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

Post-contrast acute kidney injury. Part 2: risk stratification, role of hydration and other... 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 � Dialysis schedules need not change when intravascular contrast medium is given . . . . Keywords Contrast media Acute kidney injury Metformin Haemodialysis Practice guidelines AGREE Appraisal of Guidelines for Research and Abbreviations and acronyms Evaluation ACEI Angiotensin Converting Enzyme Inhibitor AHRQ Agency for Healthcare Research and Quality ACR American College of Radiology * Henrik S. Thomsen Department of Radiology, Assistance Publique-Hôpitaux de Paris, Henrik.Thomsen@regionh.dk Hôpital Européen Georges Pompidou, 20 rue Leblanc, Paris Cedex 15, F-71015 Paris, France Department of Radiology, C2-S, Leiden University Medical Center, Department of Radiology, Zentralinstitut für medizinische Albinusdreef 2, NL-2333 ZA Leiden, The Netherlands Radiologie, Diagnostik und Intervention, Landesklinikum St. Pölten, Institute for Diagnostic and Interventional Radiology Klinikum Propst Führer-Straße 4, AT-3100 St. Pölten, Austria Karlsruhe, Moltkestraße 90, D-76133 Karlsruhe, Germany S.C. Radiologia Ospedale Maggiore, Piazza Ospitale 1, Department of Diagnostic Radiology, University Hospitals of Basel, I-34129 Trieste, Italy Petersgaben 4, CH-4033 Basel, Switzerland 4 Department of Radiology, St. Bartholomew’s Hospital, University of Service Central de Radiologie Hôpital Paul Brousse 14, av. London, West Smithfield, EC1A 7BE, London, UK P.-V.-Couturier, F-94807 Villejuif, France 5 10 Department of Radiology, University of Trieste, Strada di Fiume 447, Department of Diagnostic Radiology 54E2, Copenhagen University I-34149 Trieste, Italy Hospital Herlev, Herlev Ringvej 75, DK-2730 Herlev, Denmark Eur Radiol (2018) 28:2856–2869 2857 AKI Acute Kidney Injury acute kidney injury is not associated with gadolinium- ARB Angiotensin-II Receptor Blocker based contrast agents in doses approved for clinical mag- CA Coronary Angiography netic resonance imaging. CI-AKI Contrast-Induced Acute Kidney Injury In this second paper on PC-AKI, the following topics re- CIN Contrast-Induced Nephropathy lated to patient management are considered: CKD Chronic Kidney Disease CM Contrast Media 1. The role of questionnaires and risk scores to identify at- CMSC Contrast Media Safety Committee risk patients with reduced renal function CT Computed Tomography 2. The need to stop nephrotoxic medication before giving CTPA Computed Tomography Pulmonary Angiography D5W Dextrose 5% in Water CM eGFR Estimated Glomerular Filtration Rate 3. The optimal hydration protocols for protecting against ESUR European Society of Urogenital Radiology PC-AKI FDA Federal Drugs Administration 4. The possible role of prophylactic drug treatment in GFR Glomerular Filtration Rate preventing PC-AKI HD Haemodialysis 5. The need to adapt metformin administration when giving HF Haemofiltration CM IA Intra-Arterial 6. The need to alter schedules for dialysis in the period be- IV Intravenous fore and after CM administration NAc N-Acetylcysteine NaHCO Sodium Bicarbonate Recommendations are made for items 1–6. The recommen- NSAID Non-Steroidal Anti-Inflammatory Drug dations have been incorporated into version 10 of the ESUR NYHA New York Heart Association OCEBM Oxford Centre for Evidence Based Medicine CMSC guidelines, at the end of this paper (Table 4). PC-AKI Post-Contrast Acute Kidney Injury PCI Percutaneous Coronary Intervention PICO Patient–Intervention–Comparator–Outcome PS Propensity Score Materials and methods RAAS Renin–Angiotensin–Aldosterone System RSTN Radiological Society of the Netherlands The recommendations were prepared using the Appraisal RCT Randomised Controlled Trial of Guidelines for Research and Evaluation (AGREE) II RRT Renal Replacement Therapy document [4]. A guideline Writing Group (WG) prepared sCr Serum Creatinine ten clinical questions in PICO format [5]. Systematic WG Writing Group search strings were developed with a professional librari- an for four different biomedical literature databases (PubMed, Web of Science, Embase and the Cochrane Introduction Library). The titles and abstracts were screened for rele- vance and selected on predefined inclusion and exclusion The Contrast Media Safety Committee (CMSC) of the criteria. Emphasis was put on comparative studies with European Society of Urogenital Radiology (ESUR) pro- strong scientific evidence, such as meta-analyses and sys- duced their most recent guidelines on what was then tematic reviews, and prospective randomised controlled termed contrast-induced nephropathy (CIN) in 2011 [1]. trials (RCTs). The six systematic searches in this manu- Guidelines on the use of contrast media (CM) in patients script yielded 3402 references of which 445 were selected on dialysis and on the use of CM in diabetic patients on the basis of title and abstract. After review of the full using metformin were published in 2002 and 2014 [2, text of these 445 publications, 145 were selected for in- 3]. This review provides recommendations for updating clusion in this paper. The quality of the evidence from the the CMSC guidelines which were obtained using a struc- selected articles was evaluated according to the Oxford tured literature review based on clinical questions and Centre for Evidence Based Medicine levels of evidence: Patient–Intervention–Comparator–Outcome (PICO) for- grade A, established scientific evidence; grade B, scien- matting. Since the literature related to the topics consid- tific presumption; grade C, low level of evidence [6]. ered is so large, the results of the review have been split When there was no scientific evidence, recommendations into two papers. The review only considers post-contrast werebasedonWGconsensus andweregradedasexpert kidney injury (PC-AKI) after iodine-based CM because opinion (grade D). 2858 Eur Radiol (2018) 28:2856–2869 Table 1 PC-AKI: Risk stratification; use of nephrotoxic medication The full description of the materials and methods appears in part 1. Risk stratification The term intra-arterial injection with first pass renal In hospitals which use sCr measurements for all patients before exposure indicates that contrast medium reaches the kid- intravascular CM administration there is no benefit in using questionnaires for PC-AKI risk stratification. neys in a relatively undiluted form, e.g. injection into the left heart, thoracic and suprarenal abdominal aorta or the In hospitals which use sCr measurements selectively, Choyke questionnaires may be used to identify patients with eGFR < 45 renal arteries. The term intra-arterial injection with second ml/min/1.73 m before intra-arterial CM administration with first pass pass renal exposure indicates that contrast medium renal exposure. reaches the renal arteries after dilution either in the pul- Level of evidence D monary or peripheral circulation, e.g. injection into the Risk prediction scores are only available for coronary angiography and/or right heart, pulmonary artery, carotid, subclavian, coro- percutaneous coronary intervention, and have only modest abilities, so nary, mesenteric or infrarenal arteries. cannot be recommended to stratify the risk of PC-AKI. Level of evidence A Nephrotoxic medication Results In CKD patients receiving CM, optimal nephrologic care involves minimising the use of nephrotoxic drugs. Level of evidence D Question 5: Should questionnaires or scoring systems ACE inhibitors and angiotensin receptor blockers do not have to be be used for risk stratification by clinicians when they stopped before CM administration. request a contrast-enhanced imaging study? Level of evidence B There is insufficient evidence to recommend withholding nephrotoxic Patient questionnaires drugs such as NSAIDs, antimicrobial agents or chemotherapeutic agents before CM administration. Questionnaires, such as that proposed by Choyke [7], use Level of evidence C information about a history of renal disease or renal sur- gery, heart