Transitioning from Contrast-induced Nephropathy and Contrast-associated Nephropathy to Contrast-associated Acute Kidney Injury

INTRODUCTION Contrast-associated acute kidney injury (CA-AKI) poses a significant concern and unnerves surgeons who require imaging that uses contrast to make/exclude a diagnosis or treat a patient, especially in patients with preexisting renal conditions. CA-AKI and contrast-induced acute kidney injury (CI-AKI) are used interchangeably, leading to confusion in clinical discussions, however, it is crucial to distinguish between these two entities. While CI-AKI traditionally implied a direct link between contrast agents and AKI, recent literature favors the term CA-AKI.1-4 It acknowledges the multifactorial nature of renal impairment following contrast exposure. We aim to unravel the differences between these terms, offering insights into diagnostic nuances, optimal timing for repeat creatinine assessments, the onset of nephropathy, and guidelines for nephrologist intervention. GETTING TERMINOLOGY RIGHT CA-AKI versus CI-AKI: CA-AKI and CI-AKI both pose concerns for patients, but they have distinct characteristics that merit exploration. CI-AKI is primarily associated with the direct nephrotoxic effects of contrast agents, leading to a decline in renal function, particularly in patients with chronic kidney disease (CKD).3,4 On the other hand, CA-AKI takes a broader view, considering additional factors such as the patient's comorbidities, hemodynamic changes, and procedural variables.5,6 While CI-AKI is a subset of CA-AKI, the latter term better captures the intricate web of influences contributing to renal dysfunction after contrast exposure.2,4,6 Recognizing this difference is vital for tailoring diagnostic and management strategies. Certain patient profiles are more prone to either CA-AKI or CI-AKI, depending on their prior or preexisting health conditions. Patients with atherosclerotic disease, coronary artery disease, and peripheral vascular disease may face an increased risk of CI-AKI due to compromised renal perfusion.4 In contrast, CA-AKI is often observed in individuals with CKD, diabetes mellitus, or congestive heart failure, where the multifactorial nature of renal dysfunction comes into play.3,5 When it comes to medical imaging, the risks associated with CA-AKI and CI-AKI are nuanced. Choosing a low or iso-osmolar contrast agent can mitigate the risk of renal injury. Risk factors for contrast-associated nephropathy2,5 Diabetes mellitus increases vulnerability due to nephropathy and microvascular complications Congestive heart failure amplifies the risk CKD heightens susceptibility Age plays a role, advancing age potentially intensifying the impact. Risk factors for contrast-induced nephropathy1,6 Atherosclerotic disease is a notable risk, compromising renal blood flow Advanced age makes individuals more susceptible to contrast agents Volume depletion, from conditions such as dehydration or heart failure CKD, even if mild, heightens vulnerability. Clinical scenarios If the patient's urine output drops within 48–72 h after using contrast and the patient has risk factors of atherosclerotic disease, it is more likely CI-AKI If kidney impairment happens later, beyond the usual postprocedure timeframe, and is linked to existing kidney conditions, diabetes, or heart failure, CA-AKI becomes a significant possibility. Kidney Disease: Improving Global Outcomes (KIDIGOs) for diagnosing how serious AKI is, along with the scoring system from Sgura etal. (Mehran contrast-induced nephropathy risk score), are important for understanding risks. KIDIGO breaks it down into three stages, looking at serum creatinine, percentage increase, and urine output to get a detailed picture of the risk.7,8 The KIDIGO AKI Staging, by the 2022 guidelines, is presented in Table 1.7 Mehran CI-AKI risk scoring system was initially made for cardiac procedures, but, can be used for both CA-AKI and CI-AKI. The Mehran risk scoring system is detailed in Table 2.8 A recent study conducted by Samir etal. found that among patients experiencing contrast-induced nephropathy following primary percutaneous coronary intervention, Mehran's score exhibited remarkable sensitivity at 100%, high specificity at 96.77%, a positive predictive value of 70%, and a negative predictive value of 100%.9Table 1: Kidney disease: Improving global outcomes kidney injury staging 2022 7 Table 2: The Mehran risk scoring system for contrast-associated acute kidney injury and contrast-induced acute kidney injury, along with the categorization of risk factors 8 By considering variables such as age, existing kidney issues, and diabetes in the overall score, this system helps spot people at a higher risk of CI-AKI. Utilizing imaging studies such as Doppler ultrasound to examine renal blood flow and kidney size can be valuable in distinguishing between CI-AKI and CA-AKI.3,6 Furthermore, monitoring biomarkers beyond creatinine, such as Cystatin C or innovative urinary markers, may offer a more sensitive indication of early renal dysfunction associated with CA-AKI.2,3,5 Diagnosing CA-AKI and CI-AKI comes with its challenges, especially concerning the timing of creatinine assessments. Typically, creatinine levels are checked 48–72 h after using contrast, but recent study findings suggest that deterioration in renal function may show up later, especially in those at higher risk.4,6 Vigilant monitoring is essential, with an emphasis on recognizing early signs such as subtle creatinine elevations or diminished urine output. Understanding the role of predisposing factors, including diabetes, hypertension, and heart failure, aids in risk stratification and timely detection.7,8 Protocol-guided management strategies play an important role, before seeking advice from a nephrologist. This involves timely assessment of risks, following hydration protocols, and stopping nephrotoxic medications as initial steps. Remembering "DAAMN" (Diuretics, ACE inhibitors/ARBs, Aminoglycosides, Metformin, NSAIDs) can help recall the medications that should be stopped before contrast procedures.10,11 Maintaining renal blood flow through intravascular volume expansion is crucial by following an intravenous fluid protocol as outlined in Table 3.10,11 In some patients, pharmacological agents such as sodium bicarbonate, N-acetylcysteine, statins, ascorbic acid, theophylline, and aminophylline can be used.10,12 Depending on the severity of renal impairment, using vasodilators, forced diuresis, or renal replacement therapy may be considered.10-12 When a conservative approach falls short or signs of worsening renal function persist, a nephrologist's opinion is recommended. Indicators for this step include a significant rise in serum creatinine, ongoing low urine output, or the need for renal replacement therapy. Ensuring timely communication and collaboration between the primary care team and nephrologists becomes essential when navigating critical stages of renal impairment postcontrast exposure.Table 3: Intravenous fluid protocol to prevent contrast-associated acute kidney injury and contrast-induced acute kidney injury 9 , 11 To conclude, understanding CA-AKI and CI-AKI is like putting together puzzle pieces – knowing the terms, numbers, and how things work. Surgeons and physicians should first consider the use of noncontrast modalities of imaging in the elderly and those with multiple comorbidities, weighing the risks versus benefits of using contrast. In those where contrast has to be used the abovementioned measures should be put in place to reduce the risk of CI-AKI/CA-AKI. The adage "prevention is better than cure" holds in this real-life scenario.