Contrast Nephropathy
Legend? Myth? or Something to worry about?
Whats the question?
Is it real or is it a myth?
Why the debate?
How should It affect my decision making and practice?
First lets define the issue
- Most of the work we do in ED where this is relevant is CT related contrast use
- Other areas where we will come across it will be in IR in trauma patients and in Angio for STEMI or AAA (this is more likely to be as an OP)
So what we really want to work out is whether the CT contrast should be having an influence on our scanning and decision making
o We have all had discussion with the radiologist where they want the eGFR before scanning
o I’m sure we have also come across radiographers refusing to do the scan without the results even when approved by the radiologist
§ This has everything to do with the trust policies
So what we really want to work out is when we need to be advocating for our patients strongly in these situations or when what they are saying is completely fine – do we always need to scan right now?
o Obviously this is a little circumstantial, some scans just need to happen. The truly peritonitic 30 yo with abnormal physiology or the ruptured AAA for examples
Whats the proposed mechanism?
- Not properly understood but a has a view proposed ideas
- All centered around the idea of reduced renal perfusion
o Some of it direct – dilutional effect from administration of large volumes of contrast
o Most of it suggested as vasodilation from NO both intrarenal and systemic causing reduction in BP but also a reduction in glomerular filtration pressure
- Lab studies in animals haven’t shown renal failure with contrast unless systemic and renal circulation is compromised
- Its worth thinking about route of contrast administration as well.
o Anything delivered IV is diluted as it returns to the heart
o But anything delivered intra-arterially concentrates as it moves peripherally
§ This is relevant to angios
Why the debate?
- From 1950 there has been demonstration of renal failure following injection of IV contrast for IV pyelography
o However it is now thought that the contrast dye was poisonous and none of the studies had proper control groups and the evidence base is poor
- More modern dyes have lower osmolarity and so are much less likely to be nephrotoxic
- Contrast nephropathy is defined in a lot of studies in a creatinine rise with in 48hrs post dye administration
o Does this reflect true/genuine renal damage?
o How does this manifest clinically? (which is what we really worry about, nitrofurantoin causes a small temporary creatinine rise but we don’t talk about nitrofurantoin nephropathy)
§ What we really want to know is the long term consequences of modern contrasts and dyes ie does it cause permanent damage (as demonstrated in persistently raised Creatinine and Urea, or in the need for renal replacement therapy)
- It is unethical to do RCTs where you potentially cause renal failure, so all the studies are limited in their nature; they are all retrospective propensity studies
o RECENT STUDIES AND META-ANALYSES DON’T DEMONSTRATE ANY RELATIONSHIP BETWEEN CONSTRAST AND CREATININE ELEVATION
§ Interestingly there is one study comparing creatinine in both non con and contrast CT and there was a similar rise in both groups (https://pubmed.ncbi.nlm.nih.gov/23360742/)
§ Also there are suggestions that the average creatinine of a group of patients post contrast doesn’t change – that being said that some rise and some decrease
- In a 2015 study looking at renal bio-markers, as a proxy for renal damage, demonstrated no rise post contrast administration for 96hrs (which is as far as the study went)
o However the study was in patients who received hydration regimes
o https://pubmed.ncbi.nlm.nih.gov/25773936/
- Likewise this meta-analysis (https://pubmed.ncbi.nlm.nih.gov/28811122/) demonstrated no difference between the groups receiving contrast with their CTs and those that didn’t when looking at rates of renal insufficiency, RRT or mortality
o This looked at 28 studies involving 107335 patients
The suspicion is that there is a lot of confounding with suggestions that contrast causes AKI
- Unwell patients get AKIs (there is a conformation bias element to unwell patients developing AKIs post scan)
- A lot of the studies are observational without a true non con control group (ie they don’t compare with people who are getting CTs)
Proving a negative (ie it doesn’t cause AKI) is really hard and will take a lot of evidence and time
Can we summerise all this data?
- IV modern contrast media, particularly at lower doses, has little no evidence that it causes renal injuries
o NICE guidelines suggest there are still some at risk groups
§ Diabetics with CKD
§ eGFRs <40 as a baseline
§ Heart failure
§ Renal Transplant
§ Hypovolaemia
o Once larger quantities or intra-arterial contrast is being given then the risk increases
So how do we proceed on the shop floor?
Most of our scans that involve IV contrast are for either abdominal or aortic pathology, looking for bleeding, visceral damage or causes of an acute abdomen
In these circumstances it seems unlikely that Contrast Nephropathy is going to be something that we need to concern ourselves with.
The general view is that delaying a scan is likely to cause more harm than any potential consequences from contrast.
With this in mind we should be pushing for scans in all our sick patients regardless of the delay for an eGFR.
The hard question comes when the patient is not so unwell or potentially has significant pathology that time is important in establishing the diagnosis (ie trauma or acute abdomens)
- With these patients it becomes a judgment call and comes with the question of why we want the scan. Do we THINK that they have perforated or are they just a bit sore and we want to rule it out and actually they may just be constipated.
o It goes back to the pre-test probability question we talked about the understanding blood test section
There is evidence suggesting that the delay in the scan causes more harm compared to the nephropathy from contrast
What we can do is make sure we are mitigating the risks where we can – simply working to improve renal perfusion by good hydration (we will probably already treating them with fluids for the sick patients anyway)
Intra-arterial and particularly intra-aortic holds bigger risks but in these situations (IR and cardiac angios) the big picture of the patient makes it necessary but again we can think about ways we can improve the renal function to try and reduce the consequences (if there are any)
Nicely since this was written, RCEM and RCR have got together and released a joint statement. Read it here
https://www.rcr.ac.uk/news-policy/latest-updates/joint-advisory-statement-between-the-royal-college-of-radiologists-royal-college-emergency-medicine-regarding-emergency-computed-tomography-scans-and-the-use-of-intravenous-iodinated-contrast-agents/
Reference
https://emcrit.org/ibcc/contrast/
https://pubmed.ncbi.nlm.nih.gov/23360742/
https://litfl.com/contrast-induced-nephropathy/
https://www.ajronline.org/doi/full/10.2214/ajr.183.6.01831673
https://pubmed.ncbi.nlm.nih.gov/25773936/