Advertisement

European Radiology

, Volume 28, Issue 7, pp 2856–2869 | Cite as

Post-contrast acute kidney injury. Part 2: risk stratification, role of hydration and other prophylactic measures, patients taking metformin and chronic dialysis patients

Recommendations for updated ESUR Contrast Medium Safety Committee guidelines
  • Aart J. van der Molen
  • Peter Reimer
  • Ilona A. Dekkers
  • Georg Bongartz
  • Marie-France Bellin
  • Michele Bertolotto
  • Olivier Clement
  • Gertraud Heinz-Peer
  • Fulvio Stacul
  • Judith A. W. Webb
  • Henrik S. Thomsen
Open Access
Contrast Media

Abstract

Objectives

The Contrast Media Safety Committee (CMSC) of the European Society of Urogenital Radiology (ESUR) has updated its 2011 guidelines on the prevention of post-contrast acute kidney injury (PC-AKI). The results of the literature review and the recommendations based on it, which were used to prepare the new guidelines, are presented in two papers.

Areas covered in part 2

Topics reviewed include stratification of PC-AKI risk, the need to withdraw nephrotoxic medication, PC-AKI prophylaxis with hydration or drugs, the use of metformin in diabetic patients receiving contrast medium and the need to alter dialysis schedules in patients receiving contrast medium.

Key points

• In CKD, hydration reduces the PC-AKI risk

• Intravenous normal saline and intravenous sodium bicarbonate provide equally effective prophylaxis

• No drugs have been consistently shown to reduce the risk of PC-AKI

• Stop metformin from the time of contrast medium administration if eGFR < 30 ml/min/1.73 m 2

• Dialysis schedules need not change when intravascular contrast medium is given

Keywords

Contrast media Acute kidney injury Metformin Haemodialysis Practice guidelines 

Abbreviations and acronyms

ACEI

Angiotensin Converting Enzyme Inhibitor

ACR

American College of Radiology

AGREE

Appraisal of Guidelines for Research and Evaluation

AHRQ

Agency for Healthcare Research and Quality

AKI

Acute Kidney Injury

ARB

Angiotensin-II Receptor Blocker

CA

Coronary Angiography

CI-AKI

Contrast-Induced Acute Kidney Injury

CIN

Contrast-Induced Nephropathy

CKD

Chronic Kidney Disease

CM

Contrast Media

CMSC

Contrast Media Safety Committee

CT

Computed Tomography

CTPA

Computed Tomography Pulmonary Angiography

D5W

Dextrose 5% in Water

eGFR

Estimated Glomerular Filtration Rate

ESUR

European Society of Urogenital Radiology

FDA

Federal Drugs Administration

GFR

Glomerular Filtration Rate

HD

Haemodialysis

HF

Haemofiltration

IA

Intra-Arterial

IV

Intravenous

NAc

N-Acetylcysteine

NaHCO3

Sodium Bicarbonate

NSAID

Non-Steroidal Anti-Inflammatory Drug

NYHA

New York Heart Association

OCEBM

Oxford Centre for Evidence Based Medicine

PC-AKI

Post-Contrast Acute Kidney Injury

PCI

Percutaneous Coronary Intervention

PICO

Patient–Intervention–Comparator–Outcome

PS

Propensity Score

RAAS

Renin–Angiotensin–Aldosterone System

RSTN

Radiological Society of the Netherlands

RCT

Randomised Controlled Trial

RRT

Renal Replacement Therapy

sCr

Serum Creatinine

WG

Writing Group

Introduction

The Contrast Media Safety Committee (CMSC) of the European Society of Urogenital Radiology (ESUR) produced their most recent guidelines on what was then termed contrast-induced nephropathy (CIN) in 2011 [1]. Guidelines on the use of contrast media (CM) in patients on dialysis and on the use of CM in diabetic patients using metformin were published in 2002 and 2014 [2, 3]. This review provides recommendations for updating the CMSC guidelines which were obtained using a structured literature review based on clinical questions and Patient–Intervention–Comparator–Outcome (PICO) formatting. Since the literature related to the topics considered is so large, the results of the review have been split into two papers. The review only considers post-contrast kidney injury (PC-AKI) after iodine-based CM because acute kidney injury is not associated with gadolinium-based contrast agents in doses approved for clinical magnetic resonance imaging.

In this second paper on PC-AKI, the following topics related to patient management are considered:
  1. 1.

    The role of questionnaires and risk scores to identify at-risk patients with reduced renal function

     
  2. 2.

    The need to stop nephrotoxic medication before giving CM

     
  3. 3.

    The optimal hydration protocols for protecting against PC-AKI

     
  4. 4.

    The possible role of prophylactic drug treatment in preventing PC-AKI

     
  5. 5.

    The need to adapt metformin administration when giving CM

     
  6. 6.

    The need to alter schedules for dialysis in the period before and after CM administration

     

Recommendations are made for items 1–6. The recommendations have been incorporated into version 10 of the ESUR CMSC guidelines, at the end of this paper (Table 4).

Materials and methods

The recommendations were prepared using the Appraisal of Guidelines for Research and Evaluation (AGREE) II document [4]. A guideline Writing Group (WG) prepared ten clinical questions in PICO format [5]. Systematic search strings were developed with a professional librarian for four different biomedical literature databases (PubMed, Web of Science, Embase and the Cochrane Library). The titles and abstracts were screened for relevance and selected on predefined inclusion and exclusion criteria. Emphasis was put on comparative studies with strong scientific evidence, such as meta-analyses and systematic reviews, and prospective randomised controlled trials (RCTs). The six systematic searches in this manuscript yielded 3402 references of which 445 were selected on the basis of title and abstract. After review of the full text of these 445 publications, 145 were selected for inclusion in this paper. The quality of the evidence from the selected articles was evaluated according to the Oxford Centre for Evidence Based Medicine levels of evidence: grade A, established scientific evidence; grade B, scientific presumption; grade C, low level of evidence [6]. When there was no scientific evidence, recommendations were based on WG consensus and were graded as expert opinion (grade D).

The full description of the materials and methods appears in part 1.

The term intra-arterial injection with first pass renal exposure indicates that contrast medium reaches the kidneys in a relatively undiluted form, e.g. injection into the left heart, thoracic and suprarenal abdominal aorta or the renal arteries. The term intra-arterial injection with second pass renal exposure indicates that contrast medium reaches the renal arteries after dilution either in the pulmonary or peripheral circulation, e.g. injection into the right heart, pulmonary artery, carotid, subclavian, coronary, mesenteric or infrarenal arteries.

Results

Question 5: Should questionnaires or scoring systems be used for risk stratification by clinicians when they request a contrast-enhanced imaging study?

Patient questionnaires

Questionnaires, such as that proposed by Choyke [7], use information about a history of renal disease or renal surgery, heart failure, diabetes, proteinuria, hypertension and gout to stratify patients for their PC-AKI risk so that sCr measurements need only be done selectively. This may work well and can save resources [8]. Observational studies have shown that these questionnaires can identify patients with eGFR < 45 ml/min/1.73 m2 with adequate sensitivity, especially if they are aged less than 70 [9, 10, 11]. Since eGFR measurement can detect more patients with renal dysfunction than questionnaires [12], with easier patient logistics and similar cost-effectiveness [13, 14], many hospitals have adopted a policy of sCr measurements in all patients scheduled for intravenous (IV) CM and no longer use questionnaires for risk stratification or selection for eGFR measurement (Table 1).
Table 1

PC-AKI: Risk stratification; use of nephrotoxic medication

Risk stratification

In hospitals which use sCr measurements for all patients before intravascular CM administration there is no benefit in using questionnaires for PC-AKI risk stratification.

In hospitals which use sCr measurements selectively, Choyke questionnaires may be used to identify patients with eGFR < 45 ml/min/1.73 m2 before intra-arterial CM administration with first pass renal exposure.

Level of evidence D

Risk prediction scores are only available for coronary angiography and/or percutaneous coronary intervention, and have only modest abilities, so cannot be recommended to stratify the risk of PC-AKI.

Level of evidence A

Nephrotoxic medication

In CKD patients receiving CM, optimal nephrologic care involves minimising the use of nephrotoxic drugs.

Level of evidence D

ACE inhibitors and angiotensin receptor blockers do not have to be stopped before CM administration.

Level of evidence B

There is insufficient evidence to recommend withholding nephrotoxic drugs such as NSAIDs, antimicrobial agents or chemotherapeutic agents before CM administration.

Level of evidence C

Risk prediction models

No risk models have been produced yet for IV or IA CM administration with second pass renal exposure. For patients having coronary angiography (CA) or percutaneous coronary intervention (PCI), many different risk scores have been proposed to stratify the patient’s PC-AKI risk, and most include pre-procedural and procedural data. A model with only pre-procedural data [15] would be more practical for selecting suitable preventive measures. Risk scores should be verified in relation to improvements in clinical outcome. In clinical practice, a prediction rule would require a high discriminatory value, i.e. a C-statistic greater than 0.80 [16].

The best-known risk model is the eight-variable Mehran score [17], which has been studied in more than 15,000 patients and has been externally validated in multiple studies, but with variable C-statistic values of 0.57–0.85 [16, 18, 19, 20]. The Mehran score correlates relatively well with clinical outcomes [21]. Newer risk scores with good discriminatory value, available in user-friendly calculators or smartphone applications, still need external validation [22]. A recent systematic review of 16 risk models concluded that they had only modest predictive value [23] and a review and meta-analysis of 74 risk models noted their heterogeneity and concluded that further research was needed to evaluate the effect of such models on clinical care [24] (Table 1).

Question 6: Should nephrotoxic medication be withheld to reduce the risk of PC-AKI?

Optimal nephrologic care involves minimizing the use of nephrotoxic drugs where clinically possible [25]. Many frequently prescribed medications, such as nonselective NSAIDs, selective Cox-2 inhibitors, several classes of antimicrobial agents and chemotherapeutic agents have nephrotoxic potential and can induce AKI [26].

