Veilig gebruik van contrastmiddelen

Initiatief: NVvR Aantal modules: 48

Definities, terminologie en klinisch verloop

Disclaimer: This narrative review has been written by members of the Guideline Development Group so that non-specialized readers can follow the Modules about Hypersensitivity more easily. It was not part of the actual guideline process with structured literature analyses. 

 

Post-Contrast-AKI: Terminology and definitions

Because of the recent developments there is confusion about terminology. Terms as post-contrast acute kidney injury, contrast-associated acute kidney injury, and contrast-induced acute kidney injury or contrast-induced nephropathy are incorrectly used interchangeably.

 

Therefore, the working group suggests adaptation of the suggestion of the American College of Radiology (ACR) Committee on Drugs and Contrast Media, put forward in their Manual on Contrast Media for more uniformity (ACR Manual, 2017).

 

Post Contrast Acute Kidney Injury (PC-AKI) is a general term used to describe a sudden deterioration in renal function that occurs within 48 hours following the intravascular administration of iodine-containing contrast medium. PC-AKI may occur regardless of whether the contrast medium was the cause of the deterioration. PC-AKI is a correlative diagnosis.

 

Contrast-Induced Acute Kidney Injury (CI-AKI) or Contrast-Induced Nephropathy (CIN) is a specific term used to describe a sudden deterioration in kidney function that is caused by the intravascular administration of iodine-containing contrast medium; therefore, CI-AKI/CIN is a subgroup of PC-AKI. CI-AKI/CIN is a causative diagnosis.

 

The ACR acknowledges that very few published studies have a suitable control group to permit the differentiation of CI-AKI/CIN from PC-AKI. Therefore, the incidence of PC-AKI reported in clinical studies and the incidence of PC-AKI observed in clinical practice likely includes a combination of CI-AKI/CIN (i.e., AKI caused by contrast medium administration) and AKI unrelated to contrast medium administration (i.e., AKI coincident to, but not caused by contrast medium administration). It should be clear that these terms are not interchangeable.

 

PC-AKI is not synonymous with CI-AKI / CIN (ACR Manual, 2017).

 

Definitions and their history

In critical care, acute renal failure is a complex disorder with a wide variety of aetiologies and possible risk factors. Despite improved knowledge from animal studies, there was a lack of uniform definition of this disorder. This challenge has been taken on by multiple groups in the Nephrology community, among them the Acute Dialysis Quality Initiative (ADQI) (Bellomo, 2004) and the Kidney Disease: Improving Global Outcome (KDIGO) (Levey, 2005) groups.

 

During the first meeting of the Acute Kidney Injury Network (AKIN), a network of experts in Critical Care and Nephrology, the term Acute Kidney Injury (AKI) was suggested as the preferred uniform terminology for acute renal failure. This was diagnosed as “an abrupt (within 48 hours) reduction in kidney function currently defined as an absolute increase in serum creatinine (sCr) of ≥ 0.3 mg/dl (≥ 26.4 μmol/l), a percentage increase in serum creatinine of more than or equal to 50% (1.5-fold from baseline), or a reduction in urine output (documented oliguria of less than 0.5 ml/kg per hour for more than six hours)” (Mehta, 2007). In clinical practice a 50% increase in sCr >3 and <7 days can be used. This definition is thus applicable to all forms of AKI and is not specific for contrast-induced AKI. This was subsequently adapted into the KDIGO Practice Guidelines in 2012. According to this guideline, AKI can be subdivided in 3 stages (see Table 1) according to criteria adapted from the RIFLE (Risk, Injury, Failure, Loss, End Stage) criteria (Drüeke, 2012):

 

Table 1: KDIGO staging of AKI

Stage

Serum creatinine criteria

Urine output criteria

1

sCr increase ≥0.3 mg/dl (≥26.5 μmol/l), or

sCr increase ≥1.5 to 1.9x baseline

<0.5 ml/kg/h for 6 to 12h

2

sCr increase >2.0 to 2.9x baseline

<0.5 ml/kg/h for ≥12h

3

sCr ≥4.0 mg/dl (≥354 μmol/l)

sCr increase >3.0 x baseline or

initiation of renal replacement therapy

<0.3 ml/kg/h for ≥24h

Anuria for ≥12h

Of note 1 mg/dl serum Creatinine equals 88,4 µmol/l.

 

In the mid 1990s, the Contrast Media Safety Committee (CMSC) of the European Society of Urogenital Radiology (ESUR) was founded, a group of experienced CM researchers from Radiology, that was set out to make expert-based guidelines. The most frequently used definition of Contrast-Induced Nephropathy (CIN), is from their first renal guideline: “CIN refers to a condition in which an impairment in renal function (an increase in serum creatinine by more than 25% or 44 µmol/l (or 0.5 mg/dl) occurs within 3 days following the intravascular administration of a contrast medium in the absence of an alternative aetiology” (Morcos, 1999). More stringent definitions have been used in older studies, e.g. using a sCr increase >1 mg/dl [88 µmol/l] or 50% (Aspelin, 2003). However, these have not really been used widely in recent times.

 

This resulted in another confusion that has still not been adequately resolved by a consensus definition (Endre, 2010; Meinel, 2014). It has been shown in multiple studies that the percentage of patients with CIN is largely dependent on the definition used (Jabara, 2009; Pyxaras, 2015; Weisbord, 2008).

 

A relative increase in sCr of >25% has been the most sensitive indicator, whereas absolute value definitions led to lower rates of CIN. In some studies relative increases in sCr were found to overestimate CIN and absolute values were preferable (Budano, 2011), while in other studies relative definitions were stronger associated with prognostic relevance in coronary angiography (Pyxaras, 2015). A recent study showed that the combination of an absolute sCr increase >0.3 mg/dl [25 mol/l] or a relative sCr increase >50% might be the most optimal definition (Parsh, 2016).

However, these figures of CIN are usually not well related to hard clinical endpoints such as (short-term) renal replacement therapy dependency, morbidity or mortality. Some studies in critically ill populations have shown a benefit of the AKIN-definition of post-contrast AKI on ICU mortality (Lakhal, 2011).

