Format

Send to

Choose Destination
Nephron. 2019;141(1):31-40. doi: 10.1159/000494047. Epub 2018 Oct 26.

Intra-Arterial versus Intravenous Contrast and Renal Injury in Chronic Kidney Disease: A Propensity-Matched Analysis.

Author information

1
Division of Cardiovascular Medicine, University of Iowa, Iowa City, Iowa, USA.
2
Department of Nephrology and Hypertension, Glickman Kidney Urological Institute (GUKI), Cleveland Clinic Foundation, Cleveland, Ohio, USA.
3
Department of Cardiology, Section of Cardiovascular Imaging, Cleveland Clinic Foundation, Cleveland, Ohio, USA.
4
Department of Medicine, Cleveland Clinic Foundation, Cleveland, Ohio, USA.
5
Department of Quantitative Health Sciences, Cleveland Clinic, Cleveland, Ohio, USA.
6
Center for Populations Health Research, Cleveland Clinic, Cleveland, Ohio, USA.
7
Section of Nephrology, Baylor College of Medicine, Houston, Texas, USA.
8
Section of Nephrology, Michael E. Debakey VA Medical Center, Houston, Texas, USA.
9
Cleveland Clinic Lerner College of Medicine of CWRU, Cleveland, Ohio, USA.
10
Department of Nephrology and Hypertension, Glickman Kidney Urological Institute (GUKI), Cleveland Clinic Foundation, Cleveland, Ohio, USAnakhoug@ccf.org.
11
Cleveland Clinic Lerner College of Medicine of CWRU, Cleveland, Ohio, USAnakhoug@ccf.org.

Abstract

BACKGROUND/AIMS:

contrast-induced nephropathy (CIN) is well described following an administration of intraarterial contrast, but its occurrence after intravenous (IV) contrast is being questioned. We evaluated the incidence of acute kidney injury (AKI), post-contrast AKI (PC-AKI), CIN, dialysis and mortality in patients with chronic kidney disease (CKD) undergoing non-contrast computed tomography (NCCT) or contrast CT (CCT) or coronary angiography (CoA).

METHODS:

We identified individuals who had CoA or CCT or NCCT between 2010 and 2015 in the Cleveland Clinic CKD registry. We used propensity scores to match patients in the 3 groups. We evaluated the proportion of patients that developed AKI and CIN across the groups with chi-square tests. We generated Kaplan-Meier plots comparing mortality and ESRD among patients who developed AKI (in the NCCT group), PC (multifactorial AKI, CIN) AKI and no AKI.

RESULTS:

Out of 251 eligible patients, 200 who had CoA were matched to each of the other CT scan groups. The incidence of AKI was 27% in CoA, 24% in CCT and 24% in NCCT (p = 0.72). The incidence of CIN AKI was 16.5% in CoA and 12.5% in CCT (p = 0.26). The Kaplan-Meier survival at 2 years was 74.8 (95% CI 63.8-87.7) for those with CIN and 53.2 (95% CI 39.7-71.4) for those with multifactorial AKI and 56.5 (95% CI 43.4-73.6) for those with AKI-NCCT and 71.4 (95% CI 67.2-76.0) for those without AKI. The Kaplan-Meier ESRD-free estimates at 2 years were 89.9 (95% CI 80.8-100) for those with CIN and 89.4 (95% CI 78.7-100) for those with multifactorial AKI and 77.4 (95% CI 63.6-94.3) for those with AKI-NCCT and 94.4 (95% CI 91.9-97.1) for those without AKI.

CONCLUSION:

The administration of both IV and intra-arterial contrast is associated with a risk of AKI. Multifactorial AKI was associated with worse outcomes, while CIN was associated with better outcomes.

KEYWORDS:

Acute renal failure; Chronic kidney disease; Contrast-induced nephropathy; Intraarterial contrast; Intravenous contrast

PMID:
30368506
DOI:
10.1159/000494047

Supplemental Content

Full text links

Icon for S. Karger AG, Basel, Switzerland
Loading ...
Support Center