failure, diabetes, proteinuria, hypertension and gout to stratify patients for their PC-AKI risk so that sCr clinical outcome. In clinical practice, a prediction rule measurements need only be done selectively. This may would require a high discriminatory value, i.e. a C- work well and can save resources [8]. Observational stud- statistic greater than 0.80 [16]. ies have shown that these questionnaires can identify pa- The best-known risk model is the eight-variable Mehran tients with eGFR < 45 ml/min/1.73 m with adequate score [17], which has been studied in more than 15,000 pa- sensitivity, especially if they are aged less than 70 tients and has been externally validated in multiple studies, but [9–11]. Since eGFR measurement can detect more pa- with variable C-statistic values of 0.57–0.85 [16, 18–20]. The tients with renal dysfunction than questionnaires [12], Mehran score correlates relatively well with clinical outcomes with easier patient logistics and similar cost- [21]. Newer risk scores with good discriminatory value, avail- effectiveness [13, 14], many hospitals have adopted a pol- able in user-friendly calculators or smartphone applications, icy of sCr measurements in all patients scheduled for in- still need external validation [22]. A recent systematic review travenous (IV) CM and no longer use questionnaires for of 16 risk models concluded that they had only modest pre- risk stratification or selection for eGFR measurement dictive value [23] and a review and meta-analysis of 74 risk (Table 1). models noted their heterogeneity and concluded that further research was needed to evaluate the effect of such models on Risk prediction models clinical care [24](Table 1). No risk models have been produced yet for IV or IA CM administration with second pass renal exposure. For pa- Question 6: Should nephrotoxic medication be tients having coronary angiography (CA) or percutaneous withheld to reduce the risk of PC-AKI? coronary intervention (PCI), many different risk scores have been proposed to stratify the patient’s PC-AKI risk, Optimal nephrologic care involves minimizing the use of and most include pre-procedural and procedural data. A nephrotoxic drugs where clinically possible [25]. Many fre- model with only pre-procedural data [15] would be more quently prescribed medications, such as nonselective practical for selecting suitable preventive measures. Risk NSAIDs, selective Cox-2 inhibitors, several classes of scores should be verified in relation to improvements in Eur Radiol (2018) 28:2856–2869 2859 Table 2 PC-AKI prophylaxis: Hydration, drugs, renal replacement therapy antimicrobial agents and chemotherapeutic agents have neph- rotoxic potential and can induce AKI [26]. Hydration There is little good quality data about the relationship Preventive hydration should be used to reduce the incidence of PC-AKI between these drugs and PC-AKI [27]. A retrospective in at-risk patients. cohort study showed that concurrent use of four or more Level of evidence B nephrotoxic agents was significantly predictive for PC- Intravenous saline and bicarbonate protocols have similar efficacy for hydration. AKI in patients given IV CM [28]. A meta-analysis of PC-AKI incidence following CM-enhanced CT found that Level of evidence A concurrent administration of NSAIDs was an independent For intravenous and intra-arterial CM administration with second pass renal exposure hydrate the patient with either (a) 3 ml/kg/h bicarbonate risk factor for PC-AKI [29]. 1.4% (or 154 mmol/l solution) for 1 h before CM or (b) 1 ml/kg/h The effect of withholding angiotensin converting en- saline 0.9% for 3–4hbeforeand 4–6hafter CM. zyme inhibitors (ACEI) and angiotensin-2 receptor Level of evidence D blockers (ARB) in chronic users has been extensively For intra-arterial CM administration with first pass renal exposure hydrate evaluated. Multiple RCTs [30, 31] and observational stud- the patient with either (a) 3 ml/kg/h bicarbonate 1.4% (or 154 mmol/l ies gave conflicting results and are limited by small sam- solution) for 1 h before CM followed by 1 ml/kg/h bicarbonate 1.4% (or 154 mmol/l) for 4–6h afterCM ple sizes and significant heterogeneity [32–34]. However, meta-analyses of RCTs found no lower risk [34]. or (b) 1 ml/kg/h saline 0.9% for 3–4 h before and 4–6h afterCM. Withholding ACEI/ARB may be associated with a slight- Level of evidence D ly lowerriskofPC-AKIbut theevidenceisnot sufficient- Oral hydration as the sole means of prevention is not recommended. ly strong to recommend this (Table 1). Level of evidence D In patients with severe heart failure (NYHA grade 3–4) or patients with Question 7: What are the most cost- end-stage renal failure (CKD grade V) preventive IV hydration should be individualized by the clinician responsible for patient care. and time-effective protocols for oral and intravenous Level of evidence D hydration to reduce the risk of PC-AKI? Drugs N-Acetylcysteine has not been conclusively shown to reduce the risk of Hydration as a preventive strategy for PC-AKI PC-AKI in patients with eGFR < 45 ml/min/1.73 m receiving intravenous or intra-arterial CM, and its use is NOT recommended. Evidence for prevention of PC-AKI with IV saline hydration Level of evidence A (volume expansion) comes from RCTs in patients who re- Giving short-term, high-dose statins to patients not already taking statins ceived intra-arterial (IA) CM during percutaneous interven- has not been shown to reduce the risk of PC-AKI in patients with eGFR tion [35–37], and in patients who received bicarbonate hydra- < 45 ml/min/1.73 m receiving intravenous or intra-arterial CM, and its use is NOT recommended. tion before IV enhanced emergency CTPA [38]. One RCT Level of evidence B evaluated the evidence for IA CM administration during CA ACE inhibitors or angiotensin receptor blockers have not been shown [39]. These studies found that, for both IA and IV CM admin- conclusively to reduce the risk of PC-AKI in patients receiving istration, the incidence of PC-AKI was significantly lower in intravenous or intra-arterial CM, and their use is NOT recommended. patients who received IV hydration compared to placebo, and Level of evidence B that hydration prevented emergency dialysis [36]. Significant Vitamin C has not been shown conclusively to reduce the risk of PC-AKI differences for mortality or other adverse events were not in patients receiving intravenous or intra-arterial CM, and its use is found. There were few patients with severe renal impairment NOT recommended. (eGFR < 30 ml/min/1.73 m ) in almost all studies. The recent Level of evidence B AMACING trial showed that for patients with eGFR > 30 ml/ Renal replacement therapy min/1.73 m receiving IV CM there was no difference be- Renal replacement therapy has not been shown conclusively to reduce the tween no hydration and hydration in preventing PC-AKI [40]. risk of PC-AKI in patients receiving intravenous or intra-arterial CM, and its use is NOT recommended. Level of evidence B 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 compared to IV hydration, but the studies were limited control. Nine studies evaluated oral hydration, but were by heterogeneity and lack of hard clinical outcomes limited by small patient numbers and by the absence of [49–51]. The CMSC does not recommend the use of oral patients with severe renal impairment [39, 41–48]. Three hydration as the sole preventive strategy for PC-AKI, but meta-analyses concluded that there is no evidence that unrestricted intake of clear oral fluids in addition to IV oral hydration is associated with more risk of PC-AKI volume expansion is supported (Table 2). 