 

Already in 2006, a CIN Consensus Working Panel formed by GE Healthcare with experts from various disciplines indicated that the ADQI-RIFLE criteria may be important in the future for defining PC-AKI (McCullough, 2006). Many researchers in radiology and cardiology are now moving towards adaptation of the AKIN criteria as the standard for studies on contrast-induced AKI (Garfinkle, 2015). Therefore, we suggest, similar to the European Renal Best Practice (ERBP) working group in their comment on the KDIGO 2012 practice guidelines on AKI, that there seems to be no good reason why the definition of PC-AKI (or CI-AKI) should be different from the general definition of other forms of AKI (Fliser, 2012; Kooiman, 2016; Thomas, 2015), even though CI-AKI /CIN and PC-AKI are not completely interchangeable.

 

Clinical Course and Incidence

PC-AKI is an iatrogenic renal injury that follows intravascular administration of CM in susceptible individuals. (Rear, 2016). The proliferation in imaging methods and interventions involving administration of intravascular CM has significantly increased the number of patients exposed to CM and consequently the number of patients at risk for PC-AKI.

 

Discrimination between different causes of AKI in patients subjected to iodine-containing CM administration is difficult. In most of cases PC-AKI is mild and reversible with returning of renal function to baseline or near baseline values within 1-3 weeks (Mehran, 2006; Guitterez, 2002). As common for all forms of AKI, the occurrence of PC-AKI has shown to be a marker for increased short- and long-term morbidity and/or mortality and prolonged hospital stay (Gupta; 2005; Gruberg, 2000; Mitchell, 2015; Kooiman, 2015; Rihal, 2002; Rudnick, 2008).

 

Various studies suggest that the route of administration of iodine-containing CM (intra-arterial versus intravenous) and the type of procedure (i.e. catheter-based angiography versus CT imaging) can have a substantial impact on the incidence of PC-AKI. (Dong, 2012) However, in four retrospective studies the risk of PC-AKI and clinical course did not differ in patients who underwent both intra-arterial and intravenous contrast administration within a restricted time span. (Karlsberg, 2011; Kooiman, 2013; Tong, 2016; McDonald, 2016)

 

The cause of AKI following catheter angiography is in many instances multifactorial and may erroneously be diagnosed as PC-AKI. (Keeley, 1998) For instance, catheter-based procedures as compared to contrast-enhanced computed tomography (CE-CT) may be complicated by haemodynamic instability leading to post-interventional AKI, which may be misinterpreted as contrast-induced nephropathy (Bruce, 2009; Newhouse, 2008). In addition, cholesterol emboli, aortic plaque fragments and thrombi may be physically dislodged during catheter manipulation, leading to micro-embolization of the kidney and post-procedural impairment of kidney function (Wichmann, 2015).

 

Two recent meta-analyses of 40 and 42 studies in about 19,000 patients undergoing CE-CT revealed a weighted pooled incidence of PC-AKI of 6.4% (95%CI 5.0-8.1%) and 5.0% (95%CI 3.8-6.5%). (Kooiman, 2012; Moos, 2013) In the meta-analysis of Moos et al. chronic kidney disease (CKD), diabetes, malignancy, age >65 years and use of non-steroidal anti-inflammatory drugs (NSAID’s) and in the meta-analysis of Kooiman et al. CKD and diabetes were associated with an increased risk. In about 1% of all patients (follow-up one week to two months after CE-CT) the renal function decline persisted, but the weighted pooled incidence of renal replacement therapy was as low as 0.06%. (Kooiman, 2012) The authors of this meta-analysis conclude that, given the low incidence of PC-AKI in general and the rare occurrence of a persistent decline in renal function, CM in the setting of a CT can be safely administered to the vast majority of patients. However, as emphasized by the authors, since in most of the studies pre- and post-hydration was performed in patients at high risk for PC-AKI, the results are not generalizable to high risk patients without pre- and/or post-hydration.

 

Meta-analyses of non-randomized studies comparing outcomes of patients who underwent CT with and without iodine-containing CM bear the risk of selection bias. Recently, propensity score matching has been introduced to the field of PC-AKI. Propensity score matching is a statistical method used in observational studies with low incidence of outcome under study that takes measured confounding into account (Rosenbaum, 1984). McDonald JS, et al. performed a propensity score-based matched study in over 12,500 patients, and did not find an increased risk of PC-AKI, acute dialysis, or 30-day mortality in patients who underwent CE-CT versus those who did not. (McDonald, 2014) Using propensity-score based matching in over 17,500 patients Davenport et al. also did not observe an increased risk for AKI in patients with normal renal function after intravenous CM administration for CT, but they reported an increased incidence of AKI in patients with an eGFR <30 ml/min/1.73m2 (Davenport, 2013). These findings suggest that the incidence of CI-AKI in patients undergoing contrast-enhanced CT with intravenous iodine-containing CM administration is likely to be substantially lower than previously estimated. However, the clinical course of AKI after CE-CT may not always be so favourable as evidenced by the abovementioned studies. In a prospective observational study concerning 633 emergency department patients undergoing CE-CT without pre-hydration PC-AKI occurred in 70 patients (11%), with persistent renal failure at one-year follow-up in 11 of these patients. (Mitchell, 2015) It should be emphasized that these patients had an emergent indication for CE-CT and might therefore have other risk factors (such as haemodynamic instability) for AKI.