There is little good quality data about the relationship between these drugs and PC-AKI [27]. A retrospective cohort study showed that concurrent use of four or more nephrotoxic agents was significantly predictive for PC-AKI in patients given IV CM [28]. A meta-analysis of PC-AKI incidence following CM-enhanced CT found that concurrent administration of NSAIDs was an independent risk factor for PC-AKI [29].

The effect of withholding angiotensin converting enzyme inhibitors (ACEI) and angiotensin-2 receptor blockers (ARB) in chronic users has been extensively evaluated. Multiple RCTs [30, 31] and observational studies gave conflicting results and are limited by small sample sizes and significant heterogeneity [32, 33, 34]. However, meta-analyses of RCTs found no lower risk [34]. Withholding ACEI/ARB may be associated with a slightly lower risk of PC-AKI but the evidence is not sufficiently strong to recommend this (Table 1).

Question 7: What are the most cost- and time-effective protocols for oral and intravenous hydration to reduce the risk of PC-AKI?

Hydration as a preventive strategy for PC-AKI

Evidence for prevention of PC-AKI with IV saline hydration (volume expansion) comes from RCTs in patients who received intra-arterial (IA) CM during percutaneous intervention [35, 36, 37], and in patients who received bicarbonate hydration before IV enhanced emergency CTPA [38]. One RCT evaluated the evidence for IA CM administration during CA [39]. These studies found that, for both IA and IV CM administration, the incidence of PC-AKI was significantly lower in patients who received IV hydration compared to placebo, and that hydration prevented emergency dialysis [36]. Significant differences for mortality or other adverse events were not found. There were few patients with severe renal impairment (eGFR < 30 ml/min/1.73 m2) in almost all studies. The recent AMACING trial showed that for patients with eGFR > 30 ml/min/1.73 m2 receiving IV CM there was no difference between no hydration and hydration in preventing PC-AKI [40].

Oral hydration versus intravenous saline hydration

Oral intake of clear fluids by patients as an alternative to IV saline to prevent PC-AKI is difficult to monitor or control. Nine studies evaluated oral hydration, but were limited by small patient numbers and by the absence of patients with severe renal impairment [39, 41, 42, 43, 44, 45, 46, 47, 48]. Three meta-analyses concluded that there is no evidence that oral hydration is associated with more risk of PC-AKI compared to IV hydration, but the studies were limited by heterogeneity and lack of hard clinical outcomes [49, 50, 51]. The CMSC does not recommend the use of oral hydration as the sole preventive strategy for PC-AKI, but unrestricted intake of clear oral fluids in addition to IV volume expansion is supported (Table 2).
Table 2

PC-AKI prophylaxis: Hydration, drugs, renal replacement therapy

Hydration

Preventive hydration should be used to reduce the incidence of PC-AKI in at-risk patients.

Level of evidence B

Intravenous saline and bicarbonate protocols have similar efficacy for hydration.

Level of evidence A

For intravenous and intra-arterial CM administration with second pass renal exposure hydrate the patient with either (a) 3 ml/kg/h bicarbonate 1.4% (or 154 mmol/l solution) for 1 h before CM or (b) 1 ml/kg/h saline 0.9% for 3–4 h before and 4–6 h after CM.

Level of evidence D

For intra-arterial CM administration with first pass renal exposure hydrate the patient with either (a) 3 ml/kg/h bicarbonate 1.4% (or 154 mmol/l solution) for 1 h before CM followed by 1 ml/kg/h bicarbonate 1.4% (or 154 mmol/l) for 4–6 h after CM

or (b) 1 ml/kg/h saline 0.9% for 3–4 h before and 4–6 h after CM.

Level of evidence D

Oral hydration as the sole means of prevention is not recommended.

Level of evidence D

In patients with severe heart failure (NYHA grade 3–4) or patients with end-stage renal failure (CKD grade V) preventive IV hydration should be individualized by the clinician responsible for patient care.

Level of evidence D

Drugs

N-Acetylcysteine has not been conclusively shown to reduce the risk of PC-AKI in patients with eGFR < 45 ml/min/1.73 m2 receiving intravenous or intra-arterial CM, and its use is NOT recommended.

Level of evidence A

Giving short-term, high-dose statins to patients not already taking statins has not been shown to reduce the risk of PC-AKI in patients with eGFR < 45 ml/min/1.73 m2 receiving intravenous or intra-arterial CM, and its use is NOT recommended.

Level of evidence B

ACE inhibitors or angiotensin receptor blockers have not been shown conclusively to reduce the risk of PC-AKI in patients receiving intravenous or intra-arterial CM, and their use is NOT recommended.

Level of evidence B

Vitamin C has not been shown conclusively to reduce the risk of PC-AKI in patients receiving intravenous or intra-arterial CM, and its use is NOT recommended.

Level of evidence B

Renal replacement therapy

Renal replacement therapy has not been shown conclusively to reduce the risk of PC-AKI in patients receiving intravenous or intra-arterial CM, and its use is NOT recommended.

Level of evidence B

Intravenous hydration: saline versus bicarbonate

Normal saline (NaCl 0.9%) and sodium bicarbonate solution (1.4% or 154 mmol NaHCO3 in D5W) are the two most commonly studied crystalloid solutions. The rationale for using bicarbonate is that alkalinisation can reduce the formation of free reactive oxygen species [52]. Initial studies favoured bicarbonate [53, 54, 55, 56], but this was not replicated in later studies [57, 58, 59, 60, 61, 62], so IV hydration with bicarbonate can be considered equivalent to normal saline.

There is no consensus on the optimal hydration regime. Most studies have compared bicarbonate given pre- and post-CM for less than 6 h [53] to longer duration saline pre- and post-CM protocols (12–24 h). In all studies, there are few patients with eGFR < 30 ml/min/1.73 m2, and evidence about whether short duration bicarbonate is better than long duration saline is conflicting [63, 64, 65, 66, 67, 68, 69, 70, 71]. There is limited evidence on whether pre-hydration only is inferior to pre- and post-hydration, and only one very short duration bicarbonate protocol has been evaluated [38, 72, 73].

Most studies have been performed in cardiac patients admitted for CA or PCI. Three studies evaluated hydration protocols in patients having contrast-enhanced CT, and did not favour bicarbonate over saline [38, 72, 74]. No studies were identified assessing the beneficial effect of other crystalloids. However, balanced crystalloid solutions, such as Ringer’s lactate, may be preferable in critical care populations, because they avoid the harmful effects of hyperchloraemic acidosis.

The CMSC considers that for IV and IA CM injection with second pass renal exposure either a short bicarbonate hydration regime before CM or a conventional protocol with saline given before and after CM may be used. For IA CM injection with first pass renal exposure conventional protocols with either bicarbonate or saline given before and after CM should be used (Table 2).

Forced diuresis versus conventional hydration

Newer approaches for patients with impaired left ventricular function combine controlled saline hydration with a forced high urinary flow rate to maintain euvolemia and avoid overhydration and several RCTs showed better results than conventional hydration protocols [75, 76, 77]. Other catheter-based strategies used left ventricular end-diastolic pressure or central venous pressure to guide hydration [78, 79]. In these RCTs the incidence of PC-AKI was lower than with standard IV hydration. Since the forced diuresis studies have heterogeneous populations, interventions and control hydration protocols, their findings cannot be pooled. The CMSC considers that there is not sufficient evidence to recommend forced diuresis.

In which patients should the hydration protocol be individualized?

There is no data to suggest that patients with severe renal impairment (CKD grade V) or severe heart failure (NYHA grade 3–4) should receive different hydration protocols. However, IV hydration with large volumes may exacerbate acute heart failure and induce pulmonary oedema [40]. The opinion of the CMSC is that hydration protocols in these patients should be individualized for type, volume and duration.

Question 8: Which other strategies (pharmaceutical, vitamin, renal replacement therapy) have been proved effective in preventing PC-AKI?

N-Acetylcysteine (NAc)

Most recent RCTs or meta-analyses do not show a protective effect of NAc against PC-AKI following coronary or peripheral angiography [66, 80, 81, 82, 83, 84]. NAc also failed to affect clinical outcome in coronary or peripheral angiography [85] or to have a protective effect in CT [86, 87] or in patients with diabetes mellitus undergoing coronary or peripheral angiography [88, 89]. Comparative studies with NAc combined with saline or sodium bicarbonate protocols did not show any additional effect of protective effect of NAc [61, 90, 91, 92, 93]. However, more recent meta-analyses showed a benefit of NAc, with or without high-dose statins, when added to hydration for preventing PC-AKI [94, 95, 96].

Statins

Several meta-analyses showed lower overall PC-AKI rates with the use of high-dose, short-term statin treatment compared to controls [95, 96, 97, 98, 99, 100, 101, 102, 103, 104, 105]. Lower PC-AKI rates were also found in subgroups, such as older patients, patients with acute coronary syndromes and for high-dose statin regimes. Some of these meta-analyses showed a reduced need for RRT after statins, but no reduction in all-cause mortality [97, 102]. However, the US Agency for Healthcare Research and Quality (AHRQ) meta-analysis showed that the risk of PC-AKI was only significantly reduced when statins were added to hydration and NAc. A reduction in PC-AKI risk could not be shown when statins plus hydration were compared to hydration alone in patients not taking statins. The standard of evidence grade was low in both analyses [94].

Despite the many positive results, it is difficult to make a general recommendation for statins [106] because the patients studied were invariably cardiac, and a variety of statin and hydration protocols were used. Patients with CKD grade 3B–5 (eGFR < 45 ml/min/1.73 m2) are under-represented in the studies and results in these patients remain inconclusive [102, 103, 107, 108]. Most patients undergoing CA/PCI are already taking long-term statins, and results in these patients are unclear.