2860 Eur Radiol (2018) 28:2856–2869 Intravenous hydration: saline versus bicarbonate In which patients should the hydration protocol be individualized? Normal saline (NaCl 0.9%) and sodium bicarbonate solution (1.4% or 154 mmol NaHCO in D5W) are the two most com- There is no data to suggest that patients with severe renal monly studied crystalloid solutions. The rationale for using impairment (CKD grade V) or severe heart failure (NYHA bicarbonate is that alkalinisation can reduce the formation of grade 3–4) should receive different hydration protocols. free reactive oxygen species [52]. Initial studies favoured bi- However, IV hydration with large volumes may exacerbate carbonate [53–56], but this was not replicated in later studies acute heart failure and induce pulmonary oedema [40]. The [57–62], so IV hydration with bicarbonate can be considered opinion of the CMSC is that hydration protocols in these equivalent to normal saline. patients should be individualized for type, volume and There is no consensus on the optimal hydration re- duration. gime. Most studies have compared bicarbonate given pre- and post-CM for less than 6 h [53] to longer dura- Question 8: Which other strategies (pharmaceutical, tion saline pre- and post-CM protocols (12–24 h). In all vitamin, renal replacement therapy) have been studies, there are few patients with eGFR < 30 ml/min/ proved effective in preventing PC-AKI? 1.73 m , and evidence about whether short duration bi- carbonate is better than long duration saline is conflicting N-Acetylcysteine (NAc) [63–71]. There is limited evidence on whether pre- hydration only is inferior to pre- and post-hydration, Most recent RCTs or meta-analyses do not show a protective and only one very short duration bicarbonate protocol effect of NAc against PC-AKI following coronary or periph- has been evaluated [38, 72, 73]. eral angiography [66, 80–84]. NAc also failed to affect clinical Most studies have been performed in cardiac patients ad- outcome in coronary or peripheral angiography [85]orto have mitted for CA or PCI. Three studies evaluated hydration pro- aprotective effect in CT [86, 87] or in patients with diabetes tocols in patients having contrast-enhanced CT, and did not mellitus undergoing coronary or peripheral angiography [88, favour bicarbonate over saline [38, 72, 74]. No studies were 89]. Comparative studies with NAc combined with saline or identified assessing the beneficial effect of other crystalloids. sodium bicarbonate protocols did not show any additional However, balanced crystalloid solutions, such as Ringer’slac- effect of protective effect of NAc [61, 90–93]. However, more tate, may be preferable in critical care populations, because recent meta-analyses showed a benefit of NAc, with or with- they avoid the harmful effects of hyperchloraemic acidosis. out high-dose statins, when added to hydration for preventing The CMSC considers that for IV and IA CM injection PC-AKI [94–96]. with second pass renal exposure either a short bicarbonate hydration regime before CM or a conventional protocol with Statins saline given before and after CM may be used. For IA CM injection with first pass renal exposure conventional proto- Several meta-analyses showed lower overall PC-AKI rates cols with either bicarbonate or saline given before and after with the use of high-dose, short-term statin treatment CM should be used (Table 2). compared to controls [95–105]. Lower PC-AKI rates were also found in subgroups, such as older patients, patients with acute coronary syndromes and for high-dose statin Forced diuresis versus conventional hydration regimes. Some of these meta-analyses showed a reduced need for RRT after statins, but no reduction in all-cause Newer approaches for patients with impaired left ventricular mortality [97, 102]. However, the US Agency for function combine controlled saline hydration with a forced Healthcare Research and Quality (AHRQ) meta-analysis high urinary flow rate to maintain euvolemia and avoid showed that the risk of PC-AKI was only significantly overhydration and several RCTs showed better results than reduced when statins were added to hydration and NAc. conventional hydration protocols [75–77]. Other catheter- A reduction in PC-AKI risk could not be shown when based strategies used left ventricular end-diastolic pressure statins plus hydration were compared to hydration alone or central venous pressure to guide hydration [78, 79]. In in patients not taking statins. The standard of evidence these RCTs the incidence of PC-AKI was lower than with grade was low in both analyses [94]. standard IV hydration. Since the forced diuresis studies have Despite the many positive results, it is difficult to make a heterogeneous populations, interventions and control hydra- general recommendation for statins [106] because the patients tion protocols, their findings cannot be pooled. The CMSC studied were invariably cardiac, and a variety of statin and considers that there is not sufficient evidence to recommend hydration protocols were used. Patients with CKD grade forced diuresis. 3B–5 (eGFR < 45 ml/min/1.73 m ) are under-represented in Eur Radiol (2018) 28:2856–2869 2861 the studies and results in these patients remain inconclusive Question 9: Should administration of metformin be [102, 103, 107, 108]. Most patients undergoing CA/PCI are adapted to reduce the risk of metformin-associated already taking long-term statins, and results in these patients lactic acidosis in patients with type 2 diabetes mellitus are unclear. scheduled to receive intravascular contrast media? While the CMSC recognises the potential preventive ef- fects of short-term statins, it does not advise the use of short- Metformin is the standard drug for monotherapy of type 2 term, high-dose statins as a single strategy for preventing PC- diabetes mellitus [133]. The effect of CM on the risk of AKI (Table 2). metformin-associated lactic acidosis is indirect, since an epi- sode of AKI following intravascular CM administration may lead to metformin accumulation. The use of metformin in RAAS blockade: ACE inhibitors and angiotensin-II receptor patients with eGFR 30–59 ml/min/1.73 m is considered safe blockers if doses are reduced appropriately [134, 135]. Limiting the metformin dose to a maximum of 2000 mg/day for eGFR Administration of renin–angiotensin–aldosterone system 45–60 ml/min/1.73 m and to a maximum of 1000 mg/day (RAAS) blockade as a preventive measure for patients not tak- for eGFR 30–44 ml/min/1.73 m has been recommended. In ing these drugs did not show a significant effect on the inci- patients with eGFR 30–59 ml/min/1.73 m metformin drug dence of PC-AKI in recent meta-analyses [32, 34](Table 2). levels remain within therapeutic ranges. For patients with eGFR < 30 ml/min/1.73 m metformin administration is not approved. Vitamin C Multiple studies and meta-analyses have shown that the risk of lactic acidosis is very low and linked more to the The majority of RCTs or meta-analyses do not demon- underlying disease and possible co-morbidities rather than strate a protective effect of vitamin C against PC-AKI in the use of metformin [134, 136, 137]. Because of the lack of patients with CKD predominantly undergoing coronary published evidence on metformin and CM, early guidelines angiography [109–111]orany benefitofthe use ofvita- about the need to stop metformin before intravascular CM min C, NAc or a combination of both over the standard were based on consensus, and were strict [138, 139]. As the hydration regimen in preventing PC-AKI [112, 113] low risk of lactic acidosis became apparent, guidelines have (Table 2). Combining vitamin C with pentoxifylline also become less restrictive [3]. failed to show an advantage [114]. Only two publications Since no new published evidence is available, the CMSC [115, 116] have shown a protective effect of vitamin C in has updated its recommendations based on recent patients with CKD undergoing CA. Renal replacement therapy (RRT) Table 3 Metformin administration, dialysis schedules There is no convincing evidence in favour of preventive Metformin administration in patients at risk of PC-AKI haemodialysis or RRT alone [117–119]or combined with hy- Note that these recommendations may deviate from current EMA/FDA recommendations. dration [120] in patients with CKD, predominantly undergo- Patients with eGFR > 30 ml/min/1.73 m and no evidence of AKI ing CA (Table 2). There is no evidence of an increased risk of receiving either intravenous CM or intra-arterial CM with second pass permanent anuria in patients on peritoneal dialysis undergoing renal exposure: continue taking metformin normally. CA [121]. There is a single study showing better late-stage Patients (a) with eGFR < 30 ml/min/1.73 m receiving either intravenous (day 5–30) renal protection against PC-AKI with simulta- CM or intra-arterial CM with second pass renal exposure or (b) neous haemodialysis [122]. 