Impact of renal artery stenosis on acute kidney injury and outcomes after heart failure hospitalization.

BACKGROUND: Renal artery stenosis (RAS) is known to co-exist with heart failure (HF), however the impact of RAS on rates of acute kidney injury during an acute HF hospitalization, and adverse events after acute HF hospitalizations has not been well studied. METHODS: We performed a retrospective cohort study of subjects hospitalized for acute HF at a tertiary academic care center. We identified subjects who had a renal artery duplex ultrasound or other diagnostic study for RAS to categorize heart failure subjects as RAS+ or RAS-. AKI was defined as a rise from admission to peak creatinine of >0.3 mg/dL or >1.5 fold. In-hospital outcomes including rates of AKI were ascertained. Adverse outcomes over a two-year follow up period were also ascertained. RESULTS: A total of 93 subjects with acute HF hospitalization met the inclusion criteria and were enrolled in this study; 27 (29%) were identified as RAS+. At admission, subjects with RAS had higher rates of diabetes and prior PCI. During the HF hospitalization, subjects with RAS were more likely to develop AKI. No significant differences were identified in baseline or hospital medication use among subjects with versus without RAS. Importantly, the rate of ACE-I/ARB use was low in both groups and no significant difference in ACE-I/ARB use was demonstrated. Subjects with RAS had higher rates of recurrent HF hospitalization during the follow-up period. CONCLUSIONS: RAS is prevalent among subjects with acute HF, associated with higher rates of AKI during HF hospitalization, and associated with higher rates of recurrent HF hospitalization during follow-up.

Rare pitfall in the magnetic resonance imaging of status epilepticus.

Brain MRI in Status Epilepticus (SE) is often helpful in diagnosis, lateralization and localization of the seizure focus. MRI changes in SE include predominantly ipsilateral diffusion weighted imaging (DWI) changes in the hippocampus and pulvinar or similar changes involving basal ganglia, thalamus, cerebellum, brain stem and external capsule (Chatzikonstantinou et al., 2011 [1]). These changes are thought to be due to transient vasogenic and cytotoxic edema due to either transient damage or breakdown of blood brain barrier, proportional to the frequency and duration of the epileptic activity (Amato et al., 2001 [2]). Such changes may also be reflected on T2- weighted and T2-Fluid-Attenuated Inversion Recovery (FLAIR) sequences of MRI. Herein, we present a case of a transient FLAIR cerebrospinal fluid (CSF) hyperintensity on the second MRI brain in a patient with focal status epilepticus. This imaging finding led to diagnostic confusion and was initially thought to represent subarachnoid hemorrhage. However, lumbar puncture, brain computed tomography (CT), and a follow-up brain MRI ruled out that possibility and other CSF pathologies. We concluded that the transient FLAIR changes in the second brain MRI were related to a rare imaging pitfall caused by Gadolinium enhancement of CSF on the FLAIR sequence, popularly referred to as hyperintense acute reperfusion marker (HARM).