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 not clearly distinguishable from those of other metabolic encephalopathies, but may respond to 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 neural 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 substance less than 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

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.

Imbalance of inhibitory and excitatory neurotransmitter

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