Dialysis dementia symptoms

The neurotoxic effects of aluminum were first observed in people undergoing dialysis for treatment of kidney failure. This syndrome, called dialysis dementia, starts with speech disorders and progresses to dementia and convulsions. Symptoms corresponded with elevated aluminum levels commonly found in bone, brain, and muscle following 3 to 7 years of treatment. Elevated levels of aluminum were also found in the brains of people suffering from Alzheimer s disease. Despite considerable research, it is not clear if the aluminum accumulation in the brain is a cause of Alzheimer s disease or a result of changes in the brain associated with the disease. 

In the past several clinical patterns have been described. The most important recognized clinical patterns or types of Al toxicity include two types of encephalopathy. Firstly, the classical dialysis dementia sometimes referred to as dialysis encephalopathy syndrome (DES) or dementia dialytica [24, 28, 37, 42, 70-74] and secondly, the acute or subacute Al encephalopathy [41]. There are also two types of bone disease - either osteomalacia with bone fractures and proximal myopathy or aplastic bone disease [41, 75, 76]. There is quite some confusion in the definitions of Al toxicity in the literature. Because there seems to be an obligatory lag phase of at least several days to weeks for symptoms to occur, acute Al encephalopathy, defined as a direct result of a single overdose, probably does not exist. Because of the long lag phase of several months to years necessary to develop the chronic dialysis encephalopathy and also because acute Al encephalopathy has an abrupt, sudden onset of symptoms one can understand why the term acute is used instead of the more descriptive subacute . The descriptions dialysis dementia [37, 42, 46, 73, 74] and dialysis encephalopathy [33-36, 38, 40, 41, 78] are also unfortunate because true dementia is rare in Al encephalopathy [73] and non-dialyzed patients can also develop these symptoms [78]. There are also many dialysis-related encephalopathy syndromes unrelated to Al. As an example,... 

Clinical Symptoms of Acute Al Encephalopathy and Chronic Al Encephalopathy (also Referred to as Classical "Dialysis Dementia")... 

Davidson et al. found that the cumulative risk of death due to dialysis dementia in patients whose water supply had a mean Al concentration >200 pg/L was significantly greater (27.9% deaths in the first 40 months) than the risk in patients whose mean water Al content was <200 pg/L (2.1% deaths in the first 490 months). The relation between the mean Al concentration in the dialysate and time to death was given in the formula [24] The time in months from the first symptoms of dialysis dementia to death = 65—0.081 x [mean Al concentration (pg/L) in dialysis water]. 

Elevated aluminum levels have been implicated as the cause of dialysis encephalopathy or dementia in renal failure patients undergoing long-term hemodialysis [85]. Some patients used aluminum-containing medications. Moreover, patients with renal failure cannot remove aluminum from the blood. Dialysis dementia can arise after three to seven years of hemodialysis treatment. Speech disorders precede dementia and convulsions. Since many hemodialysis units rely on systems to purify fluoridated tap water, it is likely that many patients are being exposed inadvertently to increased concentrations of fluoride and aluminum. Increased serum fluoride concentration and fluoride intoxication have been also observed in chronic hemodialysis patients. Arnow et al. [96] reported that 12 of 15 patients receiving dialysis treatment in one room became acutely ill, with multiple non-specific symptoms and fatal ventricular fibrillation. Death was associated with longer hemodialysis time and increased age compared with other patients who became ill. 

He was hospitalized for revision of his arteriovenous shunt and postoperatively complained of symptoms of gastroesophageal reflux. This complaint prompted institution of cimetidine therapy. In view of the patient s impaired renal function, the usually prescribed dose was reduced by half. Three days later, the patient was noted to be confused. An initial diagnosis of dialysis dementia was made and the family was informed that dialysis would be discontinued. On teaching rounds, the suggestion was made that cimetidine be discontinued. Two days later the patient was alert and was discharged from the hospital to resume outpatient hemodialysis therapy. 

However, there is no doubt that aluminium can damage people whose kidney function is impaired. The condition called dialysis dementia was first noticed in patients who had received long-term haemodialysis for renal failure. Its symptoms included speech disorders, memory loss, convulsions and seizures, followed, in some cases, by death within a year. The incidence of the disease was highest when the municipal water used in the dialysis contained high concentrations of aluminium. Aluminium is, therefore, a potential neurotoxin. 

DD symptoms often develop after 2-3 years of dialysis (Chui and Damasio 1980). In typical cases of DD, the individual presents with speech arrest, dysarthria, or dysphasia, followed by myoclonic jerks, electroencephalogram abnormalities, bizarre behavior, and progressive dementia (Chokroverty et al. 1976 O Hare et al. 1983). Death often occurs within 6 months of onset (Chui and Damasio 1980). 

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