CIN Consensus Working Panel: Executive Summary

Peter A McCullough, MD, MPH
Consultant Cardiologist, William Beaumont Hospital, Michigan, USA

Address for correspondence:
Dr Peter A McCullough, MD, MPH
Consultant Cardiologist
William Beaumont Hospital, Coolidge Highway
Royal Oak, Michigan 48073, USA
Tel: +1-248-655-5929 Fax: +1-248-380-2008
Email: pmccullough@beaumont.edu

Abstract
Radiological and cardiological procedures continue to rely on the use of iodinated contrast media for the identification of vascular structures. Contrast-induced nephropathy (CIN) is an important complication in the use of iodinated contrast media which accounts for a significant number of cases of hospital-acquired renal failure, with adverse effects on prognosis and healthcare costs. CIN is likely to remain a significant challenge for clinicians since more patients are likely to undergo exposure to contrast media in the future and since the incidence of chronic kidney disease, the major risk factor for CIN, is increasing. The CIN Consensus Working Panel is an international multidisciplinary group convened to address the challenges of CIN. A total of 4370 references were identified by literature search (the MEDLINE and EMBASE databases from 1966 to February 2005), of which 865 were considered potentially relevant. The results of the literature search were used to compile reviews covering the epidemiology and pathogenesis of CIN, baseline renal function measurement, risk assessment, identification of high-risk patients, contrast medium use and preventive strategies. In this summary of the work of the panel, the consensus statements and an algorithm for the risk stratification and management of contrastinduced nephropathy are presented.

Introduction
Contrast-induced nephropathy (CIN) is an important complication in the use of iodinated contrast media which accounts for a significant number of cases of hospital-acquired acute kidney injury [1-3]. This iatrogenic condition has an adverse effect on prognosis and adds to healthcare costs. Several factors contribute to the increasing importance of this subject to radiologists, cardiologists and nephrologists. The numbers of imaging and interventional procedures continue to increase which inevitably means more patients will be exposed to intravascular iodinated contrast media. At the same time, the incidence and prevalence of chronic kidney disease (CKD), the most important risk factor for CIN, are increasing worldwide [4].

The CIN Consensus Working Panel is an international multidisciplinary group convened to address the challenges of CIN. The group systematically reviewed the published evidence on CIN and used this, together with expert opinion drawn from clinical practice, to compile a series of consensus statements and a management algorithm.

CIN Consensus Working Panel
The Working Panel comprised two radiologists, a CT expert, two cardiologists and two nephrologists practising in Europe and the USA. At the first meeting in November 2004, the overall scope and strategy for the project were agreed and at the second in September 2005, the Working Panel reviewed and discussed all the evidence and developed a series of consensus statements.

Methodology
A systematic search of the literature was undertaken to identify all references relevant to the subject of CIN, as a result of which 865 potentially relevant papers were identified and reviewed. The results of the literature search were used to compile reviews covering the epidemiology and pathogenesis of CIN, baseline renal function measurement, risk assessment, identification of high-risk patients, contrast medium use and preventive strategies [5-11]. After reviewing all the evidence, the Working Panel agreed a series of consensus statements addressing the identification of patients at risk of CIN and strategies for reducing the risk (Table 1) [12]. The results were also integrated into a proposed algorithm for the management of patients at risk of CIN (Figure 1) [12].

Epidemiology and prognostic implications of CIN Incidence
The reported incidence of CIN varies widely across the literature, depending on the patient population and the baseline risk factors. Moreover, as with any clinical event, the incidence also varies depending on the criteria by which it is defined. CIN is typically defined in the recent literature as an increase in serum creatinine occurring within the first 24 hours after contrast exposure and peaking up to 5 days afterwards. In most instances, the rise in serum creatinine is expressed either in absolute terms (0.5-1.0 mg/dl; 44.2-88.4 µmol/l) or as a proportional rise in serum creatinine of 25% or 50% above the baseline value. The most commonly used definition in clinical trials is a rise in serum creatinine of 0.5 mg/dl (44.2 µmol/l), or a 25% increase from the baseline value, assessed at 48 hours after the procedure. The European Society of Urogenital Radiology (ESUR) defines CIN as impairment in renal function (an increase in serum creatinine by more than 25% or 44.2 µmol/l [0.5 mg/dl]) within 3 days after intravascular administration of contrast medium, without an alternative aetiology [13]. Although other definitions have been used such as a rise in serum creatinine >0.3 mg/dl with oliguria, decreases in glomerular filtration rate (GFR) or creatinine clearance or increases in serum urea nitrogen (BUN), defined serum creatinine alone changes appear to be the universal benchmark measure for the occurrence of CIN.

