Contrast-Induced Nephropathy Following Angiography and Cardiac Interventions Roger Rear,1 Robert M Bell,1 Derek J Hausenloy1,2,3,4
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Education in Heart INVASIVE IMAGING, CARDIAC CATHETERISATION AND ANGIOGRAPHY Heart: first published as 10.1136/heartjnl-2014-306962 on 8 February 2016. Downloaded from Contrast-induced nephropathy following angiography and cardiac interventions Roger Rear,1 Robert M Bell,1 Derek J Hausenloy1,2,3,4 1The Hatter Cardiovascular INTRODUCTION Institute, University College Contrast-induced nephropathy (CIN), also known European Society of Cardiology (ESC) London, London, UK 2The National Institute of as contrast-induced acute kidney injury, is an iatro- curriculum section and guidelines Health Research University genic renal injury that follows intravascular admin- referenced College London Hospitals istration of radio-opaque contrast media (CM) in Biomedical Research Centre, susceptible individuals. CIN was first described ▸ 2.4 Invasive imaging: cardiac catheterisation London, UK during the 1950s in case reports of fatal acute renal 3National Heart Research and angiography. failure that had occurred following intravenous Institute Singapore, National ▸ ESC: updated contrast-induced nephropathy pyelography in patients with renal disease arising Heart Centre Singapore, (CIN) prevention guidelines 2014. Singapore, Singapore from multiple myeloma.12Despite technological 4 ▸ European Society of Urogenital Radiology: Cardiovascular and Metabolic advances, CIN remains responsible for a third of all Disorders Program, Duke- updated contrast media safety committee hospital-acquired acute kidney injury (AKI)34and National University of guidelines 2011. Singapore, Singapore, affects between 1% and 2% of the general popula- Singapore tion and up to 50% of high-risk subgroups follow- ing coronary angiography (CA) or percutaneous Correspondence to coronary intervention (PCI).5 Professor Derek Hausenloy, Learning objectives The Hatter Cardiovascular The proliferation of imaging methods and inter- Institute, Institute of ventional procedures involving administration of Cardiovascular Science, NIHR intravascular CM in both non-cardiac modalities ▸ Define CIN and recognise this as a common University College London (eg, vascular CT angiography and interventional and serious complication in susceptible patients Hospitals Biomedical Research vascular angiography) and in established (eg, CA receiving intravascular contrast media. Centre, University College ▸ London Hospital & Medical and PCI) and emerging cardiac modalities (eg, CT Understand the possible pathological School, 67 Chenies Mews, coronary angiography (CTCA) and transcatheter mechanisms underlying CIN. London WC1E 6HX, UK; aortic valve implantation (TAVI)) has significantly ▸ Describe the clinical and periprocedural risk [email protected] increased the number of patients exposed to CM factors for CIN and perform a risk assessment http://heart.bmj.com/ Received 18 March 2015 and thus the number at risk of CIN. The wide- for patients receiving contrast media. Revised 8 November 2015 spread adoption of primary PCI for the treatment ▸ Appreciate the established strategies used to Accepted 29 December 2015 of acute myocardial infarction (AMI), despite sig- prevent CIN and be aware of novel therapies. Published Online First nificantly improving cardiovascular outcomes, has ▸ Recognise the onset of CIN and manage this 8 February 2016 increased the incidence of CIN due to the inherent complication appropriately. difficulties in rapidly assessing CIN risk, instigating prophylactic measures, attendant haemodynamic compromise and higher contrast volumes, all on September 27, 2021 by guest. Protected copyright. known risk factors for the development of CIN.6 preventative therapies. The wholly iatrogenic and Despite several therapeutic approaches, the rising predictable nature of CIN makes it a particularly age and incidence of comorbidity within the broad well-suited area for ongoing cardiovascular and cohort of cardiac patients receiving CM has nephrology research, with focus on pathophysio- ensured that the prevention of CIN remains a sig- logical mechanisms as well as novel risk assessment, nificant clinical challenge.7 preventative, diagnostic and therapeutic measures. As will be discussed in the following sections, the Open Access estimated risk of an individual developing CIN can DEFINITION AND DIAGNOSTIC CRITERIA OF Scan to access more free content be calculated using known pre-existent clinical and CIN periprocedural factors, which are consistent with The generally accepted definition of CIN is a 25% the proposed pathological mechanisms of CIN. relative increase, or a 0.5 mg/dL (44 mmol/L) abso- Pre-existent stage III chronic kidney disease (CKD), lute increase, in serum creatinine (SCr) within 