Controlled contrast medium-induced nephropathy studies demonstrate a similar incidence of AKI, dialysis, and death between the contrast medium group and control group.This was just a curiousity that felt like the work of magician because no matter how many different ways that McDonald et al tried to prove there was no contrast nephropathy, I had seen it with my own eyes. I had seen young people with a normal creatinine who were completely stable go for a contrasted CT scan and then spiral into renal failure in subsequent days. No one could convince me that this was incidental renal failure. Renal failure just doesn't happen like that.
The best I could do to explain away the work of McDonald was to say that she is a radiologist so it must be biased in favor of her procedure/specialty. I know this is weak sauce but the I had seen it with my own eyes could not be silenced. Then Chertow. Here was the most prominent nephrology clinical trialist of our time coming to the exact same conclusions as the radiologists.
...the incremental risk of AKI that can be attributed to radiocontrast is modest at worst, and almost certainly over- estimated by patients, physicians, surgeons, radiologists, and other decision-makers.I have been trying to reconcile this cognitive dissonance and this is where I am. The decision to use changes in creatinine to define contrast nephropathy results in a definition that captures lots of false positives.
Definition of contrast-induced nephropathy (CIN): impairment of renal function defined as either a 25% increase in serum creatinine (SCr) from baseline or 0.5 mg/dL (44 µmol/L) increase in absolute value, within 48-72 hours of intravenous contrast administration.Note that unlike definitions of other entities like hepatorenal syndrome, there is no exception if there is alternative explanation for the renal failure. Any patient with sepsis, hypotension, and a complete breakfast of aminoglycosides, ketorolac, and ramipril that happens to get a contrasted CT scan followed by a bump in the creatinine is another case of contrast nephropathy. Though being admirably sensitive, this definition is wildly non-specific.
So the key question in evaluating the definition of contrast nephropathy is what proportion of cases are real cases of contrast nephropathy and what numbers are incidental AKI that happen to occur after contrast exposure. In other words how many of those contrast nephropathies are false postives. To reconcile my experience and Chertow’s data I have shifted my position from being mostly true positives with a small amount of noise to mostly noise with only a few cases of true contrast nephropathy.
Once you accept that the the majority of cases of contrast nephropathy are just incidental cases of AKI, other facts start to come into focus. For example, look at the risk factors for contrast nephropathy:
- CKD
- Diabetes mellitus
- Advanced age
- High contrast dose
- NSAIDs
- ACEi
- Heart failure
- Balloon pump
- Volume depletion
- Hypotension
- Shock
How about the interventions we do to reduce contrast nephropathy:
- Avoid diuretics
- Avoid NSAIDs
- Stop ACEi/ARBs
- Give IVF (and 0.9 NS is better than 0.45 NS)
Why is this important? Well for one I think our research is lying to us. I have been surprised on multiple occasions that the patients that get contrast nephropathy don’t fit the model of the high risk patient and likewise patients that are set-ups to get contrast nephropathy don’t. Our models are so overwelmed with incidental AKI that they do not give us a good idea of the people who are truly at risk of real contrast nephropathy.
I wonder, if we were to do a careful analysis of contrast nephropathy cases where we excluded every case that could have an alternative explanation of AKI, to produce a cohort of people with a very low rate of false positives. How different would the risk factors for contrast nephropathy look like in that cohort? I suspect contrast nephropathy would look more like an idiopathic condition.