 

In 5244 patients with ST-Elevation Myocardial Infarction (STEMI) treated with PCI the incidence of PC-AKI for patients with a baseline eGFR of >90, 60-90, 30-59 and <30 ml/min/1.73 m2 was 2.1%, 3.4%, 7.3% and 1.8%, respectively, underlining pre-existent CKD as a risk factor of PC-AKI. (Vavalle, 2016) The relatively low incidence of PC-AKI in the group of patients with an eGFR <30 ml/min/1.73 m2 may be related to the small number of patients (n=89) present in this subgroup. Impaired renal function at presentation and development of PC-AKI were highly associated with worse clinical outcome, including death. A meta-analysis of 39 observational studies including 139,603 participants that investigated cardiovascular outcomes in those with PC-AKI demonstrated an increased risk of mortality, cardiovascular events, renal failure and prolonged hospitalization. (James, 2013) Baseline characteristics that simultaneously predispose to both mortality and PC-AKI were regarded as confounders. The reported incidence of end stage renal disease ranged from 0% to 0.2% in those without PC-AKI and from 0.2% to 4.5% in those with PC-AKI. In a more recent study consisting of 92,317 PCI procedures performed in 90,383 patients the incidence of PC-AKI was 2.3% and of renal replacement therapy 0.3%. (Kooiman, 2015) As expected patients developing PC-AKI had a greater burden of co-morbidity at baseline and were more likely to have adverse in-hospital outcomes. Using propensity-score based matching (1,371 patients with PC-AKI versus 5,484 patients without PC-AKI) in-hospital major adverse clinical outcomes (in-hospital mortality, cardiogenic shock, heart failure, stroke, bleeding and new requirement for dialysis post-PCI were considerably and significantly higher in AKI versus non-AKI patients and nearly one-third of the in-hospital mortality risk post PCI appeared to be attributable to AKI, demonstrating its clinical importance. (Kooiman, 2015)

 

In conclusion, the incidence of PC-AKI after intravenous or intra-arterial iodine-containing CM administration in general is low and directly related to the presence and severity of CKD prior to contrast administration and concomitant co-morbidities as demonstrated by propensity-score based matching analyses. The decline in renal function is mostly transient, but in rare instances renal replacement therapy is required with reported incidences of 0.06% after CE-CT and 0.2% to 0.6% post PCI. PC-AKI is a marker of poor outcomes, including increased short- and long-term mortality. Whether there is a causal relation between PC-AKI and poor outcomes remains unclear. However, reducing the incidence of PC-AKI in high risk patients (such as those undergoing emergent PCI, or with an eGFR <30 ml/min/1.73m2) by optimal risk stratification and preventive measures, remains a major goal in clinical practice.

 

Terminology of the routes of CM administration

A difference has been made in guidelines between intravenous and intra-arterial CM administration. Intravenous CM administration implies that the CM will reach the renal arteries after dilution by circulation through the right heart and pulmonary or a systemic vascular bed. The same applies to intra-arterial CM administration with second pass renal exposure administrations, that is: administration distal to the renal arteries and to CM administration after selective catheterisation of the suprarenal aortic side branches, e.g. injections via catheters in the carotid, subclavian, brachial, coronary and mesenteric arteries, except for the minimal back flow into the aorta of which only 20% will reach the renal arteries directly. In intra-arterial CM administration with first pass renal exposure the CM will reach the renal arteries without being diluted by a capillary bed, as is the case when the CM is injected via catheters in the left ventricle, thoracic aorta, suprarenal abdominal aorta, or selectively in the renal arteries.

 

Since this guideline only uses a single cut-off value of eGFR <30 ml/min/1.73m2 for preventive IV hydration, the distinction between IV or IA iodinated CM is largely theoretical and has no prevention consequences. Therefore, both IV and IA iodinated CM administration will be referred to by the general term “intravascular CM administration”.

 

References

American College of Radiology Manual on Contrast Media, v10.3. Reston, VA: American College of Radiology, 2017. Available at: https://www.acr.org/~/media/ACR/Documents/PDF/QualitySafety/Resources/Contrast-Manual/Contrast_Media.pdf

Aspelin P, Aubry P, Fransson SG, et al. Nephrotoxicity in High-Risk Patients Study of Iso-Osmolar and Low-Osmolar Non-Ionic Contrast Media Study Investigators. Nephrotoxic effects in high-risk patients undergoing angiography. N Engl J Med. 2003;348(6):491-9.

Bellomo R, Ronco C, Kellum JA, et al. Acute Dialysis Quality Initiative workgroup. Acute renal failure-definition, outcome measures, animal models, fluid therapy and information technology needs: the Second International Consensus Conference of the Acute Dialysis Quality Initiative (ADQI) Group. Crit Care. 2004;8(4):R204-12.

Bruce RJ, Djamali A, Shinki K, et al. Background fluctuation of kidney function versus contrast-induced nephrotoxicity. AJR Am J Roentgenol. 2009;192(3):711-8.

Budano C, Levis M, D'Amico M, et al. Impact of contrast-induced acute kidney injury definition on clinical outcomes. Am Heart J. 2011;161(5):963-71.

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(3):719-28.

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(3):719-28.

Dong M, Jiao Z, Liu T, et al. Effect of administration route on the renal safety of contrast agents: a meta-analysis of randomized controlled trials. J Nephrol. 2012;25(3):290-301.

Drüeke TB, Parfrey PS. Summary of the KDIGO guideline on anemia and comment: reading between the (guide) line (s). Kidney Int. 2012;82(9):952-60.

Endre ZH, Pickering JW. Outcome definitions in non-dialysis intervention and prevention trials in acute kidney injury (AKI). Nephrol, Dial Transplant. 2010;25(1):107-18.

Fliser D, Laville M, Covic A, et al. A European Renal Best Practice (ERBP) position statement on the Kidney Disease Improving Global Outcomes (KDIGO) clinical practice guidelines on acute kidney injury: part 1: definitions, conservative management and contrast-induced nephropathy. Nephrol Dial Transplant. 2012;27(12):4263-72.

Garfinkle, MA, Stewart S, Basi R. Incidence of CT contrast agent–induced nephropathy: toward a more accurate estimation. AJR Am J Roentgenol. 2015;204(6):1146-51

Gruberg L, Mintz GS, Mehran R, et al. The prognostic implications of further renal function deterioration within 48 h of interventional coronary procedures in patients with pre-existent chronic renal insufficiency. J Am Coll Cardiol. 2000;36(5):1542-8.

Guiterrez NV, Diaz A, Timmins GC, et al. Determinants of serum creatinine trajectory in acute contrast nephropathy. J Interv Cardiol 2002; 15(5): 349-54

Gupta R, Gurm HS, Bhatt DL, et al. Renal failure after percutaneous coronary intervention is associated with high mortality. Cathet Cardiovasc Intervent. 2005;64(4):442-8.

