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CT angiography for intracerebral hemorrhage does not increase risk of acute nephropathy
Alexandra Oleinik1, Javier M Romero, Kristin Schwab
1Department of Neurology, Massachusetts General Hospital, Boston, MA 02114, USA.
Insights
CT angiography (CTA) in intracerebral hemorrhage (ICH) does not increase the risk of acute kidney injury. Patients with ICH have an 8% risk of hospital-acquired nephropathy, regardless of contrast use.
Area of Science:
- Nephrology
- Radiology
- Neurology
Background:
- CT angiography (CTA) is increasingly used for intracerebral hemorrhage (ICH) to detect vascular abnormalities and predict bleeding.
- Concerns exist regarding contrast-induced nephropathy (CIN) with CTA, but the actual risk is unclear.
Purpose of the Study:
- To evaluate the risk of acute nephropathy in patients with ICH undergoing CTA.
- To determine if CTA or contrast administration increases the incidence of acute kidney injury in ICH patients.
Main Methods:
- Retrospective analysis of a prospectively collected cohort of 539 ICH patients (2002-2007).
- Acute nephropathy defined as a creatinine rise >25% or >0.5 mg/dL, with peak >1.5 mg/dL.
- Comparison of nephropathy rates between patients who received CTA and those who did not.
Main Results:
- 65% of ICH patients (348/539) received CTA.
- Acute nephropathy occurred in 6% of CTA patients vs. 10% of non-CTA patients (P=0.1).
- Neither CTA nor contrast administration predicted nephropathy in univariate or multivariate analyses.
Conclusions:
- CT angiography does not elevate the risk of acute nephropathy in ICH patients.
- Studies on CIN may overestimate contrast's impact without proper control groups.
- ICH patients have an approximate 8% risk of hospital-acquired nephropathy.
Background And Purpose:
CT angiography (CTA) is receiving increased attention in intracerebral hemorrhage (ICH) for its role in ruling out vascular abnormalities and potentially predicting ongoing bleeding. Its use is limited by the concern for contrast induced nephropathy (CIN); however, the magnitude of this risk is not known.
Methods:
We performed a retrospective analysis of a prospectively collected cohort of consecutive patients with ICH presenting to a single tertiary care hospital from 2002 to 2007. Demographic, clinical, and radiographic data were prospectively collected for all patients. Laboratory data and clinical course over the first 48 hours were retrospectively reviewed. Acute nephropathy was defined as any rise in creatinine of >25% or >0.5 mg/dL, such that the highest creatinine value was above 1.5 mg/dL.
Results:
539 patients presented during the study period and had at least 2 creatinine measurements. 348 (65%) received a CTA. Acute nephropathy developed in 6% of patients who received a CTA and in 10% of those who did not (P=0.1). Risk of nephropathy was 14% in those receiving no contrast (130 patients), 5% in those receiving 1 contrast study (124 patients), and 6% in those receiving >1 contrast study (244 patients). Neither CTA nor any use of contrast predicted nephropathy in univariate or multivariate analysis.
Conclusions:
The risk of acute nephropathy after ICH was not increased by use of CTA. Studies of CIN that do not include a control group may overestimate the influence of contrast. Patients with ICH appear to have an 8% risk of developing "Hospital-Acquired Nephropathy."
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