CON: Contrast-induced nephropathy—should we try to avoid contrast media in patients with chronic kidney disease?

CON: Contrast-induced nephropathy—should we try to avoid contrast media in patients with... Abstract The incidence of acute kidney injury (AKI) attributed to iodinated contrast has been over-estimated and this has led clinicians to withhold potentially life-saving diagnostic and therapeutic interventions. There is mounting evidence that iodinated contrast plays only a minor role in the development of AKI in comparison with more significant risk factors such as pre-existing renal dysfunction, hemodynamic instability and exposure to nephrotoxic drugs. We will present data which challenge the dogma of avoiding iodinated contrast in patients with reduced renal function. Based on a rational and individualized risk-benefit analysis, we believe it is preferable to utilize iodinated contrast if alternate diagnostic or therapeutic options are comparatively ineffective or hazardous. acute kidney injury, angiography, contrast-induced nephropathy, creatinine, creatinine clearance SHOULD IODINATED CONTRAST BE AVOIDED IN PATIENTS WITH IMPAIRED RENAL FUNCTION? To begin the discussion, consider the following two clinical scenarios. A 60-year-old man with diabetes and chronic kidney disease with a serum creatinine (SCr) of 1.8 presents to the emergency room (ER) with a differential diagnosis that includes acute mesenteric ischemia. Computed tomography (CT) scan with iodinated intravenous contrast is the preferred diagnostic test to determine the etiology of abdominal pain and guide therapeutic intervention per the American College of Radiology appropriateness criteria [1]. Should iodinated contrast be withheld? Also consider a 70-year-old man who presents with an ST-elevation myocardial infarction (STEMI). The patient’s comorbidities include hypertension, diabetes and an SCr of 2.1 mg/dL. He is on vasopressors to maintain a systolic blood pressure of 100 mmHg. Should coronary catheterization or intervention be avoided in favor of management that does not require iodinated contrast? In both cases, it is our opinion that the clinician should choose the optimal treatment as the additional risk of acute kidney injury (AKI) due to iodinated contrast is outweighed by the benefit of the treatment. Since the first description of contrast-induced acute kidney injury (CI-AKI) in the 1950s, CI-AKI has incited clinician anxiety and frequently led to irrational deviations from optimal patient management strategies [2]. Accumulating evidence demonstrates that iodinated contrast may not be as menacing to renal function as previously believed. Although it is not disputed that iodinated contrast possesses some direct renal toxicity, it is often erroneously blamed for all cases of renal dysfunction following its administration in lieu of other contributors to AKI. AKI is most often caused by a combination of factors including dehydration, sepsis, hypotension, nephrotoxic drugs, advancing age, diabetes, arterial disease and preexisting renal dysfunction. The reported incidence of CI-AKI varies from the single digits to >50%. The described incidence is dependent on multiple factors, including how CI-AKI is defined, the specific patient population of interest, the volume or chemical composition of the contrast agent and a variety of procedure-specific factors. Also contributing to the wide variation in the published incidence of CI-AKI is the near-uniform absence of a control group with risk factors comparable to the group receiving iodinated contrast. It is virtually impossible to design a prospective randomized trial due to the ethical considerations of withholding critical diagnostic and therapeutic options [3–6]. Patients who receive contrast often have a multitude of other independent risk factors for AKI, either from their primary pathology or comorbid diseases, independent of contrast administration. In the absence of exposure to iodinated contrast, AKI is common in hospitalized patients. Based on a recent analysis of nearly 20 000 annual hospitalizations at an academic medical center, Mehran et al. [7] reported that the rate of AKI was 22.7% and AKI was associated with a more than 4-fold increase in