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. Miscellaneous Level of evidence D Dialysis schedules in relation to CM administration The data on the protective effects of several agents, such It is not necessary to adapt the timing of intravascular CM administration as trimatizidine [123, 124], theophylline [95, 125–127], in relation to the dialysis schedule in patients undergoing chronic alprostadil [128, 129], nebivolol [130], fenoldopam [131] dialysis or haemofiltration, but it may be done to minimise volume overload. and iloprost [132], is not conclusive and does not sup- port recommending their use to reduce the risk of PC- Level of evidence D AKI. 2862 Eur Radiol (2018) 28:2856–2869 Table 4 ESUR CMSC guideline Definitions (version 10) for post-contrast acute kidney injury (PC-AKI) 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 m )= −0.329 Age Female sCr ≤ 62 μmol/l: 144 × (sCr/62) ×0.993 −1.209 Age Female sCr > 62 μmol/l: 144 × (sCr/62) ×0.993 −0.411 Age Male sCr ≤ 80 μmol/l: 141 × (sCr/80) ×0.993 −1.209 Age Male sCr > 80 μmol/l: 141 × (sCr/80) ×0.993 (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 m ) = 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 m before intra-arterial contrast medium administration with first pass renal exposure or in ICU patients � eGFR less than 30 ml/min/1.73 m 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 m ) - 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 Eur Radiol (2018) 28:2856–2869 2863 Table 4 (continued) - 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 m for intra- arterial administration with first pass renal exposure and eGFR less than 30 ml/min/1.73 m 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 4–6h 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 m ) � 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 m ) < 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 m 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 m 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. 2864 Eur Radiol (2018) 28:2856–2869 Table 4 (continued) 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 Haemodialysis to remove iodine-based contrast medium is unnecessary ambulatory peritoneal dialysis recommendations from the FDA [140], and on guidelines AKI. There is no need to adapt dialysis schedules in patients from the ACR and RSTN [14, 141](Table 3). being given intravascular CM. The recommendations made in this paper have been incor- porated into the ESUR CMSC guidelines version 10 (Table 4). Question 10: Should the timing of CM administration be adapted to the schedule of haemodialysis Funding The authors state that this work has not received any funding. or haemofiltration sessions in patients on renal replacement therapy? Compliance with ethical standards Guarantor The scientific guarantor of this publication is Prof. Henrik S. Iodine-based CM can be safely removed by haemodialysis Thomsen. (HD) or haemofiltration (HF). Many factors influence the ef- fectiveness of HD, such as flow rate of blood and dialysate, Conflict of interest Aart van der Molen has received incidental pay- dialysis membrane permeability, HD duration, and CM char- ments for lectures and chairmanships at scientific meetings for contrast acteristics such as molecular size, protein binding, hydrophi- agent safety related issues (contrast agent reactions, Gd-retention) from GE, Bayer, Bracco and Guerbet. licity and electrical charge [142]. Fulvio Stacul has received lecture fees from Bracco and Guerbet. Although HF concomitant with radiological procedures Olivier Clément has received lecture fees from Bracco and Guerbet. has been shown to be feasible and well tolerated [143, 144], The other authors of this manuscript declare no relationships with any the fractional removal of iodine-based CM contrast agents is companies whose products and services may be related to the subject matter of this article. modest and several HF or HD sessions are needed to remove 95% of the administered CM [143]. Also, there is no evidence Statistics and biometry No complex statistical methods were necessary for the necessity of emergency HD after administration of for this paper. iodine-based CM in patients on chronic HD [145]. However, to avoid volume overload, CM administration may be Informed consent Written informed consent was not required for this synchronised with scheduled HF or HD (Table 3). 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. Conclusion Methodology Assessment of the risk of PC-AKI before intravascular CM is � retrospective administered is best done by measuring eGFR but the alterna- � multicentre study tive of a questionnaire for patients detects most patients with eGFR less than 45 ml/min/1.73 m . Volume expansion with Open Access This article is distributed under the terms of the Creative normal saline or sodium bicarbonate remains the mainstay of Commons Attribution 4.0 International License (http:// PC-AKI prevention, but there is still uncertainty about the creativecommons.org/licenses/by/4.0/), which permits unrestricted use, optimal protocol. The additional benefit of a number of drugs, distribution, and reproduction in any medium, provided you give appro- priate credit to the original author(s) and the source, provide a link to the such as N-acetylcysteine, statins, ACE inhibitors and Creative Commons license, and indicate if changes were made. angiotensin-II receptor blockers, and vitamin C in preventing PC-AKI has not been proved conclusively. Stopping nephro- toxic medications appears to be of limited value in preventing PC-AKI. Recommendations for discontinuing metformin References when CM is given have been relaxed and now only apply to patients with eGFR < 30 ml/min/1.73 m receiving IV CM or 1. 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Brueck M, Cengiz H, Hoeltgen R et al (2013) Usefulness of N- phropathy after coronary angiographic procedures. J Interv acetylcysteine or ascorbic acid versus placebo to prevent contrast- Cardiol 25:404–410 induced acute kidney injury in patients undergoing elective cardi- 126. Dai B, Liu Y, Fu L, Li Y, Zhang J, Mei C (2012) Effect of theoph- ac catheterization: a single-center, prospective, randomized, dou- ylline on prevention of contrast-induced acute kidney injury: a ble-blind, placebo-controlled trial. J Invasive Cardiol 25:276–283 meta-analysis of randomized controlled trials. Am J Kidney Dis 60:360–370 110. Dvorsak B, Kanic V, Ekart R, Bevc S, Hojs R (2013) Ascorbic acid for the prevention of contrast-induced nephropathy after cor- 127. Matejka J, Varvarovsky I, Vojtisek P et al (2010) Prevention of onary angiography in patients with chronic renal impairment: a contrast-induced acute kidney injury by theophylline in elderly randomized controlled trial. Ther Apher Dial 17:384–390 patients with chronic kidney disease. Heart Vessels 25:536–542 111. Li R, Chen H (2012) Prevention of contrast-induced nephropathy 128. Miao Y, Zhong Y, Yan H, Li W, Wang BY, Jin J (2013) Alprostadil with ascorbic acid. Heart 98:E211 plays a protective role in contrast-induced nephropathy in the el- 112. Albabtain MA, Almasood A, Alshurafah H, Alamri H, Tamim H derly. Int Urol Nephrol 45:1179–1185 (2013) Efficacy of ascorbic acid, N-acetylcysteine, or combination 129. Ye Z, Lu H, Guo W et al (2016) The effect of alprostadil on of both on top of saline hydration versus saline hydration alone on preventing contrast induced nephropathy for percutaneous coro- prevention of contrast-Induced nephropathy: a prospective ran- nary intervention in diabetic patients: a systematic review and domized study. J Interv Cardiol 26:90–96 meta-analysis. Medicine 95:e5306 113. Zhou L, Chen H (2012) Prevention of contrast-induced nephrop- 130. Thamcharoen N, Thongprayoon C, Edmonds PJ, Cheungpasitporn athy with ascorbic acid. Intern Med 51:531–535 W (2015) Periprocedural nebivolol for the prevention of contrast- 114. Shakeryan F, Sanati H, Fathi H et al (2013) Evaluation of combi- induced acute kidney injury: a systematic review and meta-analy- nation therapy with vitamin C and pentoxifylline on preventing sis. N Am J Med Sci 7:446–451 kidney failure secondary to intravenous contrast material in coro- 131. Naeem M, McEnteggart GE, Murphy TP, Prince E, Ahn S, Soares nary angioplasty. Iran Heart J 14:17–21 G (2015) Fenoldopam for the prevention of contrast-induced Eur Radiol (2018) 28:2856–2869 2869 nephropathy (CIN) - do we need more trials? A meta-analysis. lactic acidosis after administration of contrast medium for patients receiving metformin. Radiology 254:261–269 Clin Imaging 39:759–764 132. Kassis HM, Minsinger KD, McCullough PA, Block CA, Sidhu 139. 