eGFR = estimated glomerular filtration rate; CIN = contrast-induced nephropathy; NSAID = nonsteroidal anti-inflammatory drug; Cr = creatinine; PGE₁ = prostaglandin E₁
^† Volume expansion consisting of intravenous isotonic crystalloid 1-1.5 ml/kg per hr should be given 3-12 hours before and 6-24 hours after the procedure. ^†† Consider potentially beneficial agents such as theophylline, 3-hydroxy-3-methylglutaryl coenzyme A reductase inhibitors (statins), ascorbic acid (vitamin C), prostaglandin E1 (none approved for this indication). ^††† Plans should be made in case contrast induced nephropathy (CIN) occurs and dialysis is required. * Adapted from McCullough et al, 2006 [12]

Figure 1. Algorithm for management of patients receiving iodinated contrast media [12].

The best indication of the healthcare impact of CIN comes from large studies of hospital patients. The frequency of CIN has decreased over the past decade from a general incidence of ~15% to ~7% of patients receiving iodinated contrast, [14] due to a greater awareness of the problem, better risk prevention measures, and improved iodinated contrast media with less renal toxicity. However, many cases of CIN continue to occur because of the everincreasing numbers of procedures requiring contrast medium. Nash et al reported that radiographic contrast media were the third commonest cause of hospitalacquired renal failure (after decreased renal perfusion and nephrotoxic medications) and were responsible for 11% of cases.3 The mortality rate in cases of CIN was 14%. The proportion of cases of hospital-acquired renal failure attributed to contrast media (11%) was almost identical to an earlier series [15]. However, in the more recent study, there were more cases following cardiac procedures and fewer after non-cardiac angiography.

Using a CIN definition of a 25% rise in serum creatinine, it has been suggested that in the past the frequency of CIN after use of contrast media in an unselected group of cardiology patients may be up to 15% [16,17]. In patients with impaired renal function at baseline the risk is considerably higher and the significance of renal impairment as a risk marker is reviewed later in this paper.

It has been recognised for some time that the risk of death is increased in patients developing acute kidney injury after contrast medium administration. In a large retrospective study of over 16,000 hospital in-patients undergoing procedures requiring contrast medium, a total of 183 subjects developed CIN (defined as a 25% increase in serum creatinine) [18]. The risk of death during hospitalisation was 34% in subjects who developed CIN compared with 7% in matched controls who had received contrast medium but did not develop CIN. Even after adjusting for comorbid disease, patients with CIN had a 5.5-fold increased risk of death [18]. The high risk of inhospital death associated with CIN was also documented in a retrospective analysis of 7586 patients, of whom 3.3% developed CIN after exposure to contrast medium. Among the patients who developed CIN, the in-hospital death rate was 22% compared with only 1.4% in patients who did not develop ARF [19]. The mortality rates at 1 year after development of CIN (12.1%) and at 5 years (44.6%), were higher compared to rates of 3.7% and 14.5% respectively in patients who did not develop CIN (p<0.001), indicating that the increased risk of death persisted in the long term. A further study confirmed the high mortality in patients who develop CIN, especially in those who require dialysis: the hospital mortality was 7.1% in CIN patients and 35.7% in patients who required dialysis. By 2 years, the mortality rate in patients who required dialysis was 81.2%.16 CIN (defined as an increase =25% in serum creatinine) occurred in 37% of 439 patients with renal impairment (baseline serum creatinine 1.8 mg/dl) undergoing PCI [20]. In this group, the hospital mortality rate was 14.9% compared with 4.9% in patients without CIN (p=0.001). The cumulative 1-year mortality rates were 37.7% and 19.4% respectively. The 1-year mortality was 45.2% for patients with CIN requiring dialysis and 35.4% for those with CIN not requiring dialysis [20]. In patients undergoing primary PCI for MI, short and long-term mortality rates were also significantly higher in those who developed CIN [21,22].

In PCI patients, it has been shown that CIN is an independent predictor of mortality [23].