mortality. Using the Nationwide Inpatient Sample, Wilhelm-Leen et al. reported the overall rate of AKI in hospitalized patients was not increased in patients receiving iodinated contrast (5.5 versus 5.6%, P = not significant) [3]. Zealley et al. reviewed over 9000 general surgical patients and attempted to demonstrate an association of iodinated contrast and risk of AKI. The overall rate of AKI was 10.9% but this was not statistically associated with iodinated contrast [8]. Finally, Newhouse et al. examined the frequency and magnitude of renal function change in >30 000 hospitalized patients not exposed to iodinated contrast. They concluded that AKI was relatively common and clearly related to baseline renal function, and the adverse effect of contrast was likely overestimated [9]. These results are typical of other recent reports, showing a significant risk of AKI in hospitalized patients but failing to prove a causal relationship to iodinated contrast. For >30 years, there have been reports that suggest intravenous administration of iodinated contrast is associated with negligible risk of AKI. In a now-classic report in 1985, Cramer et al. reported that the rate of AKI following head CT was not increased by administration of iodinated contrast (60–350 mL of iodinated contrast) [10]. Six years later, Heller et al. reported a similar inability to validate an association of iodinated contrast administration for CT scan with renal impairment [11]. To compensate for the absence of a control group, propensity score and risk analysis tools have been used with some success. McDonald et al. applied a propensity scoring method to 12 500 patients receiving both contrasted and non-contrasted CT scans, demonstrating no increased risk of developing AKI after iodinated contrast [12]. In a later study, the same group reported that intravenous iodinated contrast was not an independent risk factor for subsequent dialysis or mortality (80–200 mL of iodinated contrast) [13]. Hinson et al. examined the rates of AKI over a recent 5-year period at a single large academic emergency department (80–120 mL of iodinated contrast) [14]. Contrast administration for CT scans was not associated with an increased risk of AKI, chronic kidney disease, dialysis or renal transplant at 6 months [14]. Similarly, Davenport et al. examined emergency department CT scans over a 10-year period and found no significant difference in AKI, either with or without contrast exposure in patients with a glomerular filtration rate >30 mL/h (117 mL average of iodinated contrast) [15]. These findings strongly support a policy of ordering iodinated contrast-enhanced CT scans based on clinical indications. Intravenous and intra-arterial contrast injections appear to have differing impacts on renal function. Although it stands to reason that contrast injected upstream of the renal artery will result in a higher concentration at the nephron than venous injection, other factors such as instrumentation to the renal arteries and thromboembolism make differentiating the causal factors of AKI difficult. Recently, Tong et al. [16] directly compared intravenous administration of contrast for CT scans with intra-arterial administration during cardiac catheterization. In over 1900 patients, they demonstrated no increased risk of AKI due to the mode of contrast administration (201 mL average for intra-arterial and 120 mL average for intravenous) [16]. Another study comparing intravenous CT angiography and intra-arterial contrast found no significant difference in the incidence of AKI (170 mL intravenous versus 230 mL intra-arterial iodinated contrast) [17]. In the coronary literature, there is increasing evidence that factors other than iodinated contrast play a dominant role in the development of AKI after coronary intervention. Johannes et al. reported that the incidence of AKI was 18% in consecutive patients in the Bremen STEMI Registry (148.5 mL mean of iodinated contrast) [18]. Of note, the severity of the STEMI and its hemodynamic sequela (e.g. hypotension, need for intra-aortic balloon pump) were predictive of AKI but there was no association between amount or type of iodinated contrast and the risk of AKI. The development of AKI was associated with