CONCLUSION: Uremic encephalopathy generally develops in patients with acute or chronic renal failure when the glomerular filtration rate declines below 10% of normal (Raskin 2001). The clinical features are variable, tend to occur early, are n ot clearly distinguishable from those of other metabolic encephalopathies, but may respond to hemodialysis(Fraser hemodialysis(Fraser and Arieff 1997). Features of uremic encephalopathy are characteristic of a metabolic encephalopathy and may include sluggishness, easy fatigability, daytime drowsiness and insomnia, itchiness, inability to sustain attention or to perform complex cognitive tasks, slurred speech, anorexia, nausea and vomiting, restlessness, poor memory, diminished sexual interest, emotional lability, confusion, convulsions, stupor, and preterminal coma (Lockwood 1989; Lacerda et al 2010). The coexistence of features suggestive of depression of neural activity together with those of n eural excitation (ie, twitching, agitation, myoclonus, asterixis, seizures) is somewhat distinctive to uremic encephalopathy (Raskin and Fishman 1976a; 1976b).
Uremic toxins Uremic toxins
Renal failure results in accumulation of numerous organic substances that possibly act as uremic neurotoxins, but no single metabolite has been identified as the sole cause of uremia (Vanholder et al., 2003b). Symptoms are usually alleviated by dialysis or successful renal Transplantation
Creatinine Excretion of
clearance fall to
RENAL FAILURE Nitrogenous
less than
substance
10mL/min
Uremia
Accumulation of urea, guanidino compounds, uric acid, hippuric acid, various amino acids, polypeptides, polyamines, phenols and conjugates of phenol, phenolic
Accumulation of metabolites of proteins and amino acids affect the entire neuraxis
indolic acids, acetone, glucuronic acid, carnitine, myoinositol, sulphates and phosphates
uremic brain uremia appears to use less adenosine triphosphate and to produce less adenosine diphosphate, adenosine monoposphate and lactate.
Disturbance of intermediary metabolism
Imbalance of inhibitory and excitatory neurotransmitter
These changes are associated with a decrease in both brain metabolic rate and cerebral oxygen consumption and are consistent with a generalized decrease in brain energy use.
inhibition of cerebral SOdium-potassium-ATPase
cerebral
dysfunction, particularly with
parathyroid hormone, insulin, growth hormone, glucagon, thyrotropin, prolactin, luteinizing hormone and gastrin are elevated in patients with uremia.
Hormonal disturbance
seizure activity
parathyroid hormone
Entry of calcium in tissues
alterations of brain calcium, may possibly disrupt cerebral function by interfering with any of these processes
