"Animal studies have demonstrated impressive activations of biogenic amine expressing cell groups, stress-sensitive areas, and cell groups involved in the regulation of water and electrolyte homoeostasis, as well as central autonomic cell groups, in surgically and medically induced renal failure in rats 3. Data reported indicated that the acute uraemic state is an important factor that influences a variety of neurochemicals such as the biogenic amines (noradrenaline, adrenaline, histamine, and 5-hydroxytryptamine (5-HT)), as well as various brain areas such as stress-sensitive forebrain areas, neuronal cell groups involved in the regulation of water and electrolyte homoeostasis, and central autonomic cell groups 3. Animal studies comparing acute uraemic encephalopathy with hepatic encephalopathy have demonstrated an increase in brain inflammation in conjunction with an increase in vascular permeability in uraemic encephalopathy 4. Local kidney injury may activate cytokines that cross the blood-brain barrier or activate other messengers that contribute to neuronal dysfunction. Alternatively, the retention of uraemic solutes may trigger both the inflammatory reaction and neuronal dysfunction 2."
Expected headings
"Macroscopic and microscopic features"
"There are very few studies dealing with the epidemiology of the encephalopathic aspect of renal dysfunction. One study investigated cognitive impairment in patients on haemodialysis and found that among 374 patients on haemodialysis, 55 years or older, only 12.7% were completely cognitively intact. Almost 14% demonstrated mild cognitive impairment, 36.1% demonstrated moderate cognitive impairment, and 37.3% demonstrated severe cognitive impairment 1. Uraemic retention solutes, anaemia and hyperparathyroidism may play distinct roles in the pathogenesis of uraemic encephalopathy 2."
"There are very few studies dealing with the epidemiology of the encephalopathic aspect of renal dysfunction. One study investigated cognitive impairment in patients on haemodialysis and found that among 374 patients on haemodialysis, 55 years or older, only 12.7% were completely cognitively intact. Almost 14% demonstrated mild cognitive impairment, 36.1% demonstrated moderate cognitive impairment, and 37.3% demonstrated severe cognitive impairment 1. Uraemic retention solutes, anaemia and hyperparathyroidism may play distinct roles in the pathogenesis of uraemic encephalopathy 2."
"Case reports and studies in humans have reported a number of biochemical changes in acute and chronic uraemic encephalopathy, including alterations in water transport and brain oedema, disturbances of the blood-brain barrier, and changes in cerebral metabolism 5,6. Anaemia, hyperparathyroidism and brain calcium concentrations have also been implicated in uraemic encephalopathy 7,8."
"Uraemic encephalopathy is a syndrome in which the subcortical grey and white matter, midbrain and mesial temporal lobes become oedematous due to their exquisite sensitivity to metabolic alterations which is an inherent vulnerability related to the arterial perforators which supply these areas. The imaging features are thus consistent with cytotoxic oedema, localised in those areas."
"Uraemic encephalopathy on CT typically presents as confluent bilateral hypodensity involving the basal ganglia, thalamus and midbrain. The anatomical boundaries between the deep subcortical grey matter typically appear obliterated 10."
"Uraemic encephalopathy typically presents as bilateral T2/FLAIR hyperintensities involving the basal ganglia, thalamus, midbrain and mesial temporal lobes. Restricted diffusion may or may not be present to a varying degree, but is not characteristic of uraemic encephalopathy. Enhancement is not a typical feature."
"Animal studies have demonstrated impressive activations of biogenic amine expressing cell groups, stress-sensitive areas, and cell groups involved in the regulation of water and electrolyte homoeostasis, as well as central autonomic cell groups, in surgically and medically induced renal failure in rats 3. Data reported indicated that the acute uraemic state is an important factor that influences a variety of neurochemicals such as the biogenic amines (noradrenaline, adrenaline, histamine, and 5-hydroxytryptamine (5-HT)), as well as various brain areas such as stress-sensitive forebrain areas, neuronal cell groups involved in the regulation of water and electrolyte homoeostasis, and central autonomic cell groups 3. Animal studies comparing acute uraemic encephalopathy with hepatic encephalopathy have demonstrated an increase in brain inflammation in conjunction with an increase in vascular permeability in uraemic encephalopathy 4. Local kidney injury may activate cytokines that cross the blood-brain barrier or activate other messengers that contribute to neuronal dysfunction. Alternatively, the retention of uraemic solutes may trigger both the inflammatory reaction and neuronal dysfunction 2."