Intravenous contrast material-induced nephropathy: causal or coincident phenomenon?

Abstract

Purpose: To determine the causal association and effect of intravenous iodinated contrast material exposure on the incidence of acute kidney injury (AKI), also known as contrast material-induced nephropathy (CIN).

Materials and methods: This retrospective study was approved by an institutional review board and was HIPAA compliant. Informed consent was waived. All contrast material-enhanced (contrast group) and unenhanced (noncontrast group) abdominal, pelvic, and thoracic CT scans from 2000 to 2010 were identified at a single facility. Scan recipients were sorted into low- (<1.5 mg/dL), medium- (1.5-2.0 mg/dL), and high-risk (>2.0 mg/dL) subgroups of presumed risk for CIN by using baseline serum creatinine (SCr) level. The incidence of AKI (SCr ≥ 0.5 mg/dL above baseline) was compared between contrast and noncontrast groups after propensity score adjustment by stratification, 1:1 matching, inverse weighting, and weighting by the odds methods to reduce intergroup selection bias. Counterfactual analysis was used to evaluate the causal relation between contrast material exposure and AKI by evaluating patients who underwent contrast-enhanced and unenhanced CT scans during the study period with the McNemar test.

Results: A total of 157,140 scans among 53,439 unique patients associated with 1,510,001 SCr values were identified. AKI risk was not significantly different between contrast and noncontrast groups in any risk subgroup after propensity score adjustment by using reported risk factors of CIN (low risk: odds ratio [OR], 0.93; 95% confidence interval [CI]: 0.76, 1.13; P = .47; medium risk: odds ratio, 0.97; 95% CI: 0.81, 1.16; P = .76; high risk: OR, 0.91; 95% CI: 0.66, 1.24; P = .58). Counterfactual analysis revealed no significant difference in AKI incidence between enhanced and unenhanced CT scans in the same patient (McNemar test: χ(2) = 0.63, P = .43) (OR = 0.92; 95% CI: 0.75, 1.13; P = .46).

Conclusion: Following adjustment for presumed risk factors, the incidence of CIN was not significantly different from contrast material-independent AKI. These two phenomena were clinically indistinguishable with established SCr-defined criteria, suggesting that intravenous iodinated contrast media may not be the causative agent in diminished renal function after contrast material administration.

Supplemental material: http://radiology.rsna.org/lookup/suppl/doi:10.1148/radiol.12121823/-/DC1.

Figure 1:

Study inclusion flowchart. IPTW = inverse probability of treatment weighting, O.R. = odds ratio, w/in = within. µ = mean.

Figure 2:

Chart shows distribution of propensity scores in study population. Patients who underwent contrast-enhanced CT scan (contrast group) are shown above the x-axis and patients who underwent unenhanced CT scan (noncontrast group) are shown below the x-axis. A, Distribution of the full unadjusted data set (n = 157 140) and low-, medium-, and high-risk subgroups. B, Distribution of the subset of scans included in the counterfactual analysis (n = 8530).

Figure 3:

Chart shows the relative influence of the covariates on the estimated propensity score for each risk subpopulation.

Figure 4:

Incidence of AKI within the paired counterfactual data set. Contingency tables compare the incidence of AKI after contrast-enhanced scans with the incidence of AKI after unenhanced CT scans for the entire counterfactual data set (black), the subset of patients within the counterfactual data set where the contrast-enhanced examination was performed first (red), and the subset of patients within the counterfactual data set where the unenhanced examination was performed first (blue).