a markedly increased risk of 30-day and 1-year mortality. Optimal percutaneous coronary intervention (PCI) was independently associated with a reduced risk of AKI, lending further support to the theory that the adverse hemodynamic consequences of myocardial infarction play a more significant role in the development of AKI than previously estimated. Caspi et al. reported no difference in the incidence of AKI in propensity score-matched STEMI patients treated with or without PCI (8.6% versus 10.9%, P = 0.12, 150 mL median volume of iodinated contrast) [19]. They concluded that AKI was chiefly related to older age, baseline renal dysfunction, heart failure and hemodynamic instability, and this was not demonstrated with iodinated contrast exposure. The previous studies did not show an independent association of iodinated contrast administration and AKI, and they are noteworthy as they have included adequate control groups with risk factors for AKI similar to the treatment groups. When making the clinical decision to administer iodinated contrast, it is of utmost importance to consider the individual risk factors along with the specific procedural and contrast related risk factors to evaluate if the test or procedure will benefit the patient. Patient-related risk factors for contrast nephropathy common across all venues are chronic kidney disease, diabetes mellitus, advanced age, anemia, hypotension, hypovolemia, critical limb ischemia, obesity and critical tissue ischemia [5, 20]. In terms of procedural risk factors, the use of high volumes of contrast and procedural hypotension may contribute to the AKI [21]. It has been long demonstrated that high osmolality or highly concentrated contrast also contributes some additional risk of AKI [22]. A CT angiogram of the abdomen and pelvis uses 100 mL of iodinated contrast in our institution, this is slightly more volume than in standard contrasted CT exams and has caused providers reluctance in ordering this exam. Considering past over-estimation of contrast induced nephropathy (CIN) and the patient's disease process, the benefit to this patient is significant and early diagnosis will encourage timely treatment that may improve the outcome. Acknowledging recent literature, it appears that the previously reported rates of CI-AKI have been overestimated. Newer research demonstrates that AKI is more often related to patient disease processes and procedural risk factors, which may not be directly correlated with iodinated contrast administration. If an individualized risk–benefit analysis favors the use of iodinated contrast administration, it is prudent to proceed with the intervention. In patients who possess multiple risk factors for AKI, elective procedures should be preceded by prehydration and all nephrotoxic medications should be held. The use of non-contrasted studies should be exhausted before a contrasted study is performed. However, in the acute setting, optimization is often not feasible, and the minimal risk of CI-AKI should not discourage appropriate therapy. We believe that liberalizing the use of iodinated contrast to aid in patient management should be strongly considered, as iodinated contrast likely adds a negligible risk of AKI. CONFLICT OF INTEREST STATEMENT None declared. REFERENCES 1 American College of Radiology. Appropriateness Criteria, 2012. https://acr.org/Clinical-Resources/ACR-Appropriateness-Criteria (3 January 2018, date last accessed) 2 Bartels ED, Brun GC, Gammeltoft A et al.   Acute anuria following intravenous pyelography in a patient with myelomatosis. Acta Med Scand  1954; 150: 297– 302 Google Scholar CrossRef Search ADS PubMed  3 Wilhelm-Leen E, Montez-Rath ME, Chertow G. Estimating the risk of radiocontrast-associated nephropathy. J Am Soc Nephrol  2017; 28: 653– 659 Google Scholar CrossRef Search ADS PubMed  4 Mitchell AM, Jones AE, Tumlin JA et al.   Incidence of contrast-induced nephropathy after contrast-enhanced computed tomography in the outpatient setting. Clin J Am Soc Nephrol  2010; 5: 4– 9 Google Scholar CrossRef Search ADS PubMed  5 Grossman PM, Ali SS, Aronow HD et al.   