While the CMSC recognises the potential preventive effects of short-term statins, it does not advise the use of short-term, high-dose statins as a single strategy for preventing PC-AKI (Table 2).

RAAS blockade: ACE inhibitors and angiotensin-II receptor blockers

Administration of renin–angiotensin–aldosterone system (RAAS) blockade as a preventive measure for patients not taking these drugs did not show a significant effect on the incidence of PC-AKI in recent meta-analyses [32, 34] (Table 2).

Vitamin C

The majority of RCTs or meta-analyses do not demonstrate a protective effect of vitamin C against PC-AKI in patients with CKD predominantly undergoing coronary angiography [109, 110, 111] or any benefit of the use of vitamin C, NAc or a combination of both over the standard hydration regimen in preventing PC-AKI [112, 113] (Table 2). Combining vitamin C with pentoxifylline also failed to show an advantage [114]. Only two publications [115, 116] have shown a protective effect of vitamin C in patients with CKD undergoing CA.

Renal replacement therapy (RRT)

There is no convincing evidence in favour of preventive haemodialysis or RRT alone [117, 118, 119] or combined with hydration [120] in patients with CKD, predominantly undergoing CA (Table 2). There is no evidence of an increased risk of permanent anuria in patients on peritoneal dialysis undergoing CA [121]. There is a single study showing better late-stage (day 5–30) renal protection against PC-AKI with simultaneous haemodialysis [122].

Miscellaneous

The data on the protective effects of several agents, such as trimatizidine [123, 124], theophylline [95, 125, 126, 127], alprostadil [128, 129], nebivolol [130], fenoldopam [131] and iloprost [132], is not conclusive and does not support recommending their use to reduce the risk of PC-AKI.

Question 9: Should administration of metformin be adapted to reduce the risk of metformin-associated lactic acidosis in patients with type 2 diabetes mellitus scheduled to receive intravascular contrast media?

Metformin is the standard drug for monotherapy of type 2 diabetes mellitus [133]. The effect of CM on the risk of metformin-associated lactic acidosis is indirect, since an episode of AKI following intravascular CM administration may lead to metformin accumulation. The use of metformin in patients with eGFR 30–59 ml/min/1.73 m2 is considered safe if doses are reduced appropriately [134, 135]. Limiting the metformin dose to a maximum of 2000 mg/day for eGFR 45–60 ml/min/1.73 m2 and to a maximum of 1000 mg/day for eGFR 30–44 ml/min/1.73 m2 has been recommended. In patients with eGFR 30–59 ml/min/1.73 m2 metformin drug levels remain within therapeutic ranges. For patients with eGFR < 30 ml/min/1.73 m2 metformin administration is not approved.

Multiple studies and meta-analyses have shown that the risk of lactic acidosis is very low and linked more to the underlying disease and possible co-morbidities rather than the use of metformin [134, 136, 137]. Because of the lack of published evidence on metformin and CM, early guidelines about the need to stop metformin before intravascular CM were based on consensus, and were strict [138, 139]. As the low risk of lactic acidosis became apparent, guidelines have become less restrictive [3].

Since no new published evidence is available, the CMSC has updated its recommendations based on recent recommendations from the FDA [140], and on guidelines from the ACR and RSTN [14, 141] (Table 3).
Table 3

Metformin administration, dialysis schedules

Metformin administration in patients at risk of PC-AKI

Note that these recommendations may deviate from current EMA/FDA recommendations.

Patients with eGFR > 30 ml/min/1.73 m2 and no evidence of AKI receiving either intravenous CM or intra-arterial CM with second pass renal exposure: continue taking metformin normally.

Patients (a) with eGFR < 30 ml/min/1.73 m2 receiving either intravenous CM or intra-arterial CM with second pass renal exposure or (b) receiving intra-arterial CM with first pass renal exposure or (c) with AKI: stop taking metformin from the time of CM administration: measure eGFR within 48 hours and restart metformin if renal function has not changed significantly.

Level of evidence D

Dialysis schedules in relation to CM administration

It is not necessary to adapt the timing of intravascular CM administration in relation to the dialysis schedule in patients undergoing chronic dialysis or haemofiltration, but it may be done to minimise volume overload.

Level of evidence D

Question 10: Should the timing of CM administration be adapted to the schedule of haemodialysis or haemofiltration sessions in patients on renal replacement therapy?

Iodine-based CM can be safely removed by haemodialysis (HD) or haemofiltration (HF). Many factors influence the effectiveness of HD, such as flow rate of blood and dialysate, dialysis membrane permeability, HD duration, and CM characteristics such as molecular size, protein binding, hydrophilicity and electrical charge [142].

Although HF concomitant with radiological procedures has been shown to be feasible and well tolerated [143, 144], the fractional removal of iodine-based CM contrast agents is modest and several HF or HD sessions are needed to remove 95% of the administered CM [143]. Also, there is no evidence for the necessity of emergency HD after administration of iodine-based CM in patients on chronic HD [145]. However, to avoid volume overload, CM administration may be synchronised with scheduled HF or HD (Table 3).

Conclusion

Assessment of the risk of PC-AKI before intravascular CM is administered is best done by measuring eGFR but the alternative of a questionnaire for patients detects most patients with eGFR less than 45 ml/min/1.73 m2. Volume expansion with normal saline or sodium bicarbonate remains the mainstay of PC-AKI prevention, but there is still uncertainty about the optimal protocol. The additional benefit of a number of drugs, such as N-acetylcysteine, statins, ACE inhibitors and angiotensin-II receptor blockers, and vitamin C in preventing PC-AKI has not been proved conclusively. Stopping nephrotoxic medications appears to be of limited value in preventing PC-AKI. Recommendations for discontinuing metformin when CM is given have been relaxed and now only apply to patients with eGFR < 30 ml/min/1.73 m2 receiving IV CM or IA CM with second pass renal exposure, and to all patients receiving IA CM with first pass renal exposure or who have AKI. There is no need to adapt dialysis schedules in patients being given intravascular CM.

The recommendations made in this paper have been incorporated into the ESUR CMSC guidelines version 10 (Table 4).
Table 4

ESUR CMSC guideline (version 10) for post-contrast acute kidney injury (PC-AKI)

Definitions

Post-contrast acute kidney injury (PC-AKI) is defined as an increase in serum creatinine ≥ 0.3 mg/dl (or ≥ 26.5 μmol/l), or ≥ 1.5 times baseline, within 48–72 h of intravascular administration of a contrast medium.

Intra-arterial injection with first pass renal exposure indicates that contrast medium reaches the renal arteries in a relatively undiluted form, e.g. injection into the left heart, thoracic and suprarenal abdominal aorta or the renal arteries.

Intra-arterial injection with second pass renal exposure indicates that contrast medium reaches the renal arteries after dilution either in the pulmonary or peripheral circulation e.g. injection into the right heart, pulmonary artery, carotid, subclavian, coronary, mesenteric or infra-renal arteries.

Measurement of renal function

• Estimated glomerular filtration rate (eGFR), calculated from the serum creatinine, is recommended to estimate renal function before administration of contrast medium.

• In adults ≥ 18 years, the CKD-EPI formula to estimate GFR is recommended.

eGFR (ml/min/1.73 m2) =

 Female sCr ≤ 62 μmol/l: 144 × (sCr/62)−0.329 × 0.993Age

 Female sCr > 62 μmol/l: 144 × (sCr/62)−1.209 × 0.993Age

 Male sCr ≤ 80 μmol/l: 141 × (sCr/80)−0.411 × 0.993Age

 Male sCr > 80 μmol/l: 141 × (sCr/80)−1.209 × 0.993Age

 (sCr in μmol/l; age in years)

All equations × 1.159 if African American race

• In children, the revised Schwartz formula to estimate GFR is recommended,

 eGFR (ml/min/1.73 m2) = 36.5 × Length/sCr (sCr in μmol/l; length in cm)

Note: Neither serum nor plasma creatinine is an ideal indicator of renal function and may miss decreased renal function.

Renal adverse reactions to iodine-based contrast media

RISK FACTORS FOR PC-AKI

Patient-related

• eGFR less than 45 ml/min/1.73 m2 before intra-arterial contrast medium administration with first pass renal exposure or in ICU patients

• eGFR less than 30 ml/min/1.73 m2 before intravenous contrast medium or intra-arterial contrast medium administration with second pass renal exposure

• Known or suspected acute renal failure

Procedure-related

• Intra-arterial contrast medium administration with first pass renal exposure

• Large doses of contrast medium given intra-arterially with first pass renal exposure

• High osmolality contrast media

• Multiple contrast medium injections within 48-72h

Time of referral

ELECTIVE EXAMINATION

MEASUREMENT OF RENAL FUNCTION

Measure eGFR before administering intravascular iodine-based contrast medium

 either (a) In all patients

 or (b) In patients who have a history of

  - Renal disease (eGFR < 60 ml/min/1.73 m2)

  - Kidney surgery

  - Proteinuria

  - Hypertension

  - Hyperuricemia

  - Diabetes mellitus

Timing of eGFR measurement

  - Within 7 days before contrast medium administration in patients with an acute disease, an acute deterioration of a chronic disease or who are hospital inpatients

  - Within 3 months before contrast medium administration in all other patients

EMERGENCY EXAMINATION

Identify at-risk patients (see above), if possible:

• Determine eGFR if the procedure can be deferred until the result is available without harm to the patient.

• If eGFR cannot be obtained, follow the protocols for patients with eGFR less than 45 ml/min/1.73 m2 for intra-arterial administration with first pass renal exposure and eGFR less than 30 ml/min/1.73 m2 for intravenous and intra-arterial administration with second pass renal exposure as closely as clinical circumstances permit.