Impact of CIN on clinical course and outcome
As well as an increased risk of death, CIN is also associated with other adverse outcomes including late cardiovascular events. In one registry series of 5967 PCI patients, the development of CIN was associated with an increased incidence of myocardial infarction and target vessel revascularisation at 1 year [23]. Another large PCI study documented the link between contrast-induced rises in serum creatinine, post-procedural increases in creatinine kinase MB sub-fraction (CK-MB), and the risk of late cardiovascular events [24]. In a group of 5397 patients, a postprocedural rise in serum creatinine was a more powerful predictor of late mortality than CK-MB. Creatinine increases were associated with a 16% rate of death or myocardial infarction at 1 year, rising to 26.3% when CK-MB levels were also elevated [24].

More in-hospital events such as bypass surgery, bleeding requiring transfusion and vascular complications were observed in patients who developed CIN, both in those with previous renal dysfunction and those with previously normal renal function. At one year, the cumulative rate of major adverse cardiac events (MACE) was significantly higher in patients who had developed CIN (p<0.0001 for patients with and without chronic kidney disease) [25]. However, others have observed no difference in the rates of MI and target vessel revascularisation in patients with CIN [20].

The development of CIN has also been associated with an increased hospital stay. In one series, the postprocedure hospital stay was longer in patients who developed CIN, regardless of baseline renal function [25]. In a series of 200 patients undergoing PCI for acute myocardial infarction, patients who developed CIN had a longer hospital stay, a more complicated clinical course and a significantly increased risk of death compared to those without CIN [22].

Risk of CIN requiring dialysis
While most cases of CIN reflect mild transient impairment of renal function, dialysis is needed in a small proportion of patients. The literature review conducted by the CIN Consensus Working Panel suggests that the need for dialysis after CIN varies according to patients’ underlying risks at the time of contrast administration but is generally less than 1%, [16,26,27] although it was considerably higher in some older studies with HOCM [28,29]. In contemporary studies, CIN requiring dialysis developed in 3.1% of patients with underlying renal impairment [30] and 3% of patients undergoing primary PCI for MI [22]. Although CIN requiring dialysis is relatively rare, the impact on patient prognosis is considerable, with high hospital and 1-year mortality rates [16,20].

Pathophysiology of CIN
The CIN Consensus Working Panel reviewed the pathophysiology of CIN and agreed that it certainly involves the interplay of multiple factors. These include vasoconstriction, impaired vasodilation, oxidative stress and direct tubular toxicity, all contributing to medullary hypoxia. A detailed review of pathophysiology is outside the scope of this paper and the reader is referred to the published review for further information [10].

The role of baseline renal function screening
Virtually every report describing risk factors for CIN lists abnormal baseline serum creatinine, low GFR or underlying renal disease as risk factors and almost every multivariate analysis has shown that pre-existing renal impairment is an independent risk predictor for CIN [14,16,19,26,31,32]. The consensus view of the group, after reviewing the published data, was that the risk of CIN is increased in patients with an estimated glomerular filtration rate (eGFR) <60 ml/minute (equivalent to serum creatinine of =1.3 mg/dl [=114.9 µmol/l] in men and =1.0 mg/dl [=88.4 µmol/l] in women) and that special precautions should be taken in these patients.

Measurement of baseline renal function
It is important to assess renal function before administration of contrast medium to ensure that appropriate steps are taken to reduce the risk. Since serum creatinine alone does not provide a reliable measure of renal function, the National Kidney Foundation Kidney Disease Outcome Quality Initiative (K/DOQI) recommends that clinicians should use an eGFR calculated from the serum creatinine as an index of renal function rather than using serum creatinine [33]. The CIN Consensus Working Panel agreed that eGFR should be determined prior to contrast administration, using the abbreviated Modification of Diet in Renal Disease (MDRD) formula.

Use of surveys/questionnaires
It is highly desirable to have an eGFR value (calculated from a recent serum creatinine measurement) available in order to assess the risk of CIN, but this may be impractical in some circumstances. Where renal function data are unavailable, a simple survey or questionnaire may be used to identify patients at higher risk for CIN than the general population in whom appropriate precautions should be taken to reduce the risk of CIN [34-36].

