By Daniel Sartori MD, Marty Fried MD, Shreya Trivedi MD; Illustration by Michelle Lo MD and Amy Ou MD. Quiz yourself on the 5 Pearls we will be covering:



* Are there diagnostic criteria for contrast-induced nephropathy (CIN)? (2:11 )

* Is there a difference between exposure to intra-arterial versus intra-venous contrast in terms of risk of CIN? (6:28 )

* What are the biggest risk factors for CIN? (14:48 )

* What preventive measures have been shown to best reduce the risk of CIN? (19:41 )

* Can ESRD patients on hemodialysis still suffer from CIN? (23:32 )

* Recap (25:49 )



A special thank you to Dr. Josh Farkas for peer-reviewing this podcast!

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Pearl 1: Diagnostic criteria for Contrast-Induced Nephropathy (CIN)



Most research studies define CIN as a relative increase in serum creatinine of anywhere from 25-50% or, an absolute rise in serum creatinine of 0.5 to 1mg/dL within 48-72 hours after exposure to contrast with exclusion of other causes of acute kidney injury.

Other clues are signs of acute tubular necrosis and a fractional excretion of sodium (FeNA) less than 1.



Pearl 2: Intravenous vs Intra-arterial contrast



Most data suggest that CIN is a disease entity almost entirely reserved for patients undergoing intra-arterial contrast loads, and not intra-venous contrast loads.



The incidence of AKI after arterial contrast ranges anywhere from 5-30% depending on the other risk factors present.

The incidence of AKI following intravenous contrast exposure is much lower, in the ballpark of 2-10%





Issues often with studies of arterial contrast:



Retrospective

No control group

Selection Bias

Other variables: showering atherosclerotic emboli to kidneys or volume of contrast used





Issues often with studies of venous contrast:



Also retrospective

Controlled, but poorly

Selection bias









Pearl 3: Risk Factors



* CKD



* Patients with underlying CKD are at increased risk of developing CIN

* Pinpointing the GFR at which the greatest risk occurs is very difficult because most studies lump patients into buckets with wide ranges of GFR

* What we do know:

* In patients undergoing studies with arterial contrast:



* ~ 5% of patients with GFR 30-60 develop CIN

* ~ 30% of patients with GFR <30 develop CIN









* Proteinuria



* GFR < 60 plus at least 1 g of proteinuria develop CIN at almost double the rate of patients with GFR <60 alone





* Diabetes:



* Patients with diabetes coupled with CKD demonstrated almost triple the rate of CIN compared to patients with CKD alone





* Hypovolemia:



* Given difficulty measuring volume status by exam or labs, there are no known randomized trials looking at rates of CIN in those hypovolemic vs. euvolemic

* But given data with prophylactic hydration, low effect arterial blood volume and hypoperfusion to the kidneys are thought to constitute elevated risk.





* High Osmolality Contrast



* Older contrast agents are hyper-osmolar compared to serum and associated with much higher rates of CIN

* Newer contrast agents are either iso-osmolar or hypo-osmolar and associated with rates...