Before the examination

ELECTIVE EXAMINATION

At-risk patients (see above)

• Consider an alternative imaging method not using iodine-based contrast media

• Intravenous saline and bicarbonate have similar efficacy for preventive hydration

• For intravenous contrast media administration and intra-arterial contrast media administration with second pass renal exposure hydrate the patient either with intravenous sodium bicarbonate 1.4% (or 154 mmol/l in dextrose 5% water): 3 ml/kg/h for 1 h before contrast medium or with intravenous saline 0.9%, 1 ml/kg/h for 3–4 h before and 4–6 h after contrast medium

• For intra-arterial contrast media administration with first renal exposure hydrate the patient either with intravenous sodium bicarbonate 1.4% (or 154 mmol/l in dextrose 5% water): 3 ml/kg/h for 1 h before and 1 ml/kg/h for 4–6 h after contrast medium or with intravenous saline 0.9%, 1 ml/kg/h for 3–4 h before and 4–6 h after contrast medium

• The clinician responsible for patient care should individualize preventive hydration in patients with severe congestive heart failure (NYHA grade 3–4) or patients with end-stage renal failure (eGFR < 15 ml/min/1.73 m2)

• Oral hydration is not recommended as the sole method of preventive hydration

EMERGENCY EXAMINATION

At-risk patients (see above)

• Consider an alternative imaging method not using iodine-based contrast media

• Use preventive hydration before contrast medium administration (see ‘Elective Examination’ for protocols)

Time of examination

All patients

• Use low or iso-osmolar contrast media

• Use the lowest dose of contrast medium consistent with a diagnostic result

• For intra-arterial contrast medium administration with first pass renal exposure keep either the ratio CM dose (in gram I)/absolute eGFR (in ml/min) < 1.1 or the ratio CM volume (in ml)/eGFR (in ml/min/1.73 m2) < 3.0 (assuming a contrast medium concentration of 350 mg iodine/ml)

After the examination

At-risk patients

• Continue preventive hydration if appropriate (see protocols above)

• Determine eGFR 48 h after administration of contrast medium

• If at 48 h there is a diagnosis of PC-AKI, monitor the patient clinically for at least 30 days and determine eGFR at regular intervals

Note: No pharmacological prophylaxis (with statins, renal vasodilators, receptor antagonists of endogenous vasoactive mediators or cytoprotective drugs) has been shown to offer consistent protection against PC-AKI.

Patients with diabetes mellitus taking metformin

• Patients with eGFR > 30 ml/min/1.73 m2 and no evidence of AKI receiving either intravenous or intra-arterial iodine-based contrast medium with second pass renal exposure: Continue taking metformin normally.

• Patients (a) with eGFR < 30 ml/min/1.73 m2 receiving either intravenous or intra-arterial contrast medium with second pass renal exposure or (b) receiving intra-arterial contrast medium with first pass renal exposure or (c) with AKI:

Stop taking metformin from the time of contrast medium administration. Measure eGFR within 48 h and restart metformin if renal function has not changed significantly.

Dialysis and contrast medium administration

• All iodine-based contrast media can be removed by haemodialysis or peritoneal dialysis.

• There is no evidence that haemodialysis protects patients with normal or impaired renal function from PC-AKI.

• In all patients, avoid osmotic and fluid overload.

PATIENTS ON DIALYSIS

Patients on haemodialysis

• Co-ordinating the time of the iodine-based contrast medium injection with the haemodialysis session is unnecessary

• Extra haemodialysis session to remove iodine-based contrast medium is unnecessary

Patients on continuous ambulatory peritoneal dialysis

Haemodialysis to remove iodine-based contrast medium is unnecessary

Notes

Funding

The authors state that this work has not received any funding.

Compliance with ethical standards

Guarantor

The scientific guarantor of this publication is Prof. Henrik S. Thomsen.

Conflict of interest

Aart van der Molen has received incidental payments for lectures and chairmanships at scientific meetings for contrast agent safety related issues (contrast agent reactions, Gd-retention) from GE, Bayer, Bracco and Guerbet.

Fulvio Stacul has received lecture fees from Bracco and Guerbet.

Olivier Clément has received lecture fees from Bracco and Guerbet.

The other authors of this manuscript declare no relationships with any companies whose products and services may be related to the subject matter of this article.

Statistics and biometry

No complex statistical methods were necessary for this paper.

Informed consent

Written informed consent was not required for this study because this is a special paper based on other publications. Thus informed consent is not necessary.

Ethical approval

Institutional review board approval was not required because it is a retrospective study based on other studies.