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AJR Am J Roentgenol 163:969–971 review of current guidelines, and their evidence base, on risk of http://www.deepdyve.com/assets/images/DeepDyve-Logo-lg.png European Radiology Springer Journals

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

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References (169)

Publisher
Springer Journals
Copyright
Copyright © 2018 by The Author(s)
Subject
Medicine & Public Health; Imaging / Radiology; Diagnostic Radiology; Interventional Radiology; Neuroradiology; Ultrasound; Internal Medicine
ISSN
0938-7994
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1432-1084
DOI
10.1007/s00330-017-5247-4
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29417249
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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 � Dialysis schedules need not change when intravascular contrast medium is given . . . . Keywords Contrast media Acute kidney injury Metformin Haemodialysis Practice guidelines AGREE Appraisal of Guidelines for Research and Abbreviations and acronyms Evaluation ACEI Angiotensin Converting Enzyme Inhibitor AHRQ Agency for Healthcare Research and Quality ACR American College of Radiology * Henrik S. Thomsen Department of Radiology, Assistance Publique-Hôpitaux de Paris, Henrik.Thomsen@regionh.dk Hôpital Européen Georges Pompidou, 20 rue Leblanc, Paris Cedex 15, F-71015 Paris, France Department of Radiology, C2-S, Leiden University Medical Center, Department of Radiology, Zentralinstitut für medizinische Albinusdreef 2, NL-2333 ZA Leiden, The Netherlands Radiologie, Diagnostik und Intervention, Landesklinikum St. Pölten, Institute for Diagnostic and Interventional Radiology Klinikum Propst Führer-Straße 4, AT-3100 St. Pölten, Austria Karlsruhe, Moltkestraße 90, D-76133 Karlsruhe, Germany S.C. Radiologia Ospedale Maggiore, Piazza Ospitale 1, Department of Diagnostic Radiology, University Hospitals of Basel, I-34129 Trieste, Italy Petersgaben 4, CH-4033 Basel, Switzerland 4 Department of Radiology, St. Bartholomew’s Hospital, University of Service Central de Radiologie Hôpital Paul Brousse 14, av. London, West Smithfield, EC1A 7BE, London, UK P.-V.-Couturier, F-94807 Villejuif, France 5 10 Department of Radiology, University of Trieste, Strada di Fiume 447, Department of Diagnostic Radiology 54E2, Copenhagen University I-34149 Trieste, Italy Hospital Herlev, Herlev Ringvej 75, DK-2730 Herlev, Denmark Eur Radiol (2018) 28:2856–2869 2857 AKI Acute Kidney Injury acute kidney injury is not associated with gadolinium- ARB Angiotensin-II Receptor Blocker based contrast agents in doses approved for clinical mag- CA Coronary Angiography netic resonance imaging. CI-AKI Contrast-Induced Acute Kidney Injury In this second paper on PC-AKI, the following topics re- CIN Contrast-Induced Nephropathy lated to patient management are considered: CKD Chronic Kidney Disease CM Contrast Media 1. The role of questionnaires and risk scores to identify at- CMSC Contrast Media Safety Committee risk patients with reduced renal function CT Computed Tomography 2. The need to stop nephrotoxic medication before giving CTPA Computed Tomography Pulmonary Angiography D5W Dextrose 5% in Water CM eGFR Estimated Glomerular Filtration Rate 3. The optimal hydration protocols for protecting against ESUR European Society of Urogenital Radiology PC-AKI FDA Federal Drugs Administration 4. The possible role of prophylactic drug treatment in GFR Glomerular Filtration Rate preventing PC-AKI HD Haemodialysis 5. The need to adapt metformin administration when giving HF Haemofiltration CM IA Intra-Arterial 6. The need to alter schedules for dialysis in the period be- IV Intravenous fore and after CM administration NAc N-Acetylcysteine NaHCO Sodium Bicarbonate Recommendations are made for items 1–6. The recommen- NSAID Non-Steroidal Anti-Inflammatory Drug dations have been incorporated into version 10 of the ESUR NYHA New York Heart Association OCEBM Oxford Centre for Evidence Based Medicine CMSC guidelines, at the end of this paper (Table 4). PC-AKI Post-Contrast Acute Kidney Injury PCI Percutaneous Coronary Intervention PICO Patient–Intervention–Comparator–Outcome PS Propensity Score Materials and methods RAAS Renin–Angiotensin–Aldosterone System RSTN Radiological Society of the Netherlands The recommendations were prepared using the Appraisal RCT Randomised Controlled Trial of Guidelines for Research and Evaluation (AGREE) II RRT Renal Replacement Therapy document [4]. A guideline Writing Group (WG) prepared sCr Serum Creatinine ten clinical questions in PICO format [5]. Systematic WG Writing Group search strings were developed with a professional librari- an for four different biomedical literature databases (PubMed, Web of Science, Embase and the Cochrane Introduction Library). The titles and abstracts were screened for rele- vance and selected on predefined inclusion and exclusion The Contrast Media Safety Committee (CMSC) of the criteria. Emphasis was put on comparative studies with European Society of Urogenital Radiology (ESUR) pro- strong scientific evidence, such as meta-analyses and sys- duced their most recent guidelines on what was then tematic reviews, and prospective randomised controlled termed contrast-induced nephropathy (CIN) in 2011 [1]. trials (RCTs). The six systematic searches in this manu- Guidelines on the use of contrast media (CM) in patients script yielded 3402 references of which 445 were selected on dialysis and on the use of CM in diabetic patients on the basis of title and abstract. After review of the full using metformin were published in 2002 and 2014 [2, text of these 445 publications, 145 were selected for in- 3]. This review provides recommendations for updating clusion in this paper. The quality of the evidence from the the CMSC guidelines which were obtained using a struc- selected articles was evaluated according to the Oxford tured literature review based on clinical questions and Centre for Evidence Based Medicine levels of evidence: Patient–Intervention–Comparator–Outcome (PICO) for- grade A, established scientific evidence; grade B, scien- matting. Since the literature related to the topics consid- tific presumption; grade C, low level of evidence [6]. ered is so large, the results of the review have been split When there was no scientific evidence, recommendations into two papers. The review only considers post-contrast werebasedonWGconsensus andweregradedasexpert kidney injury (PC-AKI) after iodine-based CM because opinion (grade D). 