Radiographic contrast media is considered a common cause of hospital-acquired renal insufficiency, yet the latest research on contrast-induced nephropathy (CIN) suggests there may be no relationship between contrast use and renal injury1,2. A recent article by Dr. Hinson et al published in the Annals of Emergency Medicine, found no association between acute kidney injury and IV contrast use. Hinson’s article, a single-center retrospective cohort analysis of 17,934 patients who underwent CT scan with or without contrast, is the largest controlled study of CIN, and may lead to a significant change in practice.
Contrast-induced Nephropathy is a change in creatinine of 25% from baseline, or absolute increase of 0.5 mg/dl 48-72 hours after infusion1. Early research identified CIN in patients undergoing coronary catheterization, where much larger loads of contrast was used, and before the use of low-osmolar contrast agents3. Other research has found that underlying renal disease, or already impaired renal function, may be the cause of CIN4. CIN may be due to many factors other than IV contrast. Patients undergoing a CT with IV contrast followed by a rise in creatinine may have alternative causes which are overlooked, such as nephrotoxic drug use, sepsis, or a range of other causes. The contrast is presumed to be the cause, and much of the research surrounding CIN is hindered by confounding bias due to the exposure itself and the physiology of why the patient is receiving the scan in the first place. Measuring the creatinine level in patients undergoing multiple procedures, nephrotoxic medication use, or requiring CT imaging creates a significant selection bias. When selection bias is accounted for with negative controls, renal injury rates have not been correlated with contrast use, or associated with previous renal injury5,6.
The most recent study by Hinson sought to clarify the incidence of CIN and utilized two control populations to minimize bias. The paper was a retrospective review of 17,934 patients over a 5-year period, comparing the incidence of AKI in contrast-enhanced CT, non-contrast CT, and no CT imaging, with the primary outcome of incidence of acute kidney injury. Patients were included if they were >18 years-old, received an CT scan either with or without contrast, and had both initial creatinine and 48-72 hour creatinine measurements. A second control group was also included who did not undergo CT imaging, but did have initial and secondary creatinine measurements. Patients were excluded if they already had severe renal injury, a prior renal transplant, recent prior CT imaging, or insufficient creatinine data. The study used both the classic definition of CIN, as well as the Acute Kidney Injury Network/Kidney Disease Improving Global Outcomes (AKIN/KDIGO) guideline to define renal injury as a primary outcome.
The results found that contrast used produced no significant increase in acute renal injury. Using AKIN/KDIGO scoring, the probability of AKI was 6.8% in those with contrast-enhanced CTs, 8.9% in non-contrast CTs, and 8.1% for those without any CT imaging. Classic CIN definitions found the probability of developing AKI in each group was 10.6%, 10.2%, and 10.9%, in contrast-enhanced, non-contrast, and no CT imaging groups respectively. There was also no significant change in the risk for developing chronic kidney disease in 6 months or initiating dialysis between the groups.
Although this study is retrospective and single-center, it represents the largest controlled study of CIN. The inclusion of two control groups reduces the selection bias, and the primary outcome was reported using both AKIN/KDIGO and classic CIN definitions, preventing any under-reporting of renal injury. While the article found no evidence of contrast-induced nephropathy, they do identify some nephroprotective treatment patterns as being potentially responsible. Providers were more likely to provide intravenous fluids and less likely to order contrast-enhanced studies to those with decreased renal function or comorbidities. With these results, the authors are calling for a controlled randomized prospective trial to determine if there is a causative relationship between contrast media and acute renal injury.
1. Hinson JS, Ehmann MR, Fine DM, et al. Risk of Acute Kidney Injury After Intravenous Contrast Media Administration. Ann Emerg Med 2017;69:577-86 e4.
2. Nash K, Hafeez A, Hou S. Hospital-acquired renal insufficiency. Am J Kidney Dis 2002;39:930-6.
3. Daniel J. Pallin M, MPH. Intravenous Contrast May Pose No Risk to Kidneys. 2017.
4. Pickering JW, Blunt IR, Than MP. Acute Kidney Injury and mortality prognosis in Acute Coronary Syndrome patients: A meta-analysis. Nephrology (Carlton) 2016.
5. Contrast-Induced Nephropathy: Confounding Causation - emDOCs.net - Emergency Medicine Education. 2017. at http://www.emdocs.net/contrast-induced-nephropathy-confounding-causation/.)
6. Davenport MS, Khalatbari S, Cohan RH, Dillman JR, Myles JD, Ellis JH. Contrast Material–induced Nephrotoxicity and Intravenous Low-Osmolality Iodinated Contrast Material: Risk Stratification by Using Estimated Glomerular Filtration Rate. Radiology 2013;268:719-28.
Evan Kuhl, MD is an Emergency Medicine Resident at The George Washington University Hospital