Contrast-induced nephropathy in patients undergoing endovascular peripheral vascular intervention: incidence, risk factors, and outcomes as observed in the Blue Cross Blue Shield of Michigan Cardiovascular Consortium. J Interv Cardiol  2017; 30: 274– 280 Google Scholar CrossRef Search ADS PubMed  6 Bartholomew BA, Harjai KJ, Dukkipati S et al.   Impact of nephropathy after percutaneous coronary intervention and a method for risk stratification. Am J Cardiol  2004; 93: 1515– 1519 Google Scholar CrossRef Search ADS PubMed  7 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– 1399 Google Scholar PubMed  8 Zealley I, Wang H, Donnan PT et al.   (9 December 2017) Exposure to contrast media in the perioperative period confers no additional risk of acute kidney injury in surgical patients. Nephrol Dial Transplant  2017; doi: 10.1093/ndt/gfx325 9 Newhouse JH, Kho D, Rao QA et al.   Frequency of serum creatinine changes in the absence of iodinated contrast material: implications for studies of contrast nephrotoxicity. AJR Am J Roentgenol  2008; 191: 376– 382 Google Scholar CrossRef Search ADS PubMed  10 Cramer BC, Parfrey PS, Hutchinson TA et al.   Renal function following infusion of radiologic contrast material. A prospective controlled study. Arch Intern Med  1985; 145: 87– 89 Google Scholar CrossRef Search ADS PubMed  11 Heller CA, Knapp J, Halliday J et al.   Failure to demonstrate contrast nephrotoxicity. Med J Aust  1991; 155: 329– 332 Google Scholar PubMed  12 McDonald JS, McDonald RJ, Carter RE et al.   Risk of intravenous contrast material-mediated acute kidney injury: a propensity score-matched study stratified by baseline-estimated glomerular filtration rate. Radiology  2014; 271: 65– 73 Google Scholar CrossRef Search ADS PubMed  13 McDonald RJ, McDonald JS, Carter RE et al.   Intravenous contrast material exposure is not an independent risk factor for dialysis or mortality. Radiology  2014; 273: 714– 725 Google Scholar CrossRef Search ADS PubMed  14 Hinson JS, Ehmann MR, Fine DM et al.   Risk of acute kidney injury after intravenous contrast media administration. Ann Emerg Med  2017; 69: 577– 586 Google Scholar CrossRef Search ADS PubMed  15 Davenport MS, Khalatbari S, Cohan RH et al.   Contrast material-induced nephrotoxicity and intravenous low-osmolality iodinated contrast material: risk stratification by using estimated glomerular filtration rate. Radiology  2013; 268: 719– 728 Google Scholar CrossRef Search ADS PubMed  16 Tong GE, Kumar S, Chong KC et al.   Risk of contrast-induced nephropathy for patients receiving intravenous vs. intra-arterial iodixanol administration. Abdom Radiol (NY)  2016; 41: 91– 99 Google Scholar CrossRef Search ADS PubMed  17 Karlsberg RP, Dohad SY, Sheng R. Contrast medium-induced acute kidney injury: comparison of intravenous and intraarterial administration of iodinated contrast medium. J Vasc Interv Radiol  2011; 22: 1159– 1165 Google Scholar CrossRef Search ADS PubMed  18 Johannes S, Andreas F, Matthias B et al.   (1 June 2017) Predictors of acute kidney injury in patients admitted with ST-elevation myocardial infarction – results from the Bremen STEMI-Registry. Eur Heart J Acute Cardiovasc Care  2017; doi: 10.1177/2048872617708975 19 Caspi O, Habib M, Cohen Y et al.   Acute kidney injury after primary angioplasty: is contrast‐induced nephropathy the culprit? J Am Heart Assoc  2017; 6: e005715 Google Scholar CrossRef Search ADS PubMed  20 Toprak O, Cirit M. Risk factors for contrast-induced nephropathy. Kidney Blood Press Res  2006; 29: 84– 93 Google Scholar CrossRef Search ADS PubMed  21 Keaney JJ, Hannon CM, Murray PT. Contrast-induced acute kidney injury: how much contrast is safe? Nephrol Dial Transplant  2013; 28: 1376– 1383 Google Scholar CrossRef Search ADS PubMed  22 Barrett BJ, Carlisle EJ. Metaanalysis of the relative nephrotoxicity of high- and low-osmolality iodinated contrast media. Radiology  1993; 188: 171– 178 Google Scholar CrossRef Search ADS PubMed  © The Author(s) 2018. Published by Oxford University Press on behalf of ERA-EDTA. All rights reserved. This article is published and distributed under the terms of the Oxford University Press, Standard Journals Publication Model (https://academic.oup.com/journals/pages/about_us/legal/notices) http://www.deepdyve.com/assets/images/DeepDyve-Logo-lg.png Nephrology Dialysis Transplantation Oxford University Press

