within 72 hours post-procedure. Of the patients in the atorvastatin group, 5% developed CI-AKI versus 13.2% in the placebo group (Patti et al., 2011). In addition, secondary endpoints showed that creatinine clearance, C-reactive protein peak levels, and serum creatinine were all significantly lower in the atorvastatin group versus the control group (Patti et al., 2011). These results further lend support to the early use of high-dose statin therapy as an adjunctive pharmacological prophylaxis for CI-AKI in high-risk patients.

A meta-analysis of nine randomized-controlled trials was conducted by Singh et al. (2014). This meta-analysis assessed the role of statin pretreatment in the prevention of CIAKI. Data from 5,143 patients were analyzed, of whom approximately half received statins while the other half was in the placebo group. The risk of CI-AKI was significantly reduced in the statin therapy group versus the control group of no therapy or NAC therapy, with a risk ratio of 0.47. In patients with renal impairment or diabetes mellitus, there was no significant difference in the degree of beneficial effect of statin therapy on CI-AKI between the intervention and the control groups, but it did show a 45% to 55% risk reduction of CI-AKI with the use of statins. Additionally, the meta-analysis accounted for the co-treatment of NAC in some studies. It found that the beneficial effect of statin reducing the risk of CI-AKI was independent of NAC, with a 54% risk reduction in those who also received

NAC and 49% risk reduction in those who did not. The type of statins used was also statistically analyzed. The study found there was a benefit with both atorvastatin and rosuvastatin, but with a risk reduction of 0.38 with atorvastatin and 0.53 with rosuvastatin. Irrespective of the type of statin, pretreatment with a statin had a beneficial role in preventing CI-AKI.

The advent of statin pretreatment in preventing the development or reducing the risk of CI-AKI is promising. Further large-scale studies with the same baseline prophylaxis therapy, such as intravenous normal saline in combination with the same dose and type of statin among homogenous groups, need to be performed. These studies should then be compared to conclude the logistics of statin therapy and implement it as a standardized prophylactic management for CI-AKI.

Conclusion

CI-AKI has been receiving more attention over the last several years. While CI-AKI may be an acute episodic event, some studies have shown that an injury to the kidneys may cause devastating effects, especially in high-risk patients. Because CI-AKI may be a potentially preventable condition, it is important to understand some of the effective pharmacological methods. Hydration has always been at the forefront of pharmacological management in preventing CI-AKI. Normal saline has consistently been shown to be more effective and safer than 0.45% NaCl for all patients except for patients with severe heart failure who are at risk of fluid overload. Oral hydration is now being researched as a more cost-effective and less invasive means to reduce the incidence of CI-AKI in high-risk patients, but it has not been shown to be more efficacious in acute care settings with high-risk patients.

NAC is another well-studied prophylactic therapy. Small-scale studies that have been performed with NAC have shown its benefits to be questionable. However, more recent large scale studies have found NAC to be futile, and therefore, it should not be recommended as a standardized prophylaxis regimen until more largescale studies with strong methodological quality are done to prove NAC is beneficial. At this time, the joint American College of Cardiology/ American Heart Association (ACC/ AHA) guidelines do not recommend NAC (Anderson et al., 2013).

Statin therapy is a novel prophylaxis therapy for CI-AKI in high-risk patients and has been shown to have beneficial results when used in combination with hydration. While promising, statin therapy is still relatively new and needs to be further researched with the same type and dosage of statin to make the results of the various studies comparable. However, recommendations for and the use of statin pretreatment should be initiated in hospitals because of its safety, benefit, and cost-effective nature. In addition to pharmacological management, it is important to adopt a universal definition of CI-AKI and a baseline risk for AKI before continuing to perform research studies.

Nursing Considerations

It is important to understand that nurses play a crucial role in preventing CI-AKI as well. When a nurse cares for a patient who is to undergo a procedure involving iodinated contrast medium, certain precautions should be taken. Recognizing high-risk patients who are more prone to CIAKI is the most important assessment a nurse can make because it will direct a patient's course of treatment. Another important step in preventing or monitoring CI-AKI is to obtain the patient's baseline kidney function, including serum creatinine, creatinine clearance, estimated glomerular filtration rate, and blood urea nitrogen (BUN). Understanding the pathophysiological process of how CI-AKI can develop should inform nurses of the importance of hydrating their patients before contrast injection. At this time, some of the major methods of preventing CI-AKI are with intravenous hydration using normal saline and the conservative use of contrast dye. In addition to intravenous normal saline, other pharmacological treatments are being researched in the prevention of CI-AKI. Nurses should continue to act as advocates and keep informed of recent studies on the pharmacological prevention of CI-AKI to prevent harm to or withhold beneficial treatment from patients.

