Here’s the simple explanation for why none of our observed treatments to prevent contrast-induced nephropathy – acetylcysteine, hydration, sodium bicarbonate – reliably work: CIN is a myth.
There’s a lot of observational literature evaluating the incidence of mild acute-kidney injury after iodinated contrast exposure – either CT scans or vascular procedures – and every study shows some increase in serum creatinine in a small, but significant, proportion of patients. But, as this study suggests, is this just random effects, a confounder from co-occurring medical illness, or true dose-dependent renal injury?
This study, although retrospective, is almost precisely how I would have addressed the question. This is a single-center review of ten years of patients receiving CT scans. There were 116,694 contrast-enhanced scans and 40,446 non-contrast scans for whom before-and-after serum creatinine values were available. These CT scan events were compared by both risk-stratification as well as propensity score-matched subsets, as well as a counterfactual set of patients who had both independent contrast-enhanced and non-contrast CTs in their records. With every adjusted and unadjusted analysis, regardless of baseline renal insufficiency, there was no evidence of an excess of CIN following the contrast-enhanced events.
This is retrospective, so it’s hard to say whether there are undetected confounders – other comorbid illnesses, diagnosis disparities – that influenced these results despite the large numbers analyzed. However, it is absolutely reasonable to move forward with a prospective study design based on the hypothesis that intravenous contrast-enhanced CT scans do not increase risk of AKI. These results are not yet generalizable, however, to other interventional procedures in which higher volumes of contrast might be used.
This article was also covered by James Roberts in Emergency Medical News.
“Intravenous Contrast Material-induced Nephropathy: Casual or Coincident Phenomenon”