CON: Contrast-induced nephropathy—should we try to avoid contrast media in patients with chronic kidney disease?

Loading next page...
 
/lp/ou_press/con-contrast-induced-nephropathy-should-we-try-to-avoid-contrast-media-FWRYmllREI
Publisher
Oxford University Press
Copyright
© The Author(s) 2018. Published by Oxford University Press on behalf of ERA-EDTA. All rights reserved.
ISSN
0931-0509
eISSN
1460-2385
D.O.I.
10.1093/ndt/gfy153
Publisher site
See Article on Publisher Site

Abstract

Abstract The incidence of acute kidney injury (AKI) attributed to iodinated contrast has been over-estimated and this has led clinicians to withhold potentially life-saving diagnostic and therapeutic interventions. There is mounting evidence that iodinated contrast plays only a minor role in the development of AKI in comparison with more significant risk factors such as pre-existing renal dysfunction, hemodynamic instability and exposure to nephrotoxic drugs. We will present data which challenge the dogma of avoiding iodinated contrast in patients with reduced renal function. Based on a rational and individualized risk-benefit analysis, we believe it is preferable to utilize iodinated contrast if alternate diagnostic or therapeutic options are comparatively ineffective or hazardous. acute kidney injury, angiography, contrast-induced nephropathy, creatinine, creatinine clearance SHOULD IODINATED CONTRAST BE AVOIDED IN PATIENTS WITH IMPAIRED RENAL FUNCTION? To begin the discussion, consider the following two clinical scenarios. A 60-year-old man with diabetes and chronic kidney disease with a serum creatinine (SCr) of 1.8 presents to the emergency room (ER) with a differential diagnosis that includes acute mesenteric ischemia. Computed tomography (CT) scan with iodinated intravenous contrast is the preferred diagnostic test to determine the etiology of abdominal pain and guide therapeutic intervention per the American College of Radiology appropriateness criteria [1]. Should iodinated contrast be withheld? Also consider a 70-year-old man who presents with an ST-elevation myocardial infarction (STEMI). The patient’s comorbidities include hypertension, diabetes and an SCr of 2.1 mg/dL. He is on vasopressors to maintain a systolic blood pressure of 100 mmHg. Should coronary catheterization or intervention be avoided in favor of management that does not require iodinated contrast? In both cases, it is our opinion that the clinician should choose the optimal treatment as the additional risk of acute kidney injury (AKI) due to iodinated contrast is outweighed by the benefit of the treatment. Since the first description of contrast-induced acute kidney injury (CI-AKI) in the 1950s, CI-AKI has incited clinician anxiety and frequently led to irrational deviations from optimal patient management strategies [2]. Accumulating evidence demonstrates that iodinated contrast may not be as menacing to renal function as previously believed. Although it is not disputed that iodinated contrast possesses some direct renal toxicity, it is often erroneously blamed for all cases of renal dysfunction following its administration in lieu of other contributors to AKI. AKI is most often caused by a combination of factors including dehydration, sepsis, hypotension, nephrotoxic drugs, advancing age, diabetes, arterial disease and preexisting renal dysfunction. The reported incidence of CI-AKI varies from the single digits to >50%. The described incidence is dependent on multiple factors, including how CI-AKI is defined, the specific patient population of interest, the volume or chemical composition of the contrast agent and a variety of procedure-specific factors. Also contributing to the wide variation in the published incidence of CI-AKI is the near-uniform absence of a control group with risk factors comparable to the group receiving iodinated contrast. It is virtually impossible to design a prospective randomized trial due to the ethical considerations of withholding critical diagnostic and therapeutic options [3–6]. Patients who receive contrast often have a multitude of other independent risk factors for AKI, either from their primary pathology or comorbid diseases, independent of contrast administration. In the absence of exposure to iodinated contrast, AKI is common in hospitalized patients. Based on a recent analysis of nearly 20 000 annual hospitalizations at an academic medical center, Mehran et al. [7] reported that the rate of AKI was 22.7% and AKI was associated with a more than 4-fold increase in mortality. Using the Nationwide Inpatient Sample, Wilhelm-Leen et al. reported the overall rate of AKI in