Methodology

• retrospective

• multicentre study

References

  1. 1.
    Stacul F, van der Molen AJ, Reimer P, Contrast Media Safety Committee of European Society of Urogenital Radiology (ESUR) et al (2011) Contrast induced nephropathy: updated ESUR Contrast Media Safety Committee guidelines. Eur Radiol 21:2527–2541PubMedCrossRefGoogle Scholar
  2. 2.
    Morcos SK, Thomsen HS, Webb JA, Contrast Media Safety Committee of the European Society of Urogenital Radiology (ESUR) et al (2002) Dialysis and contrast media. Eur Radiol 12:3026–3030PubMedGoogle Scholar
  3. 3.
    Contrast Media Safety Committee ESUR. Guidelines on Contrast Media v9. CMSC, 2014. http://www.esur-cm.org/index.php/en/. 15 December 2017
  4. 4.
    Brouwers M, Kho ME, Browman GP, on behalf of the AGREE Next Steps Consortium et al (2010) AGREE II: Advancing guideline development, reporting and evaluation in healthcare. Can Med Assoc J 182:E839–E842CrossRefGoogle Scholar
  5. 5.
    Guyatt GH, Oxman AD, Kunz R et al (2011) GRADE guidelines: 2. Framing the question and deciding on important outcomes. J Clin Epidemiol 64:395–400PubMedCrossRefGoogle Scholar
  6. 6.
    OCEBM Levels of Evidence Working Group. The Oxford 2011 Levels of Evidence. Oxford Centre for Evidence-Based Medicine. http://www.cebm.net/index.aspx?o=5653. Accessed 15 December 2017
  7. 7.
    Choyke PL, Cady J, DePollar SL, Austin H (1998) Determination of serum creatinine prior to iodinated contrast media: is it necessary in all patients? Tech Urol 4:65–69PubMedGoogle Scholar
  8. 8.
    Tippins RB, Torres WE, Baumgartner BR, Baumgarten DA (2000) Are screening serum creatinine levels necessary prior to outpatient CT examinations? Radiology 216:481–484PubMedCrossRefGoogle Scholar
  9. 9.
    Azzouz M, Romsing J, Thomsen HS (2014) Can a structured questionnaire identify patients with reduced renal function? Eur Radiol 24:780–784PubMedCrossRefGoogle Scholar
  10. 10.
    Too CW, Ng WY, Tan CC, Mahmood MI, Tay KH (2015) Screening for impaired renal function in outpatients before iodinated contrast injection: comparing the Choyke questionnaire with a rapid point-of-care-test. Eur J Radiol 84:1227–1231PubMedCrossRefGoogle Scholar
  11. 11.
    Zähringer C, Potthast S, Tyndall AJ, Bongartz G, Hohmann J (2015) Serum creatinine measurements: evaluation of a questionnaire according to the ESUR guidelines. Acta Radiol 56:628–634PubMedCrossRefGoogle Scholar
  12. 12.
    Chang P, Saddleton E, Laumann AE et al (2012) Comparison of the sensitivity of a pre-MRI questionnaire and point of care eGFR testing for detection of impaired renal function. Acad Radiol 19:1181–1185PubMedPubMedCentralCrossRefGoogle Scholar
  13. 13.
    Moos SI, de Weijert RS, Nagan G, Stoker J, Bipat S (2014) Cost of screening for kidney disease before intravenous contrast administration. Neth J Med 72:271–280PubMedGoogle Scholar
  14. 14.
    Van der Molen AJ, Geenen RWF, Dekkers HM et al for the Radiological Society of the Netherlands (RSTN). Guideline safe use of contrast media, part 1. Vught, RSTN: 2017. https://www.radiologen.nl/secties/nvvr/documenten/richtlijn-veilig-gebruik-van-contrastmiddelen-deel-1-full-english. Accessed 15 December 2017
  15. 15.
    Tsai TT, Patel UD, Chang TI et al (2014) Validated contemporary risk model of acute kidney injury in patients undergoing percutaneous coronary interventions: insights from the National Cardiovascular Data Registry Cath-PCI Registry. J Am Heart Assoc 3:e001380PubMedPubMedCentralCrossRefGoogle Scholar
  16. 16.
    Kooiman J, Gurm HS (2014) Predicting contrast-induced renal complications in the catheterization laboratory. Intervent Cardiol Clin 3:369–377PubMedCrossRefGoogle Scholar
  17. 17.
    Mehran R, Aymong ED, Nikolsky E et al (2004) A simple risk score for prediction of contrast-induced nephropathy after percutaneous coronary intervention: development and initial validation. J Am Coll Cardiol 44:1393–1399PubMedGoogle Scholar
  18. 18.
    Sgura FA, Bertelli L, Monopoli D et al (2010) Mehran contrast-induced nephropathy risk score predicts short- and long-term clinical outcomes in patients with ST-elevation-myocardial infarction. Circ Cardiovasc Interv 3:491–498PubMedCrossRefGoogle Scholar
  19. 19.
    Tziakas D, Chalikias G, Stakos D et al (2014) Validation of a new risk score to predict contrast-induced nephropathy after percutaneous coronary intervention. Am J Cardiol 113:1487–1493PubMedCrossRefGoogle Scholar
  20. 20.
    Abellas-Sequeiros RA, Raposeiras-Roubin S, Abu-Assi E et al (2016) Mehran contrast nephropathy risk score: is it still useful 10 years later? J Cardiol 67:262–267PubMedCrossRefGoogle Scholar
  21. 21.
    Sato A, Hoshi T, Kakefuda Y et al (2015) Effect of the Mehran risk score for the prediction of clinical outcomes after percutaneous coronary intervention. J Cardiol 66:417–422PubMedCrossRefGoogle Scholar
  22. 22.
    Gurm HS, Seth M, Kooiman J, Share D (2013) A novel tool for reliable and accurate prediction of renal complications in patients undergoing percutaneous coronary intervention. J Am Coll Cardiol 61:2242–2248PubMedCrossRefGoogle Scholar
  23. 23.
    Silver SA, Shah PS, Chertow GM, Harel S, Wald R, Harel Z (2015) Risk prediction models for contrast induced nephropathy: systematic review. BMJ 351:h4395PubMedPubMedCentralCrossRefGoogle Scholar
  24. 24.
    Allen DW, Ma B, Leung KC et al (2017) Risk prediction models for contrast-induced acute kidney injury accompanying cardiac catheterization: systematic review and meta-analysis. Can J Cardiol 33(6):724-736
  25. 25.
    Dutch Federation of Nephrology. Guideline diagnosis and management of chronic kidney disease 2016. https://www.nefro.nl/richtlijnen/diagnostiek-en-behandeling-van-chronische-nierschade-voorlopige-richtlijn-2016-0. Accessed 15 December 2017
  26. 26.
    Perazella MA (2005) Drug-induced nephropathy: an update. Expert Opin Drug Saf 4:689–704PubMedCrossRefGoogle Scholar
  27. 27.
    Diogo LP, Saitovitch D, Biehl M et al (2010) Is there an association between non-steroidal anti-inflammatory drugs and contrast nephropathy? Arq Bras Cardiol 95:726–731PubMedCrossRefGoogle Scholar
  28. 28.
    Ho YF, Hsieh KL, Kung FL, et al (2015) Nephrotoxic polypharmacy and risk of contrast medium-induced nephropathy in hospitalized patients undergoing contrast-enhanced CT. AJR Am J Roentgenol 205:703–708Google Scholar
  29. 29.
    Moos SI, van Vemde DN, Stoker J, Bipat S (2013) 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 82:e387–e399PubMedCrossRefGoogle Scholar
  30. 30.
    Rosenstock JL, Bruno R, Kim JK et al (2008) The effect of withdrawal of ACE inhibitors or angiotensin receptor blockers prior to coronary angiography on the incidence of contrast-induced nephropathy. Int Urol Nephrol 40:749–755PubMedCrossRefGoogle Scholar
  31. 31.
    Bainey KR, Rahim S, Etherington K, CAPTAIN Investigators et al (2015) Effects of withdrawing vs. continuing renin-angiotensin blockers on incidence of acute kidney injury in patients with renal insufficiency undergoing cardiac catheterization: results from the angiotensin converting enzyme inhibitor/angiotensin receptor blocker and contrast induced nephropathy in patients receiving cardiac catheterization (CAPTAIN) trial. Am Heart J 170:110–116PubMedCrossRefGoogle Scholar
  32. 32.
    Jo SH, Lee JM, Park J, Kim HS (2015) The impact of renin-angiotensin-aldosterone system blockade on contrast-induced nephropathy: a meta-analysis of 12 studies with 4,493 patients. Cardiology 130:4–14PubMedCrossRefGoogle Scholar
  33. 33.
    Peng F, Su J, Lin J, Niu W (2015) Impact of renin-angiotensin-aldosterone system-blocking agents on the risk of contrast-induced acute kidney injury: a prospective study and meta-analysis. J Cardiovasc Pharmacol 65:262–268PubMedCrossRefGoogle Scholar
  34. 34.
    Wu Z, Zhang H, Jin W et al (2015) The effect of renin-angiotensin-aldosterone system blockade medications on contrast-induced nephropathy in patients undergoing coronary angiography: a meta-analysis. PLoS One 10:e0129747PubMedPubMedCentralCrossRefGoogle Scholar
  35. 35.
    Chen SL, Zhang J, Yei F et al (2008) Clinical outcomes of contrast-induced nephropathy in patients undergoing percutaneous coronary intervention: a prospective, multicenter, randomized study to analyze the effect of hydration and acetylcysteine. Int J Cardiol 126:407–413PubMedCrossRefGoogle Scholar
  36. 36.
    Luo Y, Wang X, Ye Z, et al (2014) Remedial hydration reduces the incidence of contrast-induced nephropathy and short-term adverse events in patients with ST-segment elevation myocardial infarction: a single-center, randomized trial. Intern Med 53:2265–2272Google Scholar
  37. 37.
    Jurado-Roman A, Hernandez-Hernandez F, Garcia-Tejada J et al (2015) Role of hydration in contrast-induced nephropathy in patients who underwent primary percutaneous coronary intervention. Am J Cardiol 115:1174–1178PubMedCrossRefGoogle Scholar
  38. 38.
    Kooiman J, Sijpkens YW, van Buren M et al (2014) Randomised trial of no hydration vs. sodium bicarbonate hydration in patients with chronic kidney disease undergoing acute computed tomography-pulmonary angiography. J Thromb Haemost 12:1658–1666PubMedCrossRefGoogle Scholar
  39. 39.
    Trivedi HS, Moore H, Nasr S et al (2003) A randomized prospective trial to assess the role of saline hydration on the development of contrast nephrotoxicity. Nephron Clin Pract 93:C29–C34PubMedCrossRefGoogle Scholar
  40. 40.
    Nijssen EC, Rennenberg RJ, Nelemans PJ et al (2017) Prophylactic hydration to protect renal function from intravascular iodinated contrast material in patients at high risk of contrast-induced nephropathy (AMACING): a prospective, randomised, phase 3, controlled, open-label, non-inferiority trial. Lancet 389:1312–1322PubMedCrossRefGoogle Scholar
  41. 41.
    Taylor AJ, Hotchkiss D, Morse RW, McCabe J (1998) PREPARED: preparation for Angiography in Renal Dysfunction: a randomized trial of inpatient vs outpatient hydration protocols for cardiac catheterization in mild-to-moderate renal dysfunction. Chest 114:1570–1574PubMedCrossRefGoogle Scholar
  42. 42.
    Dussol B, Morange S, Loundoun A, Auquier P, Berland Y (2006) A randomized trial of saline hydration to prevent contrast nephropathy in chronic renal failure patients. Nephrol Dial Transplant 21:2120–2126PubMedCrossRefGoogle Scholar
  43. 43.
    Lawlor DK, Moist L, DeRose G et al (2007) Prevention of contrast-induced nephropathy in vascular surgery patients. Ann Vasc Surg 21:593–597PubMedCrossRefGoogle Scholar
  44. 44.
    Wrobel W, Sinkiewicz W, Gordon M, Wozniak-Wisniewska A (2010) Oral versus intravenous hydration and renal function in diabetic patients undergoing percutaneous coronary interventions. Kardiol Pol 68:1015–1020PubMedGoogle Scholar
  45. 45.
    Akyuz S, Karaca M, Kemaloglu OT et al (2014) Efficacy of oral hydration in the prevention of contrast-induced acute kidney injury in patients undergoing coronary angiography or intervention. Nephron Clin Pract 128:95–100PubMedCrossRefGoogle Scholar
  46. 46.
    Cho R, Javed N, Traub D, Kodali S, Atem F, Srinivasan V (2010) Oral hydration and alkalinization is noninferior to intravenous therapy for prevention of contrast-induced nephropathy in patients with chronic kidney disease. J Interv Cardiol 23:460–466PubMedCrossRefGoogle Scholar
  47. 47.
    Kong DG, Hou YF, Ma LL, Yao DK, Wang LX (2012) Comparison of oral and intravenous hydration strategies for the prevention of contrast-induced nephropathy in patients undergoing coronary angiography or angioplasty: a randomized clinical trial. Acta Cardiol 67:565–569PubMedCrossRefGoogle Scholar
  48. 48.
    Martin-Moreno PL, Varo N, Martinez-Anso E et al (2015) Comparison of intravenous and oral hydration in the prevention of contrast-induced acute kidney injury in low-risk patients: a randomized trial. Nephron 131:51–58PubMedCrossRefGoogle Scholar
  49. 49.
    Hiremath S, Akbari A, Shabana W, Fergusson DA, Knoll GA (2013) Prevention of contrast-induced acute kidney injury: is simple oral hydration similar to intravenous? A systematic review of the evidence. PLoS One 8:e60009PubMedPubMedCentralCrossRefGoogle Scholar
  50. 50.
    Cheungpasitporn W, Thongprayoon C, Brabec BA, Edmonds PJ, O'Corragain OA, Erickson SB (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. N Am J Med Sci 6:618–624PubMedPubMedCentralCrossRefGoogle Scholar
  51. 51.
    Agarwal SK, Mohareb S, Patel A et al (2015) Systematic oral hydration with water is similar to parenteral hydration for prevention of contrast-induced nephropathy: an updated meta-analysis of randomised clinical data. Open Heart 2:e000317PubMedPubMedCentralCrossRefGoogle Scholar