Jabara R, Gadesam RR, Pendyala LK, et al. Impact of the definition utilized on the rate of contrast-induced nephropathy in percutaneous coronary intervention. Am J Cardiol. 2009;103(12):1657-62.

James MT, Samuel SM, Manning MA, et al. Contrast-induced acute kidney injury and risk of adverse clinical outcomes after coronary angiography a systematic review and meta-analysis. Circulation: Cardiovasc Intervent. 2013;6(1):37-43.

Karlsberg RP, Dohad SY, Sheng R; Iodixanol Peripheral Computed Tomographic Angiography Study Investigator Panel. Contrast medium-induced acute kidney injury: comparison of intravenous and intra-arterial administration of iodinated contrast medium. J Vasc Interv Radiol. 2011 Aug;22(8):1159-65

Keeley EC, Grines CL. Scraping of aortic debris by coronary guiding catheters: a prospective evaluation of 1,000 cases. J Am Coll Cardiol. 1998;32(7):1861-5.

Kooiman J, Pasha SM, Zondag W, et al. Meta-analysis: serum creatinine changes following contrast enhanced CT imaging. Eur J Radiol. 2012 Oct;81(10):2554-61.

Kooiman J, Le Haen PA, Gezgin G, et al. Contrast-induced acute kidney injury and clinical outcomes after intra-arterial and intravenous contrast administration: risk comparison adjusted for patient characteristics by design. Am Heart J. 2013;165(5):793-99, 799.e1.

Kooiman J, Seth M, Nallamothu BK, et al. Association between acute kidney injury and in-hospital mortality in patients undergoing percutaneous coronary interventions. Circ Cardiovasc Interv. 2015;8(6):e002212.

Kooiman J. Risk and prevention of contrast-induced acute kidney injury. Thesis Leiden University, 2016.

Lakhal K, Ehrmann S, Chaari A, et al. Acute Kidney Injury Network definition of contrast-induced nephropathy in the critically ill: incidence and outcome. J Crit Care. 2011;26(6):593-9.

Levey AS, Eckardt KU, Tsukamoto Y, et al. Definition and classification of chronic kidney disease: a position statement from Kidney Disease: Improving Global Outcomes (KDIGO). Kidney Int. 2005;67(6):2089-100.

McCullough PA, Adam A, Becker CR, et al. Epidemiology and prognostic implications of contrast-induced nephropathy. Am J Cardiol 2006; 98 (Suppl): 5K-13K

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(1):65-73.

McDonald JS, Leake CB, McDonald RJ, Gulati R, Katzberg RW, Williamson EE, Kallmes DF. Acute kidney injury after intravenous versus intra-arterial contrast material administration in a paired cohort. Invest Radiol 2016; 51: 804-809

Mehran R, Nikolsky E. Contrast-induced nephropathy: definition, epidemiology, and patients at risk. Kidney Int. 2006;(100):S11-5.

Mehta RL, Kellum JA, Shah SV, et al. Acute Kidney Injury Network: report of an initiative to improve outcomes in acute kidney injury. Crit Care. 2007;11(2):R31.

Meinel FG, De Cecco CN, Schoepf UJ, et al. Contrast-induced acute kidney injury: definition, epidemiology, and outcome. Biomed Res Int. 2014;2014:859328.

Mitchell AM, Kline JA, Jones AE, et al. Major adverse events one year after acute kidney injury after contrast-enhanced computed tomography. Ann Emerg Med. 2015;66(3):267-274.e4.

Moos SI, van Vemde DN, Stoker J, et al. Contrast induced nephropathy in patients undergoing intravenous (IV) contrast enhanced computed tomography (CECT) and the relationship with risk factors: a meta-analysis. Eur J Radiol. 2013;82(9):e387-99.

Morcos SK, Thomsen HS, Webb JA. Contrast-media-induced nephrotoxicity: a consensus report. Eur Radiol. 1999;9(8):1602-13.

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(2):376-82.

Parsh J, Seth M, Briguori C, et al. The optimal definition of contrast-induced acute kidney injury for prediction of inpatient mortality in patients undergoing percutaneous coronary interventions. Am Heart J. 2016;175:160-7.

Pyxaras SA, Zhang Y, Wolf A, et al. Effect of varying definitions of contrast-induced acute kidney injury and left ventricular ejection fraction on one-year mortality in patients having transcatheter aortic valve implantation. Am J Cardiol. 2015;116(3):426-30.

Rear R, Bell RM, Hausenloy DJ. et al. Contrast-induced nephropathy following angiography and cardiac interventions. Heart. 2016;102(8):638-48.

Rihal CS, Textor SC, Grill DE, et al. Incidence and prognostic importance of acute renal failure after percutaneous coronary intervention. Circulation. 2002;105(19):2259-64.

Rosenbaum PR, Rubin RD. Reducing bias in observational studies using subclassification on the propensity score. J Am Stat Assoc. 1984(79):519-24.

Rudnick M, Feldman H. Contrast-induced nephropathy: what are the true clinical consequences? Clin J Am Soc Nephrol. 2008;3(1):263-72.

Thomas ME, Blaine C, Dawnay A, et al. The definition of acute kidney injury and its use in practice. Kidney Int. 2015;87(1):62-73.

Tong GE, Kumar S, Chong KC, et al. Risk of contrast-induced nephropathy for patients receiving intravenous vs. intra-arterial iodixanol administration. Abdom Radiol. 2016; 41: 91-9

Vavalle JP, van Diepen S, Clare RM, et al. Renal failure in patients with ST-segment elevation acute myocardial infarction treated with primary percutaneous coronary intervention: Predictors, clinical and angiographic features, and outcomes. Am Heart J. 2016;173:57-66.

Weisbord SD, Mor MK, Resnick AL, et al. Incidence and outcomes of contrast-induced AKI following computed tomography. Clin J Am Soc Nephrol. 2008. 2008;3(5):1274-81.

Wichmann JL, Katzberg RW, Litwin SE, et al. Contrast-Induced Nephropathy. Circulation. 2015;132(20):1931-6.