hospitalized patients was not increased in patients receiving iodinated contrast (5.5 versus 5.6%, P = not significant) [3]. Zealley et al. reviewed over 9000 general surgical patients and attempted to demonstrate an association of iodinated contrast and risk of AKI. The overall rate of AKI was 10.9% but this was not statistically associated with iodinated contrast [8]. Finally, Newhouse et al. examined the frequency and magnitude of renal function change in >30 000 hospitalized patients not exposed to iodinated contrast. They concluded that AKI was relatively common and clearly related to baseline renal function, and the adverse effect of contrast was likely overestimated [9]. These results are typical of other recent reports, showing a significant risk of AKI in hospitalized patients but failing to prove a causal relationship to iodinated contrast. For >30 years, there have been reports that suggest intravenous administration of iodinated contrast is associated with negligible risk of AKI. In a now-classic report in 1985, Cramer et al. reported that the rate of AKI following head CT was not increased by administration of iodinated contrast (60–350 mL of iodinated contrast) [10]. Six years later, Heller et al. reported a similar inability to validate an association of iodinated contrast administration for CT scan with renal impairment [11]. To compensate for the absence of a control group, propensity score and risk analysis tools have been used with some success. McDonald et al. applied a propensity scoring method to 12 500 patients receiving both contrasted and non-contrasted CT scans, demonstrating no increased risk of developing AKI after iodinated contrast [12]. In a later study, the same group reported that intravenous iodinated contrast was not an independent risk factor for subsequent dialysis or mortality (80–200 mL of iodinated contrast) [13]. Hinson et al. examined the rates of AKI over a recent 5-year period at a single large academic emergency department (80–120 mL of iodinated contrast) [14]. Contrast administration for CT scans was not associated with an increased risk of AKI, chronic kidney disease, dialysis or renal transplant at 6 months [14]. Similarly, Davenport et al. examined emergency department CT scans over a 10-year period and found no significant difference in AKI, either with or without contrast exposure in patients with a glomerular filtration rate >30 mL/h (117 mL average of iodinated contrast) [15]. These findings strongly support a policy of ordering iodinated contrast-enhanced CT scans based on clinical indications. Intravenous and intra-arterial contrast injections appear to have differing impacts on renal function. Although it stands to reason that contrast injected upstream of the renal artery will result in a higher concentration at the nephron than venous injection, other factors such as instrumentation to the renal arteries and thromboembolism make differentiating the causal factors of AKI difficult. Recently, Tong et al. [16] directly compared intravenous administration of contrast for CT scans with intra-arterial administration during cardiac catheterization. In over 1900 patients, they demonstrated no increased risk of AKI due to the mode of contrast administration (201 mL average for intra-arterial and 120 mL average for intravenous) [16]. Another study comparing intravenous CT angiography and intra-arterial contrast found no significant difference in the incidence of AKI (170 mL intravenous versus 230 mL intra-arterial iodinated contrast) [17]. In the coronary literature, there is increasing evidence that factors other than iodinated contrast play a dominant role in the development of AKI after coronary intervention. Johannes et al. reported that the incidence of AKI was 18% in consecutive patients in the Bremen STEMI Registry (148.5 mL mean of iodinated contrast) [18]. Of note, the severity of the STEMI and its hemodynamic sequela (e.g. hypotension, need for intra-aortic balloon pump) were predictive of AKI but there was no association between amount or type of iodinated contrast and the risk of AKI. The development of AKI was associated with a markedly increased risk of 30-day and 1-year mortality. Optimal percutaneous coronary intervention (PCI) was independently associated with a reduced risk of AKI, lending further support to the theory that the adverse hemodynamic consequences of myocardial infarction play a more significant role in the development of AKI than previously estimated. Caspi et al. reported no difference in the incidence of AKI in propensity score-matched STEMI patients treated with or without PCI (8.6% versus 