Emergency situations
In the setting of emergency procedures, where the benefit of very early imaging outweighs the risk of waiting for the results of a blood test, it may be necessary to proceed without serum creatinine assessment or GFR estimation [7]. However, where possible, an indication should be obtained of the likelihood that the patient has impaired renal function that may increase the risk of CIN, to enable suitable precautions to be taken.

Risk markers for CIN
The panel preferred the use of the term ‘risk marker’ to ‘risk factor’ since many of these indicators are non-modifiable patient characteristics that are not necessarily directly causative. The most important element of risk stratification is baseline renal filtration function which is a surrogate for reduced nephron mass and renal parenchymal function. As already noted above, abnormal baseline serum creatinine, low GFR or underlying renal disease are widely reported as risk factors and almost every multivariate analysis has shown that pre-existing renal impairment is an independent risk predictor for CIN [8]. The consensus view of the group, after reviewing the published data, was that the risk of CIN is increased in patients with an eGFR <60 ml/minute and that special precautions should be taken in these patients.

Other risk factors include diabetes mellitus, [23,37] volume depletion, [38)] nephrotoxic drugs, haemodynamic instability [24,39] and other co-morbidities. Importantly diabetes is neither necessary nor sufficient as a determinant for CIN. However, diabetes appears to act as a risk multiplier, meaning that in a patient with CKD it amplifies the risk of CIN. Several large series of PCI patients have shown an association between CIN and indicators of haemodynamic instability such as periprocedural hypotension and use of an intraaortic balloon pump (IABP) [24,25]. It is unsurprising that hypotension increases the risk of CIN since it increases the likelihood of renal ischemia and is a significant risk factor for acute renal failure in acutely ill patients. Anaemia has also been reported as a predictor of CIN [40].

The effect of risk factors is additive and the likelihood of CIN rises sharply as the number of risk factors increases [16,39]. A similar pattern of additive risk has been documented for nephropathy requiring dialysis [26].

The additive nature of risk has allowed the development of prognostic scoring schemes, [14,39] but since none of the published schemes has been adequately studied or prospectively validated in different populations, it is not appropriate to recommend routine use of any particular risk scoring in clinical practice. However, the concept is that in a patient with CKD, DM, and other comorbidities, predicted risks of CIN can approach ~50% and the risk of renal failure requiring dialysis ~15%.

High-risk situation and procedures
Many clinical situations may arise in which the risk of CIN is increased and the CIN Consensus Working Panel reviewed the published literature [5]. However the evidence is very limited for many situations and in all cases the decision to administer contrast medium is a matter for clinical judgment based on the clinical status of the patient and the expected benefits of the investigation or procedure. In particular there was insufficient evidence to make definitive statements about the risk of CIN in patients undergoing coronary artery bypass surgery after contrast exposure or in patients with cirrhosis (although cirrhosis may be a risk factor in patients undergoing transarterial chemoembolisation). As already noted, in PCI patients periprocedural haemodynamic instability may be associated with an increased risk of CIN, but no published evidence was identified on the significance of shock or hypotension in other situations. The published literature on the risk of CIN in renal transplant recipients is inconsistent [5].

Contrast medium use
Choice of contrast medium
There is good evidence that low-osmolar contrast media (LOCM) are less nephrotoxic than high-osmolar contrast media (HOCM) in patients at increased risk for CIN.

A meta-analysis published in 1992 evaluated the relative nephrotoxicity of HOCM and LOCM. The pooled odds ratio for the prevalence of CIN events (rise in serum creatinine of >44.2 µmol/l (>0.5 mg/dl)) in 25 trials was 0.61 (95% confidence interval (CI) 0.48-0.77), indicating a significant reduction in risk with LOCM [41]. Studies published since this meta-analysis generally support these findings [42].

Most studies comparing different LOCM have been small trials that have not shown clinically relevant variation between the renal effects of different LOCM and there is insufficient evidence to draw definitive conclusions about possible differences [6].

The available evidence supports the conclusion that no contrast medium is associated with a lower risk of CIN than isosmolar contrast medium (IOCM). In a prospective randomised double-blind trial in diabetic patients with renal impairment undergoing coronary or aortofemoral angiography, the mean peak increase in serum creatinine was significantly less in the iodixanol group than in the iohexol group (p=0.001). Using the most common definition of CIN (an increase of 0.5 mg/dl (44.2 µmol/l) in serum creatinine), CIN occurred in 2 of 64 patients (3%) in the iodixanol group and 17 of 65 (26%) in the iohexol group (p=0.002) [43]. The results of a prospective open-label comparison of iodixanol and iohexol were consistent with a lower incidence of CIN with iodixanol [44].