Onderbouwing

  1. American College of Radiology Manual on Contrast Media, v10.3. Reston, VA: American College of Radiology, 2017. Available at: https://www.acr.org/~/media/ACR/Documents/PDF/QualitySafety/Resources/Contrast-Manual/Contrast_Media.pdf
  2. Aspelin P, Aubry P, Fransson SG, et al. Nephrotoxicity in High-Risk Patients Study of Iso-Osmolar and Low-Osmolar Non-Ionic Contrast Media Study Investigators. Nephrotoxic effects in high-risk patients undergoing angiography. N Engl J Med. 2003;348(6):491-9.
  3. Bellomo R, Ronco C, Kellum JA, et al. Acute Dialysis Quality Initiative workgroup. Acute renal failure-definition, outcome measures, animal models, fluid therapy and information technology needs: the Second International Consensus Conference of the Acute Dialysis Quality Initiative (ADQI) Group. Crit Care. 2004;8(4):R204-12.
  4. Bruce RJ, Djamali A, Shinki K, et al. Background fluctuation of kidney function versus contrast-induced nephrotoxicity. AJR Am J Roentgenol. 2009;192(3):711-8.
  5. Budano C, Levis M, D'Amico M, et al. Impact of contrast-induced acute kidney injury definition on clinical outcomes. Am Heart J. 2011;161(5):963-71.
  6. 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(3):719-28.
  7. 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(3):719-28.
  8. Dong M, Jiao Z, Liu T, et al. Effect of administration route on the renal safety of contrast agents: a meta-analysis of randomized controlled trials. J Nephrol. 2012;25(3):290-301.
  9. Drüeke TB, Parfrey PS. Summary of the KDIGO guideline on anemia and comment: reading between the (guide) line (s). Kidney Int. 2012;82(9):952-60.
  10. Endre ZH, Pickering JW. Outcome definitions in non-dialysis intervention and prevention trials in acute kidney injury (AKI). Nephrol, Dial Transplant. 2010;25(1):107-18.
  11. Fliser D, Laville M, Covic A, et al. A European Renal Best Practice (ERBP) position statement on the Kidney Disease Improving Global Outcomes (KDIGO) clinical practice guidelines on acute kidney injury: part 1: definitions, conservative management and contrast-induced nephropathy. Nephrol Dial Transplant. 2012;27(12):4263-72.
  12. Garfinkle, MA, Stewart S, Basi R. Incidence of CT contrast agent–induced nephropathy: toward a more accurate estimation. AJR Am J Roentgenol. 2015;204(6):1146-51
  13. Gruberg L, Mintz GS, Mehran R, et al. The prognostic implications of further renal function deterioration within 48 h of interventional coronary procedures in patients with pre-existent chronic renal insufficiency. J Am Coll Cardiol. 2000;36(5):1542-8.
  14. Guiterrez NV, Diaz A, Timmins GC, et al. Determinants of serum creatinine trajectory in acute contrast nephropathy. J Interv Cardiol 2002; 15(5): 349-54
  15. Gupta R, Gurm HS, Bhatt DL, et al. Renal failure after percutaneous coronary intervention is associated with high mortality. Cathet Cardiovasc Intervent. 2005;64(4):442-8.
  16. Jabara R, Gadesam RR, Pendyala LK, et al. Impact of the definition utilized on the rate of contrast-induced nephropathy in percutaneous coronary intervention. Am J Cardiol. 2009;103(12):1657-62.
  17. James MT, Samuel SM, Manning MA, et al. Contrast-induced acute kidney injury and risk of adverse clinical outcomes after coronary angiography a systematic review and meta-analysis. Circulation: Cardiovasc Intervent. 2013;6(1):37-43.
  18. Karlsberg RP, Dohad SY, Sheng R; Iodixanol Peripheral Computed Tomographic Angiography Study Investigator Panel. Contrast medium-induced acute kidney injury: comparison of intravenous and intra-arterial administration of iodinated contrast medium. J Vasc Interv Radiol. 2011 Aug;22(8):1159-65
  19. Keeley EC, Grines CL. Scraping of aortic debris by coronary guiding catheters: a prospective evaluation of 1,000 cases. J Am Coll Cardiol. 1998;32(7):1861-5.
  20. Kooiman J, Pasha SM, Zondag W, et al. Meta-analysis: serum creatinine changes following contrast enhanced CT imaging. Eur J Radiol. 2012 Oct;81(10):2554-61.
  21. Kooiman J, Le Haen PA, Gezgin G, et al. Contrast-induced acute kidney injury and clinical outcomes after intra-arterial and intravenous contrast administration: risk comparison adjusted for patient characteristics by design. Am Heart J. 2013;165(5):793-99, 799.e1.
  22. Kooiman J, Seth M, Nallamothu BK, et al. Association between acute kidney injury and in-hospital mortality in patients undergoing percutaneous coronary interventions. Circ Cardiovasc Interv. 2015;8(6):e002212.
  23. Kooiman J. Risk and prevention of contrast-induced acute kidney injury. Thesis Leiden University, 2016.
  24. Lakhal K, Ehrmann S, Chaari A, et al. Acute Kidney Injury Network definition of contrast-induced nephropathy in the critically ill: incidence and outcome. J Crit Care. 2011;26(6):593-9.
  25. Levey AS, Eckardt KU, Tsukamoto Y, et al. Definition and classification of chronic kidney disease: a position statement from Kidney Disease: Improving Global Outcomes (KDIGO). Kidney Int. 2005;67(6):2089-100.
  26. McCullough PA, Adam A, Becker CR, et al. Epidemiology and prognostic implications of contrast-induced nephropathy. Am J Cardiol 2006; 98 (Suppl): 5K-13K
  27. 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(1):65-73.
  28. McDonald JS, Leake CB, McDonald RJ, Gulati R, Katzberg RW, Williamson EE, Kallmes DF. Acute kidney injury after intravenous versus intra-arterial contrast material administration in a paired cohort. Invest Radiol 2016; 51: 804-809
  29. Mehran R, Nikolsky E. Contrast-induced nephropathy: definition, epidemiology, and patients at risk. Kidney Int. 2006;(100):S11-5.
  30. Mehta RL, Kellum JA, Shah SV, et al. Acute Kidney Injury Network: report of an initiative to improve outcomes in acute kidney injury. Crit Care. 2007;11(2):R31.
  31. Meinel FG, De Cecco CN, Schoepf UJ, et al. Contrast-induced acute kidney injury: definition, epidemiology, and outcome. Biomed Res Int. 2014;2014:859328.
  32. Kline JA, Jones AE, et al. Major adverse events one year after acute kidney injury after contrast-enhanced computed tomography. Ann Emerg Med. 2015;66(3):267-274.e4.
  33. Moos SI, van Vemde DN, Stoker J, et al. Contrast induced nephropathy in patients undergoing intravenous (IV) contrast enhanced computed tomography (CECT) and the relationship with risk factors: a meta-analysis. Eur J Radiol. 2013;82(9):e387-99.
  34. Morcos SK, Thomsen HS, Webb JA. Contrast-media-induced nephrotoxicity: a consensus report. Eur Radiol. 1999;9(8):1602-13.
  35. 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(2):376-82.
  36. Parsh J, Seth M, Briguori C, et al. The optimal definition of contrast-induced acute kidney injury for prediction of inpatient mortality in patients undergoing percutaneous coronary interventions. Am Heart J. 2016;175:160-7.
  37. Pyxaras SA, Zhang Y, Wolf A, et al. Effect of varying definitions of contrast-induced acute kidney injury and left ventricular ejection fraction on one-year mortality in patients having transcatheter aortic valve implantation. Am J Cardiol. 2015;116(3):426-30.
  38. Rear R, Bell RM, Hausenloy DJ. et al. Contrast-induced nephropathy following angiography and cardiac interventions. Heart. 2016;102(8):638-48.
  39. Rihal CS, Textor SC, Grill DE, et al. Incidence and prognostic importance of acute renal failure after percutaneous coronary intervention. Circulation. 2002;105(19):2259-64.
  40. Rosenbaum PR, Rubin RD. Reducing bias in observational studies using subclassi?cation on the propensity score. J Am Stat Assoc. 1984(79):519-24.
  41. Rudnick M, Feldman H. Contrast-induced nephropathy: what are the true clinical consequences? Clin J Am Soc Nephrol. 2008;3(1):263-72.
  42. Thomas ME, Blaine C, Dawnay A, et al. The definition of acute kidney injury and its use in practice. Kidney Int. 2015;87(1):62-73.
  43. Tong GE, Kumar S, Chong KC, et al. Risk of contrast-induced nephropathy for patients receiving intravenous vs. intra-arterial iodixanol administration. Abdom Radiol. 2016; 41: 91-9
  44. Vavalle JP, van Diepen S, Clare RM, et al. Renal failure in patients with ST-segment elevation acute myocardial infarction treated with primary percutaneous coronary intervention: Predictors, clinical and angiographic features, and outcomes. Am Heart J. 2016;173:57-66.
  45. Weisbord SD, Mor MK, Resnick AL, et al. Incidence and outcomes of contrast-induced AKI following computed tomography. Clin J Am Soc Nephrol. 2008. 2008;3(5):1274-81.
  46. Wichmann JL, Katzberg RW, Litwin SE, et al. Contrast-Induced Nephropathy. Circulation. 2015;132(20):1931-6.