References

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American College of Radiology. (2013). Manual on contrast media, v10.2. Retrieved from http://www.acr.org/ Quality-Safety/Resources/Contrast-Manual

Anderson, J.L., Adams, C.D., Antman, E.M., Bridges, C.R., Califf, R.M., Casey, D.E., Jr., ... Yancy, C.W. (2012). 2012 ACCF/AHA focused update incorporated into the ACCF/AHA 2007 guidelines for the management of patients with unstable angina/non-ST-elevation myocardial infarction: A report of the American College of Cardiology Foundation/American Heart Association Task Force on Practice Guidelines. Journal of American College of Cardiology, 61(23), e179-e347.

Correction in Journal of American College of Cardiology, 62(11), 10401041.

Berwanger, O., Cavalcanti, A.B., Sousa, A.G., Buehler, A.M., Kodama, A.A., Carballo, M.T., ... Lima, J. (2011). Acetylcysteine for prevention of renal outcomes in patients undergoing coronary and peripheral vascular angiography: Main results from the randomized acetylcysteine for contrast-induced nephropathy trial (ACT). Circulation, 124(11), 12501259.

Brar, S.S., Aharonian, V., Mansukhani, P., Moore, N., Shen, A., Jorgensen, M., ... Kane, K. (2014). Haemodynamicguided fluid administration for the prevention of contrast-induced acute kidney injury: The POSEIDON randomized controlled trial. The Lancet, 383(9931), 1814-1823.

Cheungpasitporn, W., Thongprayoon, C., Brabec, B., Edmonds, P., O'Corragain, O. A., & Erickson, S.B. (2014). Oral hydration for prevention of contrast-induced acute kidney injury in elective radiological procedures: A systematic review and meta-analysis of randomized controlled trials. North American Journal of Medical Sciences, 6(12), 618-624.

Han, Y., Zhu, G., Han, L., Hou, F., Huang, W., Liu, H., ... Huo, Y. (2014). Short-term rosuvastatin therapy for prevention of contrast-induced acute kidney injury in patients with diabetes and chronic kidney disease. Journal of American College of Cardiology, 63(1), 62-70.

James, M.T., Samuel, S.M., Manning, M.A., Tonelli, M., Ghali, W.A., Faris, P., ... Hemmelgarn, B.R. (2013). Contrast-induced acute kidney injury and risk of adverse clinical outcomes after coronary angiography: A systematic review and meta-analysis. Circulation: Cardiovascular Interventions, 6(1), 37-43.

Kshirsagar, A.V., Poole, C., Mottl, A., Shoham, D., Franceschini, N., Tudor, G., ... Finn, W.F. (2004). N-acetylcysteine for the prevention of radiocontrast induced nephropathy: A metaanalysis of prospective controlled trials. Journal of American Society of Nephrology, 15(3), 761-769.

Lakhal, K., Ehrmann, S., Chaari, A., Laissy, J,P., Regnier, B., Wolff, M., & Pajot, O. (2011). Acute kidney injury network definition of contrast-induced nephropathy in the critically ill: Incidence and outcome. Journal of Critical Care, 26(6), 593-599.

Leoncini, M., Toso, A., Maioli, M., Tropeano, F., Villani, S., & Bellandi, F. (2014) Early high-doserosuvastatin for contrast-induced nephropathy prevention in acute coronary syndrome: Results from the PRATO-ACS study (Protective Effect of Rosuvastatin and Antiplatelet Therapy On contrast-induced acute kidney injury and myocardial damage in patients with Acute Coronary Syndrome). Journal of the American College of Cardiology, 63(1), 71-79.

McDonald, R.J., McDonald, J.S., Bida, J.P., Carter, R.E., Fleming, CJ., Misra, S., ... Kallmes, D.F. (2013). Intravenous contrast material induced nephropathy: Causal or coincident phenomenon? Radiology, 267(1), 106-118.

Meinel, F.G., De Cecco, C.N., Schoepf, UJ., & Katzberg, R. (2014). Contrast-induced acute kidney injury: Definition, epidemiology, and outcome. BioMed Research International. doi:10. 1155/2014/859328

Mittal, M., Siddiqui, M.R., Tran, K., Reddy, S.P., & Malik, A.B. (2014). Reactive oxygen species in inflammation and tissue injury. Antioxidants & Redox Signaling, 20(7), 1126-1167. doi:10.1089/ars.2012.5149

Morabito, S., Pistolesi, V., Benedetti, G., Di Roma, A., Colantonio, R., Mancone, M., ... Pierucci, A. (2012). Incidence of contrast-induced acute kidney injury associated with diagnostic or interventional coronary angiography. Journal of Nephrology, 25(6), 1098-1107. doi:10.5301/jn. 5000101

Mueller, C., Buerkle, G., Buettner, HJ., Petersen, J., Perruchoud, A.P., Eriksson, U., ... Roskamm, H. (2002). Prevention of contrast media-associated nephropathy: Randomized comparison of 2 hydration regimens in 1620 patients undergoing coronary angioplasty. Archives of Internal Medicine, 162(3), 329-336.