10.9%, P = 0.12, 150 mL median volume of iodinated contrast) [19]. They concluded that AKI was chiefly related to older age, baseline renal dysfunction, heart failure and hemodynamic instability, and this was not demonstrated with iodinated contrast exposure. The previous studies did not show an independent association of iodinated contrast administration and AKI, and they are noteworthy as they have included adequate control groups with risk factors for AKI similar to the treatment groups. When making the clinical decision to administer iodinated contrast, it is of utmost importance to consider the individual risk factors along with the specific procedural and contrast related risk factors to evaluate if the test or procedure will benefit the patient. Patient-related risk factors for contrast nephropathy common across all venues are chronic kidney disease, diabetes mellitus, advanced age, anemia, hypotension, hypovolemia, critical limb ischemia, obesity and critical tissue ischemia [5, 20]. In terms of procedural risk factors, the use of high volumes of contrast and procedural hypotension may contribute to the AKI [21]. It has been long demonstrated that high osmolality or highly concentrated contrast also contributes some additional risk of AKI [22]. A CT angiogram of the abdomen and pelvis uses 100 mL of iodinated contrast in our institution, this is slightly more volume than in standard contrasted CT exams and has caused providers reluctance in ordering this exam. Considering past over-estimation of contrast induced nephropathy (CIN) and the patient's disease process, the benefit to this patient is significant and early diagnosis will encourage timely treatment that may improve the outcome. Acknowledging recent literature, it appears that the previously reported rates of CI-AKI have been overestimated. Newer research demonstrates that AKI is more often related to patient disease processes and procedural risk factors, which may not be directly correlated with iodinated contrast administration. If an individualized risk–benefit analysis favors the use of iodinated contrast administration, it is prudent to proceed with the intervention. In patients who possess multiple risk factors for AKI, elective procedures should be preceded by prehydration and all nephrotoxic medications should be held. The use of non-contrasted studies should be exhausted before a contrasted study is performed. However, in the acute setting, optimization is often not feasible, and the minimal risk of CI-AKI should not discourage appropriate therapy. We believe that liberalizing the use of iodinated contrast to aid in patient management should be strongly considered, as iodinated contrast likely adds a negligible risk of AKI. CONFLICT OF INTEREST STATEMENT None declared. REFERENCES 1 American College of Radiology. Appropriateness Criteria, 2012. https://acr.org/Clinical-Resources/ACR-Appropriateness-Criteria (3 January 2018, date last accessed) 2 Bartels ED, Brun GC, Gammeltoft A et al.   Acute anuria following intravenous pyelography in a patient with myelomatosis. Acta Med Scand  1954; 150: 297– 302 Google Scholar CrossRef Search ADS PubMed  3 Wilhelm-Leen E, Montez-Rath ME, Chertow G. Estimating the risk of radiocontrast-associated nephropathy. J Am Soc Nephrol  2017; 28: 653– 659 Google Scholar CrossRef Search ADS PubMed  4 Mitchell AM, Jones AE, Tumlin JA et al.   Incidence of contrast-induced nephropathy after contrast-enhanced computed tomography in the outpatient setting. Clin J Am Soc Nephrol  2010; 5: 4– 9 Google Scholar CrossRef Search ADS PubMed  5 Grossman PM, Ali SS, Aronow HD et al.   Contrast-induced nephropathy in patients undergoing endovascular peripheral vascular intervention: incidence, risk factors, and outcomes as observed in the Blue Cross Blue Shield of Michigan Cardiovascular Consortium. J Interv Cardiol  2017; 30: 274– 280 Google Scholar CrossRef Search ADS PubMed  6 Bartholomew BA, Harjai KJ, Dukkipati S et al.   Impact of nephropathy after percutaneous coronary intervention and a method for risk stratification. Am J Cardiol  2004; 93: 1515– 1519 Google Scholar CrossRef Search ADS PubMed  7 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– 1399 Google Scholar PubMed  8 Zealley I, Wang H, Donnan PT et al.   (9 December 2017) Exposure to contrast media in the perioperative period confers no additional risk of acute kidney injury in surgical patients. Nephrol Dial Transplant  2017; doi: 10.1093/ndt/gfx325 9 Newhouse JH, Kho D, Rao QA et al.   