Autorisatiedatum en geldigheid

Laatst beoordeeld  : 01-07-2017

Laatst geautoriseerd  : 01-07-2017

Geplande herbeoordeling  :

Validity

The board of the Radiological Society of the Netherlands will determine at the latest in 2023 if this guideline (per module) is still valid and applicable. If necessary, a new working group will be formed to revise the guideline. The validity of a guideline can be shorter than 5 years, if new scientific or healthcare structure developments arise, that could be seen as a reason to commence revisions. The Radiological Society of the Netherlands is considered the keeper of this guideline and thus primarily responsible for the actuality of the guideline. The other scientific societies that have participated in the guideline development share the responsibility to inform the primarily responsible scientific society about relevant developments in their field.

 

Initiative

Radiological Society of the Netherlands

 

Authorization

  • The guideline is submitted for authorization to:
  • Association of Surgeons of the Netherlands
  • Dutch Association of Urology
  • Dutch Federation of Nephrology
  • Dutch Society Medical Imaging and Radiotherapy
  • Dutch Society of Intensive Care
  • Netherlands Association of Internal Medicine
  • Netherlands Society for Clinical Chemistry and Laboratory Medicine
  • Netherlands Society of Cardiology
  • Netherlands Society of Emergency Physicians
  • -Radiological Society of the Netherlands

Initiatief en autorisatie

Initiatief:
  • Nederlandse Vereniging voor Radiologie
Geautoriseerd door:
  • Nederlandse Internisten Vereniging
  • Nederlandse Vereniging van Spoedeisende Hulp Artsen
  • Nederlandse Vereniging voor Cardiologie
  • Nederlandse Vereniging voor Heelkunde
  • Nederlandse Vereniging voor Radiologie
  • Nederlandse Vereniging voor Urologie
  • Nederlandse Vereniging voor Klinische Chemie en Laboratoriumgeneeskunde
  • Nederlandse Vereniging voor Intensive Care
  • Nederlandse Vereniging Medische Beeldvorming en Radiotherapie
  • Nederlandse Federatie voor Nefrologie

Algemene gegevens

General Information

The guideline development was assisted by the Knowledge Institute of Medical Specialists (https://www.kennisinstituut.nl) and was financed by the Quality Funds for Medical Specialists (Kwaliteitsgelden Medisch Specialisten: SKMS).

Samenstelling werkgroep

Working group members

A multidisciplinary working group was formed for the development of the guideline in 2014. The working group consisted of representatives from all relevant medical specialization fields that are involved with intravascular contrast administration.

 

All working group members have been officially delegated for participation in the working group by their scientific societies. The working group has developed a guideline in the period from October 2014 until July 2017.

 

The working group is responsible for the complete text of this guideline.