Patti, G., Ricottini, E., Nusca, A., Colonna, B., Pasceri, V., D'Ambrosio, A., ... Di Sciascio, G. (2011). Short-term, high-dose Atorvastatin pretreatment to prevent contrast-induced nephropathy in patients with acute coronary syndromes undergoing percutaneous coronary intervention (from the ARMYDA-CIN [Atorvastatin for Reduction of Myocardial Damage During Angioplasty--Contrast-Induced Nephropathy] trial. American Journal of Cardiology, 108(1), 1-7.

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Solomon, R., & Dauerman, H.L. (2010). Clinician update: Contrast-induced acute kidney injury. Circulation, 122, 2451-2455. doi:10.1161/circulationaha.110.953851

Susantitaphong, P., Cruz, D.N., Cerda, J., Abulfaraj, M., Algahtani, F., Koulouridis, I., & Jaber, B.L.; the Acute Kidney Injury Advisory Group of the American Society of Nephrology. (2013). World incidence of AKI: A meta-analysis. Clinical Journal of American Society of Nephrology, 8(9), 1482-1493.

Susantitaphong, P., & Eiam-Ong, S. (2014). Nonpharmacological strategies to prevent contrast-induced acute kidney injury. BioMed Research International. doi: 10.1155/2014/463608

Tepel, M., van der Giet, M., Schwarzfeld, C., Laufer, U., Liermann, D., & Zidek, W. (2000). Prevention of radiographic-contrast-agent-induced reductions in renal function by acetylcysteine. The New England Journal of Medicine, 343(3), 180-184.

Webb, J.G., Pate, G.E., Humphries, K.H., Buller, C.E., Shalansky, S., Al Shamari, A., ... Levin, A. (2004). A randomized controlled trial of intravenous N-acetylcysteine for the preventing of contrast-induced nephropathy after cardiac catheterization: Lack of effect. American Heart Journal, 148(3), 422-429.

Weisbord, S.D., & Palevsky, P.M. (2008). Prevention of contrast-induced nephropathy with volume expansion. Clinical Journal of the American Society of Nephrology, 3(1), 273-280.

Wrobel, W., Sinkiewicz, W., Gordon, M., & Wozniak-Wisniewska, A. (2010). Oral versus intravenous hydration and renal function in diabetic patients undergoing percutaneous coronary interventions. Kardiologia Polska, 68(9), 1015-1020.

Diya Nahar, ACNP-BC, BSN, RN, is a member of the CANP and is currently working as a hospitalist with Platinum Care LA, a private Internal Medicine group.

Author's Note: Special thanks to Acute Care Nurse Practitioner Miguel Castro in the Department of Nursing at California State University, Los Angeles, CA, for suggestions to the content of this document.

Statement of Disclosure: The author reported no actual or potential conflict of interest in relation to this continuing nursing education activity.

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Prophylactic Management of Contrast-Induced Acute Kidney Injury in High-Risk Patients
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In accordance with ANCC governing rules Nephrology Nursing Journal Editorial Board statements of disclosure are published with each CNE offering. The statements of disclosure for this offering are published below.

Paula Dutka MSN, RN, CNN, disclosed that she is a coordinator of Clinical Trials for the following sponsors: Amgen, Rockwell Medical, Keryx Biopharmaceuticals, Akebia Therapeutics, and Dynavax Technologies.

Norma J. Gomez, MBA, MSN, CNNe, disclosed that she is a member of the ZS Pharma Advisory Council.

Tamara M. Kear, PhD, RN, CNS, CNN, disclosed that she is a member of the ANNA Board of Directors, serves on the Scientific Advisory Board for Kibow Biotech, Inc., and is employed by Fresenius Kidney Care as an acute hemodialysis RN.

All other members of the Editorial Board had no actual or potential conflict of interest in relation to this continuing nursing education activity.

This article was reviewed and formatted for contact hour credit by Beth Ulrich, EdD, RN, FACHE, FAAN, Nephrology Nursing Journal Editor, and Sally Russell, MN, CMSRN, CPP, ANNA Education Director.

American Nephrology Nurses Association - Provider is accredited with distinction as a provider of continuing nursing education by the American Nurses Credentialing Center's Commission on Accreditation.

ANNA is a provider approved by the California Board of Registered Nursing, provider number CEP 00910.

This CNE article meets the Nephrology Nursing Certification Commission's (NNCC's) continuing nursing education requirements for certification and recertification.
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Author:Nahar, Diya
Publication:Nephrology Nursing Journal
Article Type:Report
Geographic Code:1USA
Date:May 1, 2017
Words:5457
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