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


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).


CONCLUSIONS
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.


BACKGROUND
http://radiology.rsna.org/lookup/suppl/doi:10.1148/radiol.12121823/-/DC1.
Clinician Investigator Training Program, Department of Radiology, College of Medicine, Mayo Clinic, 200 1st St SW, Rochester, MN 55905, USA. mcdonald.robert@mayo.edu
Robert J
RJ
McDonald
Jennifer S
JS
McDonald
John P
JP
Bida
Rickey E
RE
Carter
Chad J
CJ
Fleming
Sanjay
S
Misra
Eric E
EE
Williamson
David F
DF
Kallmes
D000368:Aged; D002140:California / Q000453:epidemiology; D015984:Causality; D016009:Chi-Square Distribution; D003287:Contrast Media / Q000009:adverse effects*; D005260:Female; D006801:Humans; D015994:Incidence; D007674:Kidney Diseases / Q000139:chemically induced* / Q000000981:diagnostic imaging* / Q000453:epidemiology; D008297:Male; D008875:Middle Aged; D057216:Propensity Score; D012189:Retrospective Studies; D014057:Tomography, X-Ray Computed
D003287:Contrast Media