 

Working group

Cobbaert C., clinical chemist, Leiden University Medical Centre (member of advisory board from September 2015)

Danse P., interventional cardiologist, Rijnstate Hospital, Arnhem

Dekker H.M., radiologist, Radboud University Medical Centre, Nijmegen

Geenen R.W.F., radiologist, Noordwest Ziekenhuisgroep (NWZ), Alkmaar/Den Helder

Hoogeveen E.K., nephrologist, Jeroen Bosch Hospital, ‘s-Hertogenbosch

Kooiman J., research physician, Leiden University Medical Centre, Leiden

Oudemans - van Straaten H.M., internist-intensive care specialist, Free University Medical Centre, Amsterdam

Pels Rijcken T.H., interventional radiologist, Tergooi, Hilversum

Sijpkens Y.W.J., nephrologist, Haaglanden Medical Centre, The Hague

Vainas T., vascular surgeon, University Medical Centre Groningen (until September 2015)

van den Meiracker A.H., internist-vascular medicine, Erasmus Medical Centre, Rotterdam

van der Molen A.J., radiologist, Leiden University Medical Centre, Leiden (chairman)

Wikkeling O.R.M., vascular surgeon, Heelkunde Friesland Groep, location: Nij Smellinghe Hospital, Drachten (from September 2015)

 

Advisory board

Demir A.Y., clinical chemist, Meander Medical Center, Amersfoort, (member of working group until September 2015)

Hubbers R., patient representative, Dutch Kidney Patient Association

Mazel J., urologist, Spaarne Gasthuis, Haarlem

Moos S., resident in Radiology, HAGA Hospital, The Hague

Prantl K., Coordinator Quality & Research, Dutch Kidney Patient Association

van den Wijngaard J., resident in Clinical Chemistry, Leiden University Medical Center

 

Methodological support

Boschman J., advisor, Knowledge Institute of Medical Specialists (from May 2017)

Burger K., senior advisor, Knowledge Institute of Medical Specialists (until March 2015)

Harmsen W., advisor, Knowledge Institute of Medical Specialists (from May 2017)

Mostovaya I.M., advisor, Knowledge Institute of Medical Specialists

Persoon S., advisor, Knowledge Institute of Medical Specialists (March 2016 – September 2016)

van Enst A., senior advisor, Knowledge Institute of Medical Specialists (from January 2017)

Belangenverklaringen

Conflicts of interest

The working group members have provided written statements about (financially supported) relations with commercial companies, organisations or institutions that are related to the subject matter of the guideline. Furthermore, inquiries have been made regarding personal financial interests, interests due to personal relationships, interests related to reputation management, interest related to externally financed research and interests related to knowledge valorisation. The statements on conflict of interest can be requested at the administrative office of the Knowledge Institute of Medical Specialists and are summarised below.

 

Member

Function

Other offices

Personal financial interests

Personal relationships

Reputation management

Externally financed research

Knowledge-valorisation

Other potential conflicts of interest

Signed

Workgroup

Burger

Advisor, Knowledge Institute of Medical Specialists

None

None

None

None

None

None

None

Yes

Cobbaert

Member, physician clinical chemistry

Head of clinical chemistry department in Leiden LUMC.

Tutor for post-academic training of clinical chemists, coordinator/host for the Leiden region

Member of several working groups within the Dutch Society for Clinical Chemistry and member of several international working groups for clinical chemistry

None

None

Member of several working groups within the Dutch Society for Clinical Chemistry and member of several international working groups for clinical chemistry

None

None

None

Yes

Danse

Member, cardiologist

Board member committee of Quality, Dutch society for Cardiology (unpaid)

Board member Conference committee DRES (unpaid)

None

None

None

None

None

None

Yes

Dekker

Member, radiologist

None

None

None

None

None

None

None

Yes

Geenen

Member, radiologist

Member Contrast Media Safety Committee of the European Society of Urogenital Radiology (unpaid, meetings are partially funded by CM industry)))

None

None

None

None

None

Has been a public speaker during symposia organised by GE Healthcare about contrast agents (most recently in June 2014)

Yes

Hoogeveen

Member, nephrologist

Member of Guideline Committee of Dutch Federation of Nephrology

None

None

Member of Guideline Committee of Dutch Society for Nephrology

Grant from the Dutch Kidney Foundation to study effect of  fish oil on kidney function in post-MI patients

None

None

Yes

Kooiman

Member, research physician

Resident in department of gynaecology & obstetrics

None

None

None

None

None

None

Yes

Mostovaya

Advisor, Knowledge Institute of Medical Specialists

None

None

None

None

None

None

None

Yes

Oudemans – van Straaten

Member, intensive care medical specialist

Professor Intensive Care

none

None

None

None

None

None

None

Yes

Pels Rijcken

Member, interventional radiologist

None

None

None

None

None

None

None

Yes

Sijpkens

Member, nephrologist

None

None

None

None

None

None

None

Yes

Vainas

Member, vascular surgeon

None

None

None

None

None

None

None

Yes

Van den Meiracker

Member, internist vascular medicine

None

None

None

None

None

None

None

Yes

Van der Molen

Chairman, radiologist

Member Contrast Media Safety Committee of the European Society of Urogenital Radiology (unpaid,CMSC meetings are partially funded by CM industry))

None

None

Secretary section of Abdominal Radiology; Radiological Society of the Netherlands (until spring of 2015)

None

None

Receives Royalties for books: Contrast Media Safety, ESUR guidelines, 3rd ed. Springer, 2015

Received speaker fees for lectures on CM safety by GE Healthcare, Guerbet, Bayer Healthcare and Bracco Imaging (2015-2016)

Yes

Wikkeling

Member, vascular surgeon

None

None

None

None

None

None

None

Yes

Advisory Board

Demir

Member, physician clinical chemistry

None

None

None

None

None

None

None

Yes

Hubbers

Member, patient’s representative, Dutch Society of Kidney Patients

None

None

None

None

None

None

None

Yes

Mazel

Member, urologist

None

None

None

None

None

None

None

Yes

Prantl

Member, policy maker, Dutch Society of Kidney Patients

None

None

None

None

None

None

None

Yes

Van den Wijngaard

Member, resident clinical chemistry

Reviewer for several journals (such as American Journal of Physiology)

None

None

None

None

None

None

Yes

Inbreng patiëntenperspectief

Input of patient’s perspective

Patients’ perspective was represented, firstly by membership and involvement in the advisory board of a policy maker and a patients’ representative from the Dutch Kidney Patient Association. Furthermore, an online survey was organized by the Dutch Kidney Patient Association about the subject matter of the guideline. A summary of the results of this survey has been discussed during a working group meeting at the beginning of the guideline development process. Subjects that were deemed relevant by patients were included in the outline of the guideline. The concept guideline has also been submitted for feedback during the comment process to the Dutch Patient and Consumer Federation, who have reported their feedback through the Dutch Kidney Patient Association.