  52. 52.
    Heyman SN, Rosen S, Khamaisi M, Idée JM, Rosenberger C (2010) Reactive oxygen species and the pathogenesis of radiocontrast-induced nephorpathy. Invest Radiol 45:188–193PubMedCrossRefGoogle Scholar
  53. 53.
    Merten GJ, Burgess WP, Gray LV et al (2004) Prevention of contrast-induced nephropathy with sodium bicarbonate: a randomized controlled trial. JAMA 291:2328–2334PubMedCrossRefGoogle Scholar
  54. 54.
    Masuda M, Yamada T, Mine T et al (2007) Comparison of usefulness of sodium bicarbonate versus sodium chloride to prevent contrast-induced nephropathy in patients undergoing an emergent coronary procedure. Am J Cardiol 100:781–786PubMedCrossRefGoogle Scholar
  55. 55.
    Ozcan EE, Guneri S, Akdeniz B et al (2007) Sodium bicarbonate, N-acetylcysteine, and saline for prevention of radiocontrast-induced nephropathy. A comparison of 3 regimens for protecting contrast-induced nephropathy in patients undergoing coronary procedures. A single-center prospective controlled trial. Am Heart J 154:539–544PubMedCrossRefGoogle Scholar
  56. 56.
    Recio-Mayoral A, Chaparro M, Prado B et al (2007) The reno-protective effect of hydration with sodium bicarbonate plus N-acetylcysteine in patients undergoing emergency percutaneous coronary intervention: the RENO Study. J Am Coll Cardiol 49:1283–1288PubMedCrossRefGoogle Scholar
  57. 57.
    Adolph E, Holdt-Lehmann B, Chatterjee T et al (2008) Renal Insufficiency Following Radiocontrast Exposure Trial (REINFORCE): a randomized comparison of sodium bicarbonate versus sodium chloride hydration for the prevention of contrast-induced nephropathy. Coron Artery Dis 19:413–419PubMedGoogle Scholar
  58. 58.
    Brar SS, Shen AY, Jorgensen MB et al (2008) Sodium bicarbonate vs sodium chloride for the prevention of contrast medium-induced nephropathy in patients undergoing coronary angiography: a randomized trial. JAMA 300:1038–1046PubMedCrossRefGoogle Scholar
  59. 59.
    Boucek P, Havrdova T, Oliyarnyk O et al (2013) Prevention of contrast-induced nephropathy in diabetic patients with impaired renal function: a randomized, double blind trial of sodium bicarbonate versus sodium chloride-based hydration. Diabetes Res Clin Pract 101:303–308PubMedCrossRefGoogle Scholar
  60. 60.
    Gomes VO, Lasevitch R, Lima VC et al (2012) Hydration with sodium bicarbonate does not prevent contrast nephropathy: a multicenter clinical trial. Arq Bras Cardiol 99:1129–1134PubMedCrossRefGoogle Scholar
  61. 61.
    Ratcliffe JA, Thiagarajah P, Chen J et al (2009) Prevention of contrast-induced nephropathy: a randomized controlled trial of sodium bicarbonate and N-acetylcysteine. Int J Angiol 18:193–197PubMedPubMedCentralCrossRefGoogle Scholar
  62. 62.
    Solomon R, Gordon P, Manoukian SV et al (2015) Randomized trial of bicarbonate or saline study for the prevention of contrast-induced nephropathy in patients with CKD. Clin J Am Soc Nephrol 10:1519–1524PubMedPubMedCentralCrossRefGoogle Scholar
  63. 63.
    Briguori C, Airoldi F, D'Andrea D et al (2007) Renal Insufficiency Following Contrast Media Administration Trial (REMEDIAL): a randomized comparison of 3 preventive strategies. Circulation 115:1211–1217PubMedGoogle Scholar
  64. 64.
    Castini D, Lucreziotti S, Bosotti L et al (2010) Prevention of contrast-induced nephropathy: a single center randomized study. Clin Cardiol 33:E63–E68PubMedCrossRefGoogle Scholar
  65. 65.
    Chong E, Poh KK, Lu Q et al (2015) Comparison of combination therapy of high-dose oral N-acetylcysteine and intravenous sodium bicarbonate hydration with individual therapies in the reduction of Contrast-induced Nephropathy during Cardiac Catheterisation and Percutaneous Coronary Intervention (CONTRAST): a multi-centre, randomised, controlled trial. Int J Cardiol 201:237–242PubMedCrossRefPubMedCentralGoogle Scholar
  66. 66.
    Hafiz AM, Jan MF, Mori N et al (2012) Prevention of contrast-induced acute kidney injury in patients with stable chronic renal disease undergoing elective percutaneous coronary and peripheral interventions: randomized comparison of two preventive strategies. Catheter Cardiovasc Interv 79:929–937PubMedCrossRefGoogle Scholar
  67. 67.
    Koc F, Ozdemir K, Altunkas F et al (2013) Sodium bicarbonate versus isotonic saline for the prevention of contrast-induced nephropathy in patients with diabetes mellitus undergoing coronary angiography and/or intervention: a multicenter prospective randomized study. J Investig Med 61:872–877PubMedCrossRefGoogle Scholar
  68. 68.
    Klima T, Christ A, Marana I et al (2012) Sodium chloride vs. sodium bicarbonate for the prevention of contrast medium-induced nephropathy: a randomized controlled trial. Eur Heart J 33:2071–2079PubMedCrossRefGoogle Scholar
  69. 69.
    Lee SW, Kim WJ, Kim YH et al (2011) Preventive strategies of renal insufficiency in patients with diabetes undergoing intervention or arteriography (the PREVENT Trial). Am J Cardiol 107:1447–1452PubMedCrossRefGoogle Scholar
  70. 70.
    Maioli M, Toso A, Leoncini M et al (2008) Sodium bicarbonate versus saline for the prevention of contrast-induced nephropathy in patients with renal dysfunction undergoing coronary angiography or intervention. J Am Coll Cardiol 52:599–604PubMedCrossRefGoogle Scholar
  71. 71.
    Shavit L, Korenfeld R, Lifschitz M, Butnaru A, Slotki I (2009) Sodium bicarbonate versus sodium chloride and oral N-acetylcysteine for the prevention of contrast-induced nephropathy in advanced chronic kidney disease. J Interv Cardiol 22:556–563PubMedCrossRefGoogle Scholar
  72. 72.
    Kooiman J, Sijpkens YW, de Vries JP et al (2014) A randomized comparison of 1-h sodium bicarbonate hydration versus standard peri-procedural saline hydration in patients with chronic kidney disease undergoing intravenous contrast-enhanced computerized tomography. Nephrol Dial Transplant 29:1029–1036PubMedCrossRefGoogle Scholar
  73. 73.
    Kooiman J, de Vries JP, van der Heyden J et al (2014) Randomized trial of 1-hour sodium bicarbonate vs. Standard saline hydration in patients with chronic kidney disease undergoing intra-arterial contrast administration [abstr]. Circulation 130:A17645Google Scholar
  74. 74.
    Kama A, Yilmaz S, Yaka E et al (2014) Comparison of short-term infusion regimens of N-acetylcysteine plus intravenous fluids, sodium bicarbonate plus intravenous fluids, and intravenous fluids alone for prevention of contrast-induced nephropathy in the emergency department. Acad Emerg Med 21:615–622PubMedCrossRefGoogle Scholar
  75. 75.
    Briguori C, Visconti G, Focaccio A et al (2011) Renal Insufficiency After Contrast Media Administration Trial II (REMEDIAL II): RenalGuard System in high-risk patients for contrast-induced acute kidney injury. Circulation 124:1260–1269PubMedCrossRefGoogle Scholar
  76. 76.
    Marenzi G, Ferrari C, Marana I et al (2012) Prevention of contrast nephropathy by furosemide with matched hydration: the MYTHOS (Induced Diuresis With Matched Hydration Compared to Standard Hydration for Contrast Induced Nephropathy Prevention) trial. JACC Cardiovasc Interv 5:90–97PubMedCrossRefGoogle Scholar
  77. 77.
    Usmiani T, Andreis A, Budano C et al (2016) AKIGUARD (Acute Kidney Injury GUARding Device) trial: in-hospital and one-year outcomes. J Cardiovasc Med 17:530–537CrossRefGoogle Scholar
  78. 78.
    Brar SS, Aharonian V, Mansukhani P et al (2014) Haemodynamic-guided fluid administration for the prevention of contrast-induced acute kidney injury: the POSEIDON randomised controlled trial. Lancet 383:1814–1823PubMedCrossRefGoogle Scholar
  79. 79.
    Qian G, Fu Z, Guo J, Cao F, Chen Y (2016) Prevention of contrast-induced nephropathy by central venous pressure-guided fluid administration in chronic kidney disease and congestive heart failure patients. JACC Cardiovasc Interv 9:89–96PubMedCrossRefGoogle Scholar
  80. 80.
    Aslanger E, Uslu B, Akdeniz C, Polat N, Cizgici Y, Oflaz H (2012) Intrarenal application of N-acetylcysteine for the prevention of contrast medium-induced nephropathy in primary angioplasty. Coron Artery Dis 23:265–270PubMedCrossRefPubMedCentralGoogle Scholar
  81. 81.
    Inda-Filho AJ, Caixeta A, Manggini M, Schor N (2014) Do intravenous N-acetylcysteine and sodium bicarbonate prevent high osmolal contrast-induced acute kidney injury? A randomized controlled trial. PLoS One 9:e107602PubMedPubMedCentralCrossRefGoogle Scholar
  82. 82.
    Jaffery Z, Verma A, White CJ et al (2012) A randomized trial of intravenous n-acetylcysteine to prevent contrast induced nephropathy in acute coronary syndromes. Catheter Cardiovasc Interv 79:921–926PubMedCrossRefPubMedCentralGoogle Scholar
  83. 83.
    O'Sullivan S, Healy DA, Moloney MC, Grace PA, Walsh SR (2013) The role of N-acetylcysteine in the prevention of contrast-induced nephropathy in patients undergoing peripheral angiography: a structured review and meta-analysis. Angiology 64:576–582PubMedCrossRefGoogle Scholar
  84. 84.
    Sun Z, Fu Q, Cao L, Jin W, Cheng L, Li Z (2013) Intravenous N-acetylcysteine for prevention of contrast-induced nephropathy: a meta-analysis of randomized, controlled trials. PLoS One 8:e55124PubMedPubMedCentralCrossRefGoogle Scholar
  85. 85.
    Loomba RS, Shah PH, Aggarwal S, Arora RR (2016) Role of N-acetylcysteine to prevent contrast-induced nephropathy: a meta-analysis. Am J Ther 23:e172–e183PubMedCrossRefGoogle Scholar
  86. 86.
    Traub SJ, Mitchell AM, Jones AE et al (2013) N-acetylcysteine plus intravenous fluids versus intravenous fluids alone to prevent contrast-induced nephropathy in emergency computed tomography. Ann Emerg Med 62:511–520PubMedCrossRefPubMedCentralGoogle Scholar
  87. 87.
    Poletti PA, Platon A, De Seigneux S et al (2013) N-acetylcysteine does not prevent contrast nephropathy in patients with renal impairment undergoing emergency CT: a randomized study. BMC Nephrol 14:119PubMedPubMedCentralCrossRefGoogle Scholar
  88. 88.
    Berwanger O, Cavalcanti AB, Sousa AM et al (2013) Acetylcysteine for the prevention of renal outcomes in patients with diabetes mellitus undergoing coronary and peripheral vascular angiography: a substudy of the acetylcysteine for contrast-induced nephropathy trial. Circ Cardiovasc Interv 6:139–145PubMedCrossRefPubMedCentralGoogle Scholar
  89. 89.
    Kang X, Hu DY, Li CB, Ai ZS, Peng A (2015) N-acetylcysteine for the prevention of contrast-induced nephropathy in patients with pre-existing renal insufficiency or diabetes: a systematic review and meta-analysis. Ren Fail 37:297–303PubMedCrossRefGoogle Scholar
  90. 90.
    Brown JR, Block CA, Malenka DJ, O'Connor GT, Schoolwerth AC, Thompson CA (2009) Sodium bicarbonate plus N-acetylcysteine prophylaxis: a meta-analysis. JACC Cardiovasc Interv 2:1116–1124PubMedCrossRefGoogle Scholar
  91. 91.
    Carbonell N, Blasco M, Sanjuan R et al (2007) Intravenous N-acetylcysteine for preventing contrast-induced nephropathy: a randomised trial. Int J Cardiol 115:57–62PubMedCrossRefPubMedCentralGoogle Scholar
  92. 92.
    Heng AE, Cellarier E, Aublet-Cuvelier B et al (2008) Is treatment with N-acetylcysteine to prevent contrast-induced nephropathy when using bicarbonate hydration out of date? Clin Nephrol 70:475–484PubMedCrossRefPubMedCentralGoogle Scholar
  93. 93.
    Staniloae CS, Doucet S, Sharma SK et al (2009) N-Acetylcysteine added to volume expansion with sodium bicarbonate does not further prevent contrast-induced nephropathy: results from the cardiac angiography in renally impaired patients study. J Interv Cardiol 22:261–265PubMedCrossRefGoogle Scholar
  94. 94.
    Subramaniam RM, Suarez-Cuervo C, Wilson RF et al (2016) Effectiveness of prevention strategies for contrast-induced nephropathy: a systematic review and meta-analysis. Ann Intern Med 164:406–416PubMedCrossRefGoogle Scholar
  95. 95.
    Ali-Hassan-Sayegh S, Mirhosseini SJ, Ghodratipour Z et al (2017) Strategies preventing contrast-induced nephropathy after coronary angiography: a comprehensive meta-analysis and systematic review of 125 randomized controlled trials. Angiology 68:389–413CrossRefGoogle Scholar
  96. 96.
    Su X, Xie X, Liu L et al (2017) Comparative effectiveness of 12 treatment strategies for preventing contrast-induced acute kidney injury: A systematic review and Bayesian network analysis. Am J Kidney Dis 69:69–77PubMedCrossRefGoogle Scholar
  97. 97.
    Briasoulis A, Mallikethi-Reddy S, Sharma S, Briasouli AA, Afonso L (2015) 3-Hydroxy-3-methylglutaryl-CoA reductase enzyme inhibitors for prevention of contrast-induced nephropathy: a meta-analysis of prospective randomized controlled studies. Am J Ther 22:e158–e166PubMedCrossRefGoogle Scholar