2858 Eur Radiol (2018) 28:2856–2869 Table 1 PC-AKI: Risk stratification; use of nephrotoxic medication The full description of the materials and methods appears in part 1. Risk stratification The term intra-arterial injection with first pass renal In hospitals which use sCr measurements for all patients before exposure indicates that contrast medium reaches the kid- intravascular CM administration there is no benefit in using questionnaires for PC-AKI risk stratification. neys in a relatively undiluted form, e.g. injection into the left heart, thoracic and suprarenal abdominal aorta or the In hospitals which use sCr measurements selectively, Choyke questionnaires may be used to identify patients with eGFR < 45 renal arteries. The term intra-arterial injection with second ml/min/1.73 m before intra-arterial CM administration with first pass pass renal exposure indicates that contrast medium renal exposure. reaches the renal arteries after dilution either in the pul- Level of evidence D monary or peripheral circulation, e.g. injection into the Risk prediction scores are only available for coronary angiography and/or right heart, pulmonary artery, carotid, subclavian, coro- percutaneous coronary intervention, and have only modest abilities, so nary, mesenteric or infrarenal arteries. cannot be recommended to stratify the risk of PC-AKI. Level of evidence A Nephrotoxic medication Results In CKD patients receiving CM, optimal nephrologic care involves minimising the use of nephrotoxic drugs. Level of evidence D Question 5: Should questionnaires or scoring systems ACE inhibitors and angiotensin receptor blockers do not have to be be used for risk stratification by clinicians when they stopped before CM administration. request a contrast-enhanced imaging study? Level of evidence B There is insufficient evidence to recommend withholding nephrotoxic Patient questionnaires drugs such as NSAIDs, antimicrobial agents or chemotherapeutic agents before CM administration. Questionnaires, such as that proposed by Choyke [7], use Level of evidence C information about a history of renal disease or renal sur- gery, heart failure, diabetes, proteinuria, hypertension and gout to stratify patients for their PC-AKI risk so that sCr clinical outcome. In clinical practice, a prediction rule measurements need only be done selectively. This may would require a high discriminatory value, i.e. a C- work well and can save resources [8]. Observational stud- statistic greater than 0.80 [16]. ies have shown that these questionnaires can identify pa- The best-known risk model is the eight-variable Mehran tients with eGFR < 45 ml/min/1.73 m with adequate score [17], which has been studied in more than 15,000 pa- sensitivity, especially if they are aged less than 70 tients and has been externally validated in multiple studies, but [9–11]. Since eGFR measurement can detect more pa- with variable C-statistic values of 0.57–0.85 [16, 18–20]. The tients with renal dysfunction than questionnaires [12], Mehran score correlates relatively well with clinical outcomes with easier patient logistics and similar cost- [21]. Newer risk scores with good discriminatory value, avail- effectiveness [13, 14], many hospitals have adopted a pol- able in user-friendly calculators or smartphone applications, icy of sCr measurements in all patients scheduled for in- still need external validation [22]. A recent systematic review travenous (IV) CM and no longer use questionnaires for of 16 risk models concluded that they had only modest pre- risk stratification or selection for eGFR measurement dictive value [23] and a review and meta-analysis of 74 risk (Table 1). models noted their heterogeneity and concluded that further research was needed to evaluate the effect of such models on Risk prediction models clinical care [24](Table 1). No risk models have been produced yet for IV or IA CM administration with second pass renal exposure. For pa- Question 6: Should nephrotoxic medication be tients having coronary angiography (CA) or percutaneous withheld to reduce the risk of PC-AKI? coronary intervention (PCI), many different risk scores have been proposed to stratify the patient’s PC-AKI risk, Optimal nephrologic care involves minimizing the use of and most include pre-procedural and procedural data. A nephrotoxic drugs where clinically possible [25]. Many fre- model with only pre-procedural data [15] would be more quently prescribed medications, such as nonselective practical for selecting suitable preventive measures. Risk NSAIDs, selective Cox-2 inhibitors, several classes of scores should be verified in relation to improvements in Eur Radiol (2018) 28:2856–2869 2859 Table 2 PC-AKI prophylaxis: Hydration, drugs, renal replacement therapy antimicrobial agents and chemotherapeutic agents have neph- rotoxic potential and can induce AKI [26]. Hydration There is little good quality data about the relationship Preventive hydration should be used to reduce the incidence of PC-AKI between these drugs and PC-AKI [27]. A retrospective in at-risk patients. cohort study showed that concurrent use of four or more Level of evidence B nephrotoxic agents was significantly predictive for PC- Intravenous saline and bicarbonate protocols have similar efficacy for hydration. AKI in patients given IV CM [28]. A meta-analysis of PC-AKI incidence following CM-enhanced CT found that Level of evidence A concurrent administration of NSAIDs was an independent For intravenous and intra-arterial CM administration with second pass renal exposure hydrate the patient with either (a) 3 ml/kg/h bicarbonate risk factor for PC-AKI [29]. 1.4% (or 154 mmol/l solution) for 1 h before CM or (b) 1 ml/kg/h The effect of withholding angiotensin converting en- saline 0.9% for 3–4hbeforeand 4–6hafter CM. zyme inhibitors (ACEI) and angiotensin-2 receptor Level of evidence D blockers (ARB) in chronic users has been extensively For intra-arterial CM administration with first pass renal exposure hydrate evaluated. Multiple RCTs [30, 31] and observational stud- the patient with either (a) 3 ml/kg/h bicarbonate 1.4% (or 154 mmol/l ies gave conflicting results and are limited by small sam- solution) for 1 h before CM followed by 1 ml/kg/h bicarbonate 1.4% (or 154 mmol/l) for 4–6h afterCM ple sizes and significant heterogeneity [32–34]. However, meta-analyses of RCTs found no lower risk [34]. or (b) 1 ml/kg/h saline 0.9% for 3–4 h before and 4–6h afterCM. Withholding ACEI/ARB may be associated with a slight- Level of evidence D ly lowerriskofPC-AKIbut theevidenceisnot sufficient- Oral hydration as the sole means of prevention is not recommended. ly strong to recommend this (Table 1). Level of evidence D In patients with severe heart failure (NYHA grade 3–4) or patients with Question 7: What are the most cost- end-stage renal failure (CKD grade V) preventive IV hydration should be individualized by the clinician responsible for patient care. and time-effective protocols for oral and intravenous Level of evidence D hydration to reduce the risk of PC-AKI? Drugs N-Acetylcysteine has not been conclusively shown to reduce the risk of Hydration as a preventive strategy for PC-AKI PC-AKI in patients with eGFR < 45 ml/min/1.73 m receiving intravenous or intra-arterial CM, and its use is NOT recommended. Evidence for prevention of PC-AKI with IV saline hydration Level of evidence A (volume expansion) comes from RCTs in patients who re- Giving short-term, high-dose statins to patients not already taking statins ceived intra-arterial (IA) CM during percutaneous interven- has not been shown to reduce the risk of PC-AKI in patients with eGFR tion [35–37], and in patients who received bicarbonate hydra- < 45 ml/min/1.73 m receiving intravenous or intra-arterial CM, and its use is NOT recommended. tion before IV enhanced emergency CTPA [38]. One RCT Level of evidence B evaluated the evidence for IA CM administration during CA ACE inhibitors or angiotensin receptor blockers have not been shown [39]. These studies found that, for both IA and IV CM admin- conclusively to reduce the risk of PC-AKI in patients receiving istration, the incidence of PC-AKI was significantly lower in intravenous or intra-arterial CM, and their use is NOT recommended. patients who received IV hydration compared to placebo, and Level of evidence B that hydration prevented emergency dialysis [36]. Significant Vitamin C has not been shown conclusively to reduce the risk of PC-AKI differences for mortality or other