Implementatie

Implementation

In the different phases of guideline development, the implementation of the guideline and the practical enforceability of the guideline were taken into account. The factors that could facilitate or hinder the introduction of the guideline in clinical practice have been explicitly considered. The implementation plan can be found with the Related Products. Furthermore, quality indicators were developed to enhance the implementation of the guideline. The indicators can also be found with the Related Products.

Werkwijze

Methodology

 

AGREE

This guideline has been developed conforming to the requirements of the report of Guidelines for Medical Specialists 2.0; the advisory committee of the Quality Counsel (www.kwaliteitskoepel.nl). This report is based on the AGREE II instrument (Appraisal of Guidelines for Research & Evaluation II) (www.agreetrust.org), a broadly accepted instrument in the international community and on the national quality standards for guidelines: “Guidelines for guidelines” (www.zorginstituutnederland.nl).

 

Identification of subject matter

During the initial phase of the guideline development, the chairman, working group and the advisor inventory the relevant subject matter for the guideline. Furthermore, an Invitational Conference was organized, where additional relevant subjects were suggested by the Dutch Kidney Patient Association, Dutch Society for Emergency Physicians, and Dutch Society for Urology. A report of this meeting can be found in Related Products.

 

Clinical questions and outcomes

During the initial phase of guideline development, the chairman, working group and advisor identified relevant subject matter for the guideline. Furthermore, input was acquired for the outline of the guideline during an Invitational Conference. The working group then formulated definitive clinical questions and defined relevant outcome measures (both beneficial land harmful effects). The working group rated the outcome measures as critical, important and not important. Furthermore, where applicable, the working group defined relevant clinical differences.

 

Strategy for search and selection of literature

For the separate clinical questions, specific search terms were formulated and published scientific articles were sought after in (several) electronic databases. Furthermore, studies were looked for by cross-referencing other included studies. The studies with potentially the highest quality of research were looked for first. The working group members selected literature in pairs (independently of each other) based on title and abstract. A second selection was performed based on full text. The databases search terms and selection criteria are described in the modules containing the clinical questions.

 

Quality assessment of individual studies

Individual studies were systematically assessed, based on methodological quality criteria that were determined prior to the search, so that risk of bias could be estimated. This is described in the “risk of bias” tables.

 

Summary of literature

The relevant research findings of all selected articles are shown in evidence tables. The most important findings in literature are described in literature summaries. When there were enough similarities between studies, the study data were pooled.

 

Grading the strength of scientific evidence

 

A)           For intervention questions

The strength of the conclusions of the scientific publications was determined using the GRADE-method. GRADE stands for Grading Recommendations Assessment, Development and Evaluation (see http://www.gradeworkinggroup.org/) (Atkins, 2004).

 

GRADE defines four gradations for the quality of scientific evidence: high, moderate, low or very low. These gradations provide information about the amount of certainty about the literature conclusions. (http://www.guidelinedevelopment.org/handbook/).

 

B)           For diagnostic, etiological, prognostic or adverse effect questions

The GRADE-methodology cannot (yet) be applied. The quality of evidence of the conclusion is determined by the EBRO method (van Everdingen, 2004).

 

Formulating conclusion

For diagnostic, etiological, prognostic or adverse effect questions, the evidence was summarized in one or more conclusions, and the level of the most relevant evidence was reported. For intervention questions, the conclusion was drawn based on the body of evidence (not one or several articles). The working groups weighed the beneficial and harmful effects of the intervention.

 

Considerations

Aspects such as expertise of working group members, patient preferences, costs, availability of facilities, and organization of healthcare aspects are important to consider when formulating a recommendation. These aspects were discussed in the paragraph Considerations.

 

Formulating recommendations

The recommendations answer the clinical question and were based on the available scientific evidence and the most relevant considerations.

 

Constraints (organization of healthcare)

During the development of the outline of the guideline and the rest of the guideline development process, the organization of healthcare was explicitly taken into account. Constraints that were relevant for certain clinical questions were discussed in the Consideration paragraphs of those clinical questions. The comprehensive and additional aspects of the organization of healthcare were discussed in a separate chapter.

 

Development of quality indicators

Internal (meant for use by scientific society or its members) quality indicators are developed simultaneously with the guideline. Furthermore, existing indicators on this subject were critically appraised; and the working group produces an advice about such indicators. Additional information on the development of quality indicators is available by contacting the Knowledge Institute for Medical Specialists. (secretariaat@kennisinstituut.nl).

 

Knowledge Gaps

During the development of the guideline, a systematic literature search was performed the results of which help to answer the clinical questions. For each clinical question the working group determined if additional scientific research on this subject was desirable. An overview of recommendations for further research is available in the appendix Knowledge Gaps.

 

Comment- and authorisation phase

The concept guideline was subjected to commentaries by the involved scientific societies. The commentaries were collected and discussed with the working group. The feedback was used to improve the guideline; afterwards the working group made the guideline definitive. The final version of the guideline was offered for authorization to the involved scientific societies, and was authorized.

 

References

Atkins D, Eccles M, Flottorp S, et al. GRADE Working Group. Systems for grading the quality of evidence and the strength of recommendations I: critical appraisal of existing approaches The GRADE Working Group. BMC Health Serv Res. 2004 Dec 22;4(1):38.

Van Everdingen JJE, Burgers JS, Assendelft WJJ, et al. Evidence-based richtlijnontwikkeling. Bohn Stafleu van Loghum. Houten, 2004

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