CIN Is Much Less Common Than Once Believed
CIN is much less common than previously thought. Most patients have little or no CIN risk. Saline prophylaxis is not indicated, if the eGFR is above 30.
Why are we questioning CIN?
Data on contrast-induced nephropathy (CIN) are mixed, which has caused some confusion in radiology. Matthew Davenport, University of Michigan, has sorted the data concluding: „CIN does exist – for now”.
He reminded the audience of the two studies that have led to doubts about CIN:
- Rao (2006) showed that only 1.3% of CIN studies had dealt with IV contrast. Only 2 of 40 studies had used a control.
- Newhouse (2008) found that AKI (acute kidney injury) rates in patients not receiving contrast were similar to CIN cases in patients with contrast.
Serum creatinine – the main CIN-biomarker – decreased in more patients after contrast administration than in patients without contrast. “We know that serum creatinine is not a very good biomarker”, commented Davenport.
Many more reasons made him question the early data: The studies relied on now outdated contrast, they did not differentiate between intravenous injections and intraarterial (IA) injections for coronary angiograms, CIN definitions varied, many studies were “contaminated” by low-risk patients. “Most importantly, not all post-contrast AKI is CIN”, he said.
Two definitions – PC-AKI and CIN
Davenport differentiated two definitions which need to be used when appraising the literature:
- Post-contrast acute kidney injury (PC-AKI) is a generic term describing a sudden degeneration in renal function within 48 hours after intravascular contrast administration. It is a correlative diagnosis. Contrast may not be the reason of this degeneration.
- CIN is a specific term for contrast being the cause of renal degeneration. It is thus a subgroup of PC-AKI.
“Most studies do not have a control group, so when they describe CIN, they actually talk about PC-AKI”, underlined Davenport. “That is a very important distinction.”
Super-prevalent or non-existing?
Advanced retrospective controls in recent years from the Mayo Clinic and the University of Michigan have caused a major shift in thinking.
The studies showed “lots of PC-AKI”, but the vast majority of patients has little or no risk of CIN.
With one exception: CIN was prevalent in the high-risk group with an estimated glomerular filtration rate (eGFR) of less than 30 mL/min/1.73m2. However, only 2.1% of inpatients and 0.2% of outpatients have an eGFR <30. Of the 36% with PC-AKI in this group, 17% had CIN. The other 19% had AKI from other causes. “If we use PC-AKI to diagnose CIN in these highest risk patients, for every 10 correct CIN diagnoses we also get 11 incorrect CIN diagnosis”. The historically reported CIN risk seems to be “much overblown”, concluded Davenport.
If the eGFR is less than 30, and contrast is necessary and CT and MRI are diagnostically equivalent*:
- Low-osmolar and iso-osmolar iodinated contrast is preferred in patients with chronic anuric dialysis. “The kidneys are done anyway”, added Davenport.<
- Low-risk gadolinium-based contrast is preferred (single dose, if possible) in non-anuric patients or patient who a not on chronic dialysis.
The University of Michigan Rules
“In patients with an eGFR of less than thirty, we pick up the phone and talk to our colleagues – what are you trying to figure out, what is the number needed to harm, do we need to do that study”, explained Davenport.
Patient screening is reduced to taking patient history of renal disease – this aspect is not in line with the American College of Radiologists’ (ACR) Manual on Contrast Media. If the scan is emergent, patients will not be screened at all.
Prophylaxis with acetylcysteine and bicarbonate are not recommended (Weisbord 2018). Prior volume expansion with saline in patients with an eGFR between 30 and 59 mL/min/1.73m2 does not make a difference regarding kidney function. However, saline infusion leads to complications in 5.5% of the patients (Nijssen 2017) “So no prophylaxis for this group”, concluded Davenport.
*Note: Bayer's position does not change. Bayer recommends in the small group of the remaining renal high-risk patients (eGFR<30) a strict indication for imaging with a careful assessment of risk benefits of all available alternatives in close consolation with the referring physician and a renal specialist – most likely there is not one protocol to be followed.
Newhouse JN et al. Frequency of Serum Creatinine Changes in the Absence of Iodinated Contrast Material: Implications for Studies of Contrast Nephrotoxicity. American Journal of Roentgenology. 2008;191:376-82.
Nijssen EC et al. Prophylactic hydration to protect renal function from intravascular iodinated contrast material in patients at high risk of contrast-induced nephropathy (AMACING): a prospective, randomised, phase 3, controlled, open-label, non-inferiority trial. Lancet 2017;389(10076):1312-22.
Rao QA, Newhouse JH. Risk of nephropathy after intravenous administration of contrast material: a critical literature analysis. Radiology. 2006;239(2):392-7.
Weisbord SD et al. Outcomes after Angiography with Sodium Bicarbonate and Acetylcysteine. N Engl J Med. 2018;378(7):603-14.
Presentation Title: CIN: Does it exist? If not, why are we trying so hard to prevent it
Speaker: Matthew Davenport, University of Michigan
Session code: RC407-1