Frequency of serum creatinine changes in the absence of iodinated contrast material: implications for studies of contrast nephrotoxicity. AJR Am J Roentgenol  2008; 191: 376– 382 Google Scholar CrossRef Search ADS PubMed  10 Cramer BC, Parfrey PS, Hutchinson TA et al.   Renal function following infusion of radiologic contrast material. A prospective controlled study. Arch Intern Med  1985; 145: 87– 89 Google Scholar CrossRef Search ADS PubMed  11 Heller CA, Knapp J, Halliday J et al.   Failure to demonstrate contrast nephrotoxicity. Med J Aust  1991; 155: 329– 332 Google Scholar PubMed  12 McDonald JS, McDonald RJ, Carter RE et al.   Risk of intravenous contrast material-mediated acute kidney injury: a propensity score-matched study stratified by baseline-estimated glomerular filtration rate. Radiology  2014; 271: 65– 73 Google Scholar CrossRef Search ADS PubMed  13 McDonald RJ, McDonald JS, Carter RE et al.   Intravenous contrast material exposure is not an independent risk factor for dialysis or mortality. Radiology  2014; 273: 714– 725 Google Scholar CrossRef Search ADS PubMed  14 Hinson JS, Ehmann MR, Fine DM et al.   Risk of acute kidney injury after intravenous contrast media administration. Ann Emerg Med  2017; 69: 577– 586 Google Scholar CrossRef Search ADS PubMed  15 Davenport MS, Khalatbari S, Cohan RH et al.   Contrast material-induced nephrotoxicity and intravenous low-osmolality iodinated contrast material: risk stratification by using estimated glomerular filtration rate. Radiology  2013; 268: 719– 728 Google Scholar CrossRef Search ADS PubMed  16 Tong GE, Kumar S, Chong KC et al.   Risk of contrast-induced nephropathy for patients receiving intravenous vs. intra-arterial iodixanol administration. Abdom Radiol (NY)  2016; 41: 91– 99 Google Scholar CrossRef Search ADS PubMed  17 Karlsberg RP, Dohad SY, Sheng R. Contrast medium-induced acute kidney injury: comparison of intravenous and intraarterial administration of iodinated contrast medium. J Vasc Interv Radiol  2011; 22: 1159– 1165 Google Scholar CrossRef Search ADS PubMed  18 Johannes S, Andreas F, Matthias B et al.   (1 June 2017) Predictors of acute kidney injury in patients admitted with ST-elevation myocardial infarction – results from the Bremen STEMI-Registry. Eur Heart J Acute Cardiovasc Care  2017; doi: 10.1177/2048872617708975 19 Caspi O, Habib M, Cohen Y et al.   Acute kidney injury after primary angioplasty: is contrast‐induced nephropathy the culprit? J Am Heart Assoc  2017; 6: e005715 Google Scholar CrossRef Search ADS PubMed  20 Toprak O, Cirit M. Risk factors for contrast-induced nephropathy. Kidney Blood Press Res  2006; 29: 84– 93 Google Scholar CrossRef Search ADS PubMed  21 Keaney JJ, Hannon CM, Murray PT. Contrast-induced acute kidney injury: how much contrast is safe? Nephrol Dial Transplant  2013; 28: 1376– 1383 Google Scholar CrossRef Search ADS PubMed  22 Barrett BJ, Carlisle EJ. Metaanalysis of the relative nephrotoxicity of high- and low-osmolality iodinated contrast media. Radiology  1993; 188: 171– 178 Google Scholar CrossRef Search ADS PubMed  © The Author(s) 2018. Published by Oxford University Press on behalf of ERA-EDTA. All rights reserved. This article is published and distributed under the terms of the Oxford University Press, Standard Journals Publication Model (https://academic.oup.com/journals/pages/about_us/legal/notices)

Journal

Nephrology Dialysis TransplantationOxford University Press

Published: Jun 3, 2018

There are no references for this article.

You’re reading a free preview. Subscribe to read the entire article.


DeepDyve is your
personal research library

It’s your single place to instantly
discover and read the research
that matters to you.

Enjoy affordable access to
over 18 million articles from more than
15,000 peer-reviewed journals.

All for just $49/month

Explore the DeepDyve Library

Search

Query the DeepDyve database, plus search all of PubMed and Google Scholar seamlessly

Organize

Save any article or search result from DeepDyve, PubMed, and Google Scholar... all in one place.

Access

Get unlimited, online access to over 18 million full-text articles from more than 15,000 scientific journals.

Your journals are on DeepDyve

Read from thousands of the leading scholarly journals from SpringerNature, Elsevier, Wiley-Blackwell, Oxford University Press and more.

All the latest content is available, no embargo periods.

See the journals in your area

DeepDyve

Freelancer

DeepDyve

Pro

Price

FREE

$49/month
$360/year

Save searches from
Google Scholar,
PubMed

Create lists to
organize your research

Export lists, citations

Read DeepDyve articles

Abstract access only

Unlimited access to over
18 million full-text articles

Print

20 pages / month

PDF Discount

20% off