72 h defined as an estimated glomerular filtration rate of contrast exposure, in the absence of an alterna- 2 (eGFR)<60 mL/min/1.73 m for greater than tive explanation.10 Criticisms of this definition 3 months, is the most commonly identified risk include the lack of sensitivity to minor increases in factor for CIN; however, CIN can occur in the SCr that have been shown to correlate with adverse absence of underlying CKD if a number of other events,11 12 the combination of both relative and 5 risk factors are also present. Risk scoring systems absolute SCr changes and the absence of any func- 89 To cite: Rear R, Bell RM, have been developed from cohort studies that tional assessment such as changes in urine output, Hausenloy DJ. Heart have enabled clinicians to predict the likelihood of as used in the RIFLE,13 AKIN14 and KDIGO15 – 2016;102:638 648. CIN occurrence and have allowed targeted use of classification systems. However, this definition has 638 Rear R, et al. Heart 2016;102:638–648. doi:10.1136/heartjnl-2014-306962 Education in Heart 23 normalise after approximately 1–3 weeks. Heart: first published as 10.1136/heartjnl-2014-306962 on 8 February 2016. Downloaded from Table 1 CIN severity grading system (adapted from Harjai el al16) However, CIN is of clinical importance as a CIN grade Change in serum creatinine 6 month outcomes number of clinical trials have revealed that it por- tends a multitude of short-term and long-term Grade 0 SCr increase <25% and <0.5 mg/dL above baseline MACE 12.4% 24 Mortality 10.2% adverse events. After adjusting for comorbidities, Grade 1 SCr increase ≥25% and <0.5 mg/dL above baseline MACE 19.4% observational studies have demonstrated that Mortality 10.4% in-hospital mortality is approximately five times Grade 2 SCr increase ≥0.5 mg/dL above baseline MACE 28.6% higher in patients who suffer CIN compared with Mortality 40.9% patients receiving CM who do not,25 and mortality CIN, contrast-induced nephropathy; MACE, major adverse cardiovascular event; SCr, serum creatinine. rates at 1 and 5 years are approximately four times higher,26 with some demonstrating a 1-year mortal- ity rates of between 20%12 and 38%.27 In other observational studies, as many as 20% of those the advantage of being widely used as the end developing CIN suffer persistent worsening renal point in most CIN studies and it correlates well function after CM exposure,28 with renal replace- with adverse clinical end points. ment therapy occurring in between 0.7%25 and An alternative definition proposed by Harjai 7%27 of patients with CIN (table 2). As such the et al16 aims to classify CIN according to three additional healthcare costs associated with CIN are grades corresponding to three relative and absolute thought to be considerable.12 creatinine rise cut-offs, including a group with only However, it is important to recognise that a minor rise (<25% or 0.5 mg/dL), which also corre- direct causal relationship between CIN and mortal- lates with long-term adverse outcomes (table 1). ity has not been established in these observational A significant problem with SCr is that it is rela- studies. The onset of CIN is more likely to occur in tively insensitive to the rapid GFR changes seen in the presence of severe cardiac injury or disease, AKI, particularly in patients with normal baseline which alone conveys a poor prognosis. As such renal function.17 Elevations in SCr typically take CIN may be a marker of adverse cardiovascular 2–3 days to reach the current diagnostic threshold outcomes rather than an independent risk factor. following an acute renal insult, thus reducing its A recent meta-analysis by James et al,29 reviewed usefulness as a marker of AKI. However early and 39 observational studies that investigated cardiovas- minor incremental changes in SCr may be a useful cular outcomes in those with CIN and demon- marker of CIN; a recent clinical trial performed by strated an increased risk of mortality, cardiovascular Ribichini et al,18 which included 216 at-risk events, renal failure and prolonged hospitalisation. patients undergoing CA, demonstrated that at 12 h However, it was found that baseline clinical a 5% increase in SCr from baseline was a sensitive characteristics that simultaneously predispose to (75%) and specific (72%) marker of CIN at 48 h both CIN and mortality were strong confounders, http://heart.bmj.com/ and persistent worsening of renal function at especially so in unadjusted studies. Even with 30 days. appropriate adjustment for comorbidity, the Several novel renal biomarkers, including authors recommend that any firm conclusions NGAL,19 Cystatin C,20 urinary Kim-121 and about causality should be interpreted with caution. interleukin-1822 have been proposed to specifically Nonetheless, a number of plausible pathological detect CIN within minutes to hours of the renal mechanisms exist that