  98. 98.
    Cheungpasitporn W, Thongprayoon C, Kittanamongkolchai W, et al (2015) Periprocedural effects of statins on the incidence of contrast-induced acute kidney injury: a systematic review and meta-analysis of randomized controlled trials. Ren Fail 37:664–671Google Scholar
  99. 99.
    Li H, Wang C, Liu C, Li R, Zou M, Cheng G (2016) Efficacy of short-term statin treatment for the prevention of contrast-induced acute kidney injury in patients undergoing coronary angiography/percutaneous coronary intervention: a meta-analysis of 21 randomized controlled trials. Am J Cardiovasc Drugs 16:201–219PubMedCrossRefGoogle Scholar
  100. 100.
    Liu YH, Liu Y, Duan CY et al (2015) Statins for the prevention of contrast-induced nephropathy after coronary angiography/percutaneous interventions: a meta-analysis of randomized controlled trials. J Cardiovasc Pharmacol Ther 20:181–192PubMedCrossRefGoogle Scholar
  101. 101.
    Marenzi G, Cosentino N, Werba JP, Tedesco CC, Veglia F, Bartorelli AL (2015) A meta-analysis of randomized controlled trials on statins for the prevention of contrast-induced acute kidney injury in patients with and without acute coronary syndromes. Int J Cardiol 183:47–53PubMedCrossRefGoogle Scholar
  102. 102.
    Thompson K, Razi R, Lee MS et al (2016) Statin use prior to angiography for the prevention of contrast-induced acute kidney injury: a meta-analysis of 19 randomised trials. EuroIntervention 12:366–374PubMedCrossRefGoogle Scholar
  103. 103.
    Wang N, Qian P, Yan TD, Phan K (2016) Periprocedural effects of statins on the incidence of contrast-induced acute kidney injury: A systematic review and trial sequential analysis. Int J Cardiol 206:143–152PubMedCrossRefGoogle Scholar
  104. 104.
    Wu H, Li D, Fang M, Han H, Wang H (2015) Meta-analysis of short-term high versus low doses of atorvastatin preventing contrast-induced acute kidney injury in patients undergoing coronary angiography/percutaneous coronary intervention. J Clin Pharmacol 55:123–131PubMedCrossRefGoogle Scholar
  105. 105.
    Yang Y, Wu YX, Hu YZ (2015) Rosuvastatin treatment for preventing contrast-induced acute kidney injury after cardiac catheterization: a meta-analysis of randomized controlled trials. Medicine 94:e1226PubMedPubMedCentralCrossRefGoogle Scholar
  106. 106.
    Vanmassenhove J, Vanholder R, Lameire N (2016) Statins for the prevention of contrast-induced acute kidney injury. Curr Opin Nephrol Hypertens 25:508–517PubMedCrossRefGoogle Scholar
  107. 107.
    Giacoppo D, Capodanno D, Capranzano P, Aruta P, Tamburino C (2014) Meta-analysis of randomized controlled trials of preprocedural statin administration for reducing contrast-induced acute kidney injury in patients undergoing coronary catheterization. Am J Cardiol 114:541–548PubMedCrossRefGoogle Scholar
  108. 108.
    Han Y, Zhu G, Han L et al (2014) Short-term rosuvastatin therapy for prevention of contrast-induced acute kidney injury in patients with diabetes and chronic kidney disease. J Am Coll Cardiol 63:62–70PubMedCrossRefGoogle Scholar
  109. 109.
    Brueck M, Cengiz H, Hoeltgen R et al (2013) Usefulness of N-acetylcysteine or ascorbic acid versus placebo to prevent contrast-induced acute kidney injury in patients undergoing elective cardiac catheterization: a single-center, prospective, randomized, double-blind, placebo-controlled trial. J Invasive Cardiol 25:276–283PubMedPubMedCentralGoogle Scholar
  110. 110.
    Dvorsak B, Kanic V, Ekart R, Bevc S, Hojs R (2013) Ascorbic acid for the prevention of contrast-induced nephropathy after coronary angiography in patients with chronic renal impairment: a randomized controlled trial. Ther Apher Dial 17:384–390PubMedCrossRefGoogle Scholar
  111. 111.
    Li R, Chen H (2012) Prevention of contrast-induced nephropathy with ascorbic acid. Heart 98:E211CrossRefGoogle Scholar
  112. 112.
    Albabtain MA, Almasood A, Alshurafah H, Alamri H, Tamim H (2013) Efficacy of ascorbic acid, N-acetylcysteine, or combination of both on top of saline hydration versus saline hydration alone on prevention of contrast-Induced nephropathy: a prospective randomized study. J Interv Cardiol 26:90–96PubMedCrossRefGoogle Scholar
  113. 113.
    Zhou L, Chen H (2012) Prevention of contrast-induced nephropathy with ascorbic acid. Intern Med 51:531–535PubMedCrossRefGoogle Scholar
  114. 114.
    Shakeryan F, Sanati H, Fathi H et al (2013) Evaluation of combination therapy with vitamin C and pentoxifylline on preventing kidney failure secondary to intravenous contrast material in coronary angioplasty. Iran Heart J 14:17–21Google Scholar
  115. 115.
    Sadat U, Usman A, Gillard JH, Boyle JR (2013) Does ascorbic acid protect against contrast-induced acute kidney injury in patients undergoing coronary angiography: a systematic review with meta-analysis of randomized, controlled trials. J Am Coll Cardiol 62:2167–2175PubMedCrossRefGoogle Scholar
  116. 116.
    Wang XT, Yan J, Li L, Su Q (2014) Anti-oxidative vitamin for the prevention of contrast-induced acute kidney injury in patients with chronic kidney disease: meta-analysis of randomized controlled trials. Exp Clin Cardiol 20:1385–1410Google Scholar
  117. 117.
    Cruz DN, Perazella MA, Bellomo R et al (2006) Extracorporeal blood purification therapies for prevention of radiocontrast-induced nephropathy: a systematic review. Am J Kidney Dis 48:361–371PubMedCrossRefGoogle Scholar
  118. 118.
    Cruz DN, Goh CY, Marenzi G, Corradi V, Ronco C, Perazella MA (2012) Renal replacement therapies for prevention of radiocontrast-induced nephropathy: a systematic review. Am J Med 125:66–78PubMedCrossRefGoogle Scholar
  119. 119.
    Song K, Jiang S, Shi Y, Shen H, Shi X, Jing D (2010) Renal replacement therapy for prevention of contrast-induced acute kidney injury: a meta-analysis of randomized controlled trials. Am J Nephrol 32:497–504PubMedCrossRefGoogle Scholar
  120. 120.
    Reinecke H, Fobker M, Wellmann J et al (2007) A randomized controlled trial comparing hydration therapy to additional hemodialysis or N-acetylcysteine for the prevention of contrast medium-induced nephropathy: the Dialysis-versus-Diuresis (DVD) trial. Clin Res Cardiol 96:130–139PubMedCrossRefGoogle Scholar
  121. 121.
    Weisbord SD, Bernardini J, Mor MK et al (2006) The effect of coronary angiography on residual renal function in patients on peritoneal dialysis. Clin Cardiol 29:494–497PubMedCrossRefGoogle Scholar
  122. 122.
    Choi MJ, Yoon JW, Han SJ et al (2014) The prevention of contrast-induced nephropathy by simultaneous hemofiltration during coronary angiographic procedures: a comparison with periprocedural hemofiltration. Int J Cardiol 176:941–945PubMedCrossRefGoogle Scholar
  123. 123.
    Nadkarni GN, Konstantinidis I, Patel A et al (2015) Trimetazidine decreases risk of contrast-induced nephropathy in patients with chronic kidney disease: a meta-analysis of randomized controlled trials. J Cardiovasc Pharmacol Ther 20:539–546PubMedCrossRefGoogle Scholar
  124. 124.
    Ye Z, Lu H, Su Q et al (2017) Clinical effect of trimetazidine on prevention of contrast-induced nephropathy in patients with renal insufficiency: an updated systematic review and meta-analysis. Medicine 96:e6059PubMedPubMedCentralCrossRefGoogle Scholar
  125. 125.
    Bilasy ME, Oraby MA, Ismail HM, Maklady FA (2012) Effectiveness of theophylline in preventing contrast-induced nephropathy after coronary angiographic procedures. J Interv Cardiol 25:404–410PubMedCrossRefGoogle Scholar
  126. 126.
    Dai B, Liu Y, Fu L, Li Y, Zhang J, Mei C (2012) Effect of theophylline on prevention of contrast-induced acute kidney injury: a meta-analysis of randomized controlled trials. Am J Kidney Dis 60:360–370PubMedCrossRefGoogle Scholar
  127. 127.
    Matejka J, Varvarovsky I, Vojtisek P et al (2010) Prevention of contrast-induced acute kidney injury by theophylline in elderly patients with chronic kidney disease. Heart Vessels 25:536–542PubMedCrossRefGoogle Scholar
  128. 128.
    Miao Y, Zhong Y, Yan H, Li W, Wang BY, Jin J (2013) Alprostadil plays a protective role in contrast-induced nephropathy in the elderly. Int Urol Nephrol 45:1179–1185PubMedCrossRefGoogle Scholar
  129. 129.
    Ye Z, Lu H, Guo W et al (2016) The effect of alprostadil on preventing contrast induced nephropathy for percutaneous coronary intervention in diabetic patients: a systematic review and meta-analysis. Medicine 95:e5306PubMedPubMedCentralCrossRefGoogle Scholar
  130. 130.
    Thamcharoen N, Thongprayoon C, Edmonds PJ, Cheungpasitporn W (2015) Periprocedural nebivolol for the prevention of contrast-induced acute kidney injury: a systematic review and meta-analysis. N Am J Med Sci 7:446–451PubMedPubMedCentralCrossRefGoogle Scholar
  131. 131.
    Naeem M, McEnteggart GE, Murphy TP, Prince E, Ahn S, Soares G (2015) Fenoldopam for the prevention of contrast-induced nephropathy (CIN) - do we need more trials? A meta-analysis. Clin Imaging 39:759–764PubMedCrossRefGoogle Scholar
  132. 132.
    Kassis HM, Minsinger KD, McCullough PA, Block CA, Sidhu MS, Brown JR (2015) A review of the use of Iloprost, a synthetic prostacyclin, in the prevention of radiocontrast nephropathy in patients undergoing coronary angiography and intervention. Clin Cardiol 38:492–498PubMedCrossRefGoogle Scholar
  133. 133.
    Inzucchi SE, Bergenstal RM, Buse JB et al (2015) Management of hyperglycemia in type 2 diabetes, 2015: a patient-centered approach: update to a position statement of the American Diabetes Association and the European Association for the Study of Diabetes. Diabetes Care 38:140–149PubMedCrossRefGoogle Scholar
  134. 134.
    Inzucchi SE, Lipska KJ, Mayo H, Bailey CJ, McGuire DK (2014) Metformin in patients with type 2 diabetes and kidney disease: a systematic review. JAMA 312:2668–2675PubMedPubMedCentralCrossRefGoogle Scholar
  135. 135.
    Lu WR, Defilippi J, Braun A (2013) Unleash metformin: reconsideration of the contraindication in patients with renal impairment. Ann Pharmacother 47:1488–1497PubMedCrossRefGoogle Scholar
  136. 136.
    Richy FF, Sabido-Espin M, Guedes S, Corvino FA, Gottwald-Hostalek U (2014) Incidence of lactic acidosis in patients with type 2 diabetes with and without renal impairment treated with metformin: a retrospective cohort study. Diabetes Care 37:2291–2295PubMedCrossRefGoogle Scholar
  137. 137.
    Salpeter SR, Greyber E, Pasternak GA, Salpeter EE (2010) Risk of fatal and nonfatal lactic acidosis with metformin use in type 2 diabetes mellitus. Cochrane Database Syst Rev 14:CD002967Google Scholar
  138. 138.
    Goergen SK, Rumbold G, Compton G, Harris C (2010) Systematic review of current guidelines, and their evidence base, on risk of lactic acidosis after administration of contrast medium for patients receiving metformin. Radiology 254:261–269PubMedCrossRefGoogle Scholar
  139. 139.
    Thomsen HS, Morcos SK, ESUR CMSC (1999) Contrast media and metformin: guidelines to diminish the risk of lactic acidosis in non-insulin-dependent diabetics after administration of contrast media. Eur Radiol 9:738-740Google Scholar
  140. 140.
    Food and Drug Administration (FDA) (2016) FDA revises warnings regarding use of the diabetes medicine metformin in certain patients with reduced kidney function. http://www.fda.gov/Drugs/DrugSafety/ucm493244.htm. Accessed 15 December 2017
  141. 141.
    ACR Committee on Drugs and Contrast Media (2017) ACR manual on contrast media, v10.3. American College of Radiology. https://www.acr.org/-/media/ACR/Files/Clinical-Resources/Contrast_Media.pdf. Accessed 15 December 2017
  142. 142.
    Morcos SK, Thomsen HS, Webb JA (2002) Dialysis and contrast media. Eur Radiol 12:3026–3030PubMedGoogle Scholar
  143. 143.
    Gabutti L (2003) Does continuous venovenous hemodiafiltration concomitant with radiological procedures provide a significant and safe removal of the iodinated contrast ioversol? Blood Purif 21:152–157PubMedCrossRefGoogle Scholar
  144. 144.
    Shinoda T, Hata T, Nakajima K, Yoshimoto H, Niwa A (2002) Time-course of iodine elimination by hemodialysis in patients with renal failure after angiography. Ther Apher 6:437–442PubMedCrossRefGoogle Scholar
  145. 145.
    Younathan CM, Kaude JV, Cook MD, Shaw GS, Peterson JC (1994) Dialysis is not indicated immediately after administration of nonionic contrast agents in patients with end-stage renal disease treated by maintenance dialysis. AJR Am J Roentgenol 163:969–971PubMedCrossRefGoogle Scholar