adverse events were not in patients receiving intravenous or intra-arterial CM, and its use is found. There were few patients with severe renal impairment NOT recommended. (eGFR < 30 ml/min/1.73 m ) in almost all studies. The recent Level of evidence B AMACING trial showed that for patients with eGFR > 30 ml/ Renal replacement therapy min/1.73 m receiving IV CM there was no difference be- Renal replacement therapy has not been shown conclusively to reduce the tween no hydration and hydration in preventing PC-AKI [40]. risk of PC-AKI in patients receiving intravenous or intra-arterial CM, and its use is NOT recommended. Level of evidence B 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 compared to IV hydration, but the studies were limited control. Nine studies evaluated oral hydration, but were by heterogeneity and lack of hard clinical outcomes limited by small patient numbers and by the absence of [49–51]. The CMSC does not recommend the use of oral patients with severe renal impairment [39, 41–48]. Three hydration as the sole preventive strategy for PC-AKI, but meta-analyses concluded that there is no evidence that unrestricted intake of clear oral fluids in addition to IV oral hydration is associated with more risk of PC-AKI volume expansion is supported (Table 2). 2860 Eur Radiol (2018) 28:2856–2869 Intravenous hydration: saline versus bicarbonate In which patients should the hydration protocol be individualized? Normal saline (NaCl 0.9%) and sodium bicarbonate solution (1.4% or 154 mmol NaHCO in D5W) are the two most com- There is no data to suggest that patients with severe renal monly studied crystalloid solutions. The rationale for using impairment (CKD grade V) or severe heart failure (NYHA bicarbonate is that alkalinisation can reduce the formation of grade 3–4) should receive different hydration protocols. free reactive oxygen species [52]. Initial studies favoured bi- However, IV hydration with large volumes may exacerbate carbonate [53–56], but this was not replicated in later studies acute heart failure and induce pulmonary oedema [40]. The [57–62], so IV hydration with bicarbonate can be considered opinion of the CMSC is that hydration protocols in these equivalent to normal saline. patients should be individualized for type, volume and There is no consensus on the optimal hydration re- duration. gime. Most studies have compared bicarbonate given pre- and post-CM for less than 6 h [53] to longer dura- Question 8: Which other strategies (pharmaceutical, tion saline pre- and post-CM protocols (12–24 h). In all vitamin, renal replacement therapy) have been studies, there are few patients with eGFR < 30 ml/min/ proved effective in preventing PC-AKI? 1.73 m , and evidence about whether short duration bi- carbonate is better than long duration saline is conflicting N-Acetylcysteine (NAc) [63–71]. There is limited evidence on whether pre- hydration only is inferior to pre- and post-hydration, Most recent RCTs or meta-analyses do not show a protective and only one very short duration bicarbonate protocol effect of NAc against PC-AKI following coronary or periph- has been evaluated [38, 72, 73]. eral angiography [66, 80–84]. NAc also failed to affect clinical Most studies have been performed in cardiac patients ad- outcome in coronary or peripheral angiography [85]orto have mitted for CA or PCI. Three studies evaluated hydration pro- aprotective effect in CT [86, 87] or in patients with diabetes tocols in patients having contrast-enhanced CT, and did not mellitus undergoing coronary or peripheral angiography [88, favour bicarbonate over saline [38, 72, 74]. No studies were 89]. Comparative studies with NAc combined with saline or identified assessing the beneficial effect of other crystalloids. sodium bicarbonate protocols did not show any additional However, balanced crystalloid solutions, such as Ringer’slac- effect of protective effect of NAc [61, 90–93]. However, more tate, may be preferable in critical care populations, because recent meta-analyses showed a benefit of NAc, with or with- they avoid the harmful effects of hyperchloraemic acidosis. out high-dose statins, when added to hydration for preventing The CMSC considers that for IV and IA CM injection PC-AKI [94–96]. with second pass renal exposure either a short bicarbonate hydration regime before CM or a conventional protocol with Statins saline given before and after CM may be used. For IA CM injection with first pass renal exposure conventional proto- Several meta-analyses showed lower overall PC-AKI rates cols with either bicarbonate or saline given before and after with the use of high-dose, short-term statin treatment CM should be used (Table 2). compared to controls [95–105]. Lower PC-AKI rates were also found in subgroups, such as older patients, patients with acute coronary syndromes and for high-dose statin Forced diuresis versus conventional hydration regimes. Some of these meta-analyses showed a reduced need for RRT after statins, but no reduction in all-cause Newer approaches for patients with impaired left ventricular mortality [97, 102]. However, the US Agency for function combine controlled saline hydration with a forced Healthcare Research and Quality (AHRQ) meta-analysis high urinary flow rate to maintain euvolemia and avoid showed that the risk of PC-AKI was only significantly overhydration and several RCTs showed better results than reduced when statins were added to hydration and NAc. conventional hydration protocols [75–77]. Other catheter- A reduction in PC-AKI risk could not be shown when based strategies used left ventricular end-diastolic pressure statins plus hydration were compared to hydration alone or central venous pressure to guide hydration [78, 79]. In in patients not taking statins. The standard of evidence these RCTs the incidence of PC-AKI was lower than with grade was low in both analyses [94]. standard IV hydration. Since the forced diuresis studies have Despite the many positive results, it is difficult to make a heterogeneous populations, interventions and control hydra- general recommendation for statins [106] because the patients tion protocols, their findings cannot be pooled. The CMSC studied were invariably cardiac, and a variety of statin and considers that there is not sufficient evidence to recommend hydration protocols were used. Patients with CKD grade forced diuresis. 3B–5 (eGFR < 45 ml/min/1.73 m ) are under-represented in Eur Radiol (2018) 28:2856–2869 2861 the studies and results in these patients remain inconclusive Question 9: Should administration of metformin be [102, 103, 107, 108]. Most patients undergoing CA/PCI are adapted to reduce the risk of metformin-associated already taking long-term statins, and results in these patients lactic acidosis in patients with type 2 diabetes mellitus are unclear. scheduled to receive intravascular contrast media? While the CMSC recognises the potential preventive ef- fects of short-term statins, it does not advise the use of short- Metformin is the standard drug for monotherapy of type 2 term, high-dose statins as a single strategy for preventing PC- diabetes mellitus [133]. The effect of CM on the risk of AKI (Table 2). metformin-associated lactic acidosis is indirect, since an epi- sode of AKI following intravascular CM administration may lead to metformin accumulation. The use of metformin in RAAS blockade: ACE inhibitors and angiotensin-II receptor patients with eGFR 30–59 ml/min/1.73 m is considered safe blockers if doses are reduced appropriately [134, 135]. Limiting the metformin dose to a maximum of 2000 mg/day for eGFR Administration of renin–angiotensin–aldosterone system 45–60 ml/min/1.73 m and to a maximum of 1000 mg/day (RAAS) blockade as a preventive measure for patients not tak- for eGFR 30–44 ml/min/1.73 m has been recommended. In ing these drugs did not show a significant effect on the inci- patients with eGFR 30–59 ml/min/1.73 m metformin drug dence of PC-AKI in recent meta-analyses [32, 34](Table 2). levels remain within therapeutic ranges. For patients with