A systematic review by Solomon was also consistent with a low rate of contrast nephropathy with iodixanol [45)]. A total of 17 prospective clinical trials (1365 patients) were included, but only two of these trials were randomised comparisons of LOCM and IOCM and the other data came from the placebo arms of 13 trials of preventive strategies for CIN and the LOCM arms of 2 trials comparing LOCM and HOCM. Finally, a meta-analysis of the renal tolerability of another IOCM, iotrolan 280, provides further evidence that IOCM are associated with a lower risk of post-procedure renal impairment [46]. In an analysis of 14 double-blind studies, it was found that iotrolan had less effect on renal function than the LOCM with which it was compared (iopamidol, iohexol, iopromide).

On the basis of these results, the CIN Consensus Working Panel concluded that in patients with CKD and particularly those with DM undergoing angiographic procedures, current evidence suggests no contrast medium presents a lower risk for CIN than nonionic, iso-osmolar contrast. This consensus view was incorporated in an algorithm for patient management which indicates that in patients with CKD (eGFR <60 ml/min/1.73 m²), the choice of iodinated contrast medium should be considered.

Volume of contrast
Numerous studies have shown that the volume of contrast medium is a risk factor for CIN and that the mean contrast volume is higher in patients with CIN, and most multivariate analyses have shown that contrast volume is an independent predictor of CIN [16,23,26,39]. However, even small volumes (~30 ml) of contrast medium can have adverse effects on renal function in patients at particularly high risk [47].

Intra-arterial versus intravenous administration
A number of studies have provided circumstantial evidence that the risk of CIN may be higher following intra-arterial administration than after intravenous injection [48,49]. However, none of these studies provides an insight into the significance of the route of administration for CIN risk in contemporary practice, especially with regard to CT studies, when a comparatively large volume of contrast medium may be given as a compact intravenous bolus rather than an infusion. The limited evidence that is available suggests that there is a significant risk of CIN in these circumstances [50].

Other strategies for reducing the risk of CIN
Volume expansion
Volume expansion and treatment of dehydration has a well established role in reducing the risk of CIN, although few studies address this theme directly. There are limited data on the most appropriate choice of intravenous fluid, but the evidence indicates that isotonic saline is more effective than half-normal saline [51]. Additional confirmatory trials with sodium bicarbonate [52] are needed.

There is also no clear evidence to guide the choice of the optimal rate and duration of infusion. However, good urine output (>150 ml/hr) in the six hours after the procedure has been associated with reduced rates of CIN in one study [53]. Oral volume expansion may have some benefit, but there is not enough evidence to show that it is as effective as intravenous volume expansion [54].

Dialysis and haemofiltration
Contrast medium is removed by dialysis, but there is no clinical evidence that prophylactic dialysis reduces the risk of CIN, even when carried out within 1 hour or simultaneously with contrast administration. Haemofiltration performed before and after contrast deserves further investigation given reports of reduced mortality and need for haemodialysis, [55] but the high cost and need for ICU admission will also limit the utility of this prophylactic approach.

Pharmacological strategies
The CIN Consensus Working Panel considered that, of the pharmacological agents that have been evaluated, theophylline, statins, ascorbic acid and prostaglandin E₁ deserve further evaluation [9]. N-acetylcysteine is not consistently effective in reducing the risk of CIN. Nine published meta-analyses were identified, all documenting the significant heterogeneity between studies and pooled odds ratios for N-acetylcysteine approaching unity. Fenoldopam, dopamine, calcium channel blockers, atrial natriuretic peptide and L-arginine have not been shown to be effective. Furosemide, mannitol and an endothelin receptor antagonist are potentially detrimental [9].

Conclusion
Ten consensus statements and an accompanying algorithm have been developed. These can be used to guide the management of patients receiving iodinated contrast medium. This consensus programme is important as it is the first attempt to systematically review all relevant information on CIN, a common and serious problem. It integrates the viewpoints of cardiologists, nephrologists and radiologists. Guidelines and quality programmes can be developed from this base of work in the future.

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02-2007 BUY1154818/JB2548/MB002444/SC 13th edition

 

Source: C2I2, Volume V, Issue 1, 2007

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