Syndrome of uremic encephalopathy and bilateral basal ganglia lesions in non-diabetic hemodialysis patient: a case report

Abstract

BackgroundUremic encephalopathy (UE), a toxic metabolic encephalopathy, is an uncommon complication resulting from endogenous uremic toxins in patients with severe renal failure. UE syndrome can range from mild inattention to coma. The imaging findings of UE include cortical or subcortical involvement, basal ganglia involvement and white matter involvement. The basal ganglia type is uncommon, although previous cases have reported that Asian patients with diabetes mellitus (DM) are usually affected.Case presentationA 32 year-old woman with a history of non-diabetic hemodialysis for 3 years suffered from severe involuntary movement, and brain magnetic resonance imaging showed symmetrical T2-weighted imaging (T2WI) and T2/fluid-attenuated inversion recovery (T2FLAIR) hyperintense nonhemorrhagic lesions in the bilateral basal ganglia. She was diagnosed with UE as syndrome of bilateral basal ganglia lesions, due to a combined effect of uremic toxins and hyperthyroidism. After treatment with high frequency and high flux dialysis, hyperbaric oxygen therapy and declining parathyroid hormone, the patient achieved complete remission with normal body movement and was discharged.ConclusionUE with basal ganglia involvement is uncommon, although generally seen in Asian patients with DM. Our case reported a hemodialysis patient that had non-diabetic UE with typical bilateral basal ganglia lesions, presenting with involuntary movement.

Uremic encephalopathy: A definite diagnosis by magnetic resonance imaging?

“… 24 However, in a case study in 2018 Liu reported a non-diabetic UE with typical bilateral basal ganglia lesions. 25 In our study, none of the 20 patients showed symptoms of basal ganglia involvement on their MRI images. Since the presence of DM was considered as an exclusion criterion in our study, the DM can be suggested as an exacerbating, not a definite, factor for basal ganglia involvement.…”

Unmasking Uremic Encephalopathy: Choreoathetoid Movements Mimicking Alcohol Withdrawal in a Person with an Alcohol Use Disorder

“…The patient's deteriorating renal function, as indicated by elevated serum creatinine and blood urea nitrogen (BUN) levels, provided a crucial clue for considering uremic encephalopathy in the differential diagnosis. Chronic alcoholism can lead to renal impairment through multiple mechanisms, such as direct toxic effects of alcohol on the kidneys and dehydration secondary to alcohol consumption [5].…”

Extensive multiregional urea elevations in a case-control study of vascular dementia point toward a novel shared mechanism of disease amongst the age-related dementias

“…As there are currently no clinical methods that can quantify cerebral urea levels in vivo , the literature surrounding uremic encephalopathy has mainly focused on evidence derived from plasma creatinine and blood-urea nitrogen levels. Case reports of patients with uremic encephalopathy caused by renal failure showed an estimated 1.82–3.59 FC decrease in blood-urea nitrogen levels following dialysis and remission of symptoms related to uremic encephalopathy ( Kim et al, 2016 ; Jia et al, 2017 ; Gong et al, 2018 ). Although these reports reflect systemic urea levels, and, thus, cannot be directly compared with corresponding measurements from the cerebral tissues, the case-control FC observed in the present study of VaD approximates those present in cases of uremic encephalopathy.…”