eGFR < 30 ml/min/1.73 m metformin administration is not approved. Vitamin C Multiple studies and meta-analyses have shown that the risk of lactic acidosis is very low and linked more to the The majority of RCTs or meta-analyses do not demon- underlying disease and possible co-morbidities rather than strate a protective effect of vitamin C against PC-AKI in the use of metformin [134, 136, 137]. Because of the lack of patients with CKD predominantly undergoing coronary published evidence on metformin and CM, early guidelines angiography [109–111]orany benefitofthe use ofvita- about the need to stop metformin before intravascular CM min C, NAc or a combination of both over the standard were based on consensus, and were strict [138, 139]. As the hydration regimen in preventing PC-AKI [112, 113] low risk of lactic acidosis became apparent, guidelines have (Table 2). Combining vitamin C with pentoxifylline also become less restrictive [3]. failed to show an advantage [114]. Only two publications Since no new published evidence is available, the CMSC [115, 116] have shown a protective effect of vitamin C in has updated its recommendations based on recent patients with CKD undergoing CA. Renal replacement therapy (RRT) Table 3 Metformin administration, dialysis schedules There is no convincing evidence in favour of preventive Metformin administration in patients at risk of PC-AKI haemodialysis or RRT alone [117–119]or combined with hy- Note that these recommendations may deviate from current EMA/FDA recommendations. dration [120] in patients with CKD, predominantly undergo- Patients with eGFR > 30 ml/min/1.73 m and no evidence of AKI ing CA (Table 2). There is no evidence of an increased risk of receiving either intravenous CM or intra-arterial CM with second pass permanent anuria in patients on peritoneal dialysis undergoing renal exposure: continue taking metformin normally. CA [121]. There is a single study showing better late-stage Patients (a) with eGFR < 30 ml/min/1.73 m receiving either intravenous (day 5–30) renal protection against PC-AKI with simulta- CM or intra-arterial CM with second pass renal exposure or (b) neous haemodialysis [122]. 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. Miscellaneous Level of evidence D Dialysis schedules in relation to CM administration The data on the protective effects of several agents, such It is not necessary to adapt the timing of intravascular CM administration as trimatizidine [123, 124], theophylline [95, 125–127], in relation to the dialysis schedule in patients undergoing chronic alprostadil [128, 129], nebivolol [130], fenoldopam [131] dialysis or haemofiltration, but it may be done to minimise volume overload. and iloprost [132], is not conclusive and does not sup- port recommending their use to reduce the risk of PC- Level of evidence D AKI. 2862 Eur Radiol (2018) 28:2856–2869 Table 4 ESUR CMSC guideline Definitions (version 10) for post-contrast acute kidney injury (PC-AKI) 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 m )= −0.329 Age Female sCr ≤ 62 μmol/l: 144 × (sCr/62) ×0.993 −1.209 Age Female sCr > 62 μmol/l: 144 × (sCr/62) ×0.993 −0.411 Age Male sCr ≤ 80 μmol/l: 141 × (sCr/80) ×0.993 −1.209 Age Male sCr > 80 μmol/l: 141 × (sCr/80) ×0.993 (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 m ) = 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 m before intra-arterial contrast medium administration with first pass renal exposure or in ICU patients � eGFR less than 30 ml/min/1.73 m 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 m ) - 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 Eur Radiol (2018) 28:2856–2869 2863 Table 4 (continued) - 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 m for intra- arterial administration with first pass renal exposure and eGFR less than 30 ml/min/1.73 m 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 4–6h 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 m ) � 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 m ) < 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 m 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 m 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. 2864 Eur Radiol (2018) 28:2856–2869 Table 4 (continued) 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 Haemodialysis to remove iodine-based contrast medium is unnecessary ambulatory peritoneal dialysis recommendations from the FDA [140], and on guidelines AKI. There is no need to adapt dialysis schedules in patients from the ACR and RSTN [14, 141](Table 3). being given intravascular CM. The recommendations made in this paper have been incor- porated into the ESUR CMSC guidelines version 10 (Table 4). Question 10: Should the timing of CM administration be adapted to the schedule of haemodialysis Funding The authors state that this work has not received any funding. or haemofiltration sessions in patients on renal replacement therapy? Compliance with ethical standards Guarantor The scientific guarantor of this publication is Prof. Henrik S. Iodine-based CM can be safely removed by haemodialysis Thomsen. (HD) or haemofiltration (HF). Many factors influence the ef- fectiveness of HD, such as flow rate of blood and dialysate, Conflict of interest Aart van der Molen has received incidental pay- dialysis membrane permeability, HD duration, and CM char- ments for lectures and chairmanships at scientific meetings for contrast acteristics such as molecular size, protein binding, hydrophi- agent safety related issues (contrast agent reactions, Gd-retention) from GE, Bayer, Bracco and Guerbet. licity and electrical charge [142]. Fulvio Stacul has received lecture fees from Bracco and Guerbet. Although HF concomitant with radiological procedures Olivier Clément has received lecture fees from Bracco and Guerbet. has been shown to be feasible and well tolerated [143, 144], The other authors of this manuscript declare no relationships with any the fractional removal of iodine-based CM contrast agents is companies whose products and services may be related to the subject matter of this article. modest and several HF or HD sessions are needed to remove 95% of the administered CM [143]. Also, there is no evidence Statistics and biometry No complex statistical methods were necessary for the necessity of emergency HD after administration of for this paper. iodine-based CM in patients on chronic HD [145]. However, to avoid volume overload, CM administration may be Informed consent Written informed consent was not required for this synchronised with scheduled HF or HD (Table 3). 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. Conclusion Methodology Assessment of the risk of PC-AKI before intravascular CM is � retrospective administered is best done by measuring eGFR but the alterna- � multicentre study tive of a questionnaire for patients detects most patients with eGFR less than 45 ml/min/1.73 m . Volume expansion with Open Access This article is distributed under the terms of the Creative normal saline or sodium bicarbonate remains the mainstay of Commons Attribution 4.0 International License (http:// PC-AKI prevention, but there is still uncertainty about the creativecommons.org/licenses/by/4.0/), which permits unrestricted use, optimal protocol. The additional benefit of a number of drugs, distribution, and reproduction in any medium, provided you give appro- priate credit to the original author(s) and the source, provide a link to the such as N-acetylcysteine, statins, ACE inhibitors and Creative Commons license, and indicate if changes were made. angiotensin-II receptor blockers, and vitamin C in preventing PC-AKI has not been proved conclusively. Stopping nephro- toxic medications appears to be of limited value in preventing PC-AKI. Recommendations for discontinuing metformin References when CM is given have been relaxed and now only apply to patients with eGFR < 30 ml/min/1.73 m receiving IV CM or 1. 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Published: Feb 7, 2018

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