Copyright information

© The Author(s) 2018

Open Access This article is distributed under the terms of the Creative Commons Attribution 4.0 International License (http://creativecommons.org/licenses/by/4.0/), which permits unrestricted use, distribution, and reproduction in any medium, provided you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made.

Authors and Affiliations

  • Aart J. van der Molen
    • 1
  • Peter Reimer
    • 2
  • Ilona A. Dekkers
    • 1
  • Georg Bongartz
    • 3
  • Marie-France Bellin
    • 4
  • Michele Bertolotto
    • 5
  • Olivier Clement
    • 6
  • Gertraud Heinz-Peer
    • 7
  • Fulvio Stacul
    • 8
  • Judith A. W. Webb
    • 9
  • Henrik S. Thomsen
    • 10
  1. 1.Department of Radiology, C2-SLeiden University Medical CenterLeidenThe Netherlands
  2. 2.Institute for Diagnostic and Interventional Radiology Klinikum KarlsruheKarlsruheGermany
  3. 3.Department of Diagnostic RadiologyUniversity Hospitals of BaselBaselSwitzerland
  4. 4.Service Central de Radiologie Hôpital Paul Brousse 14VillejuifFrance
  5. 5.Department of RadiologyUniversity of TriesteTriesteItaly
  6. 6.Department of Radiology, Assistance Publique-Hôpitaux de ParisHôpital Européen Georges PompidouParisFrance
  7. 7.Department of Radiology, Zentralinstitut für medizinische Radiologie, Diagnostik und InterventionLandesklinikum St. PöltenSt. PöltenAustria
  8. 8.S.C. Radiologia Ospedale MaggioreTriesteItaly
  9. 9.Department of Radiology, St. Bartholomew’s HospitalUniversity of LondonLondonUK
  10. 10.Department of Diagnostic Radiology 54E2Copenhagen University Hospital HerlevHerlevDenmark

Personalised recommendations