Written by Thomas Davis, MD.
There are good data to support contrast-associated acute kidney injury (CA-AKI). With the use of low osmolar contrast agents, the risk may be lower. However, none of the myth-busting studies are good enough to exclude the risk of CA-AKI, especially in the most vulnerable patients.
Why does this matter?
Contrast is used to improve the diagnostic accuracy of CT and is essential to evaluate vascular pathology. However, it seems that every group of radiologists has a different renal threshold for which they are willing to scan. This variation begs the question: Is contrast-associated acute kidney injury for real?
Yes, contrast nephropathy is real!
First, there is a strong physiologic explanation. Multiple animal studies have shown that iodinated contrast leads to decreased renal blood flow, decreased partial pressure of oxygen in the outer renal medulla, and generation of free oxygen radicals. MRI studies in healthy human volunteers have confirmed decreased renal blood flow after iodinated contrast administration.
Second, there seems to be a dose-response relationship between contrast administration and AKI. While low osmolar contrast may be less toxic to the kidneys, its safety is yet to be conclusively demonstrated.
Studies that have questioned the existence of CA-AKI are severely limited by being retrospective observational studies that excluded the most vulnerable patients. If we know that contrast definitively harms the kidney, do we really believe that a lower osmolar solution is somehow renal protective—or at least renal neutral? Until an RCT explicitly tests patients with just a few remaining functional nephrons, we must continue to assume that low osmolar contrast agents can cause clinically significant AKI in patients with advanced CKD.
Contrast-associated acute kidney injury is a myth: No. Intensive Care Med. 2017 Dec 14. doi: 10.1007/s00134-017-5015-6. [Epub ahead of print]
Peer reviewed by Clay Smith, MD.