Renal failure dialysis dementia

The major population at risk for aluminum loading and toxicity consists of individuals with renal failure. In a study by Alfrey (1980), 82% of nondialyzed uremic patients and 100% of dialyzed uremic patients had an increased body burden of aluminum. The decreased renal function and loss of the ability to excrete aluminum, ingestion of aluminum compounds to lessen gastrointestinal absorption of phosphate, the aluminum present in the water used for dialysate, and the possible increase in gastrointestinal absorption of aluminum in uremic patients can result in elevated aluminum body burdens. The increased body burdens in uremic patients has been associated with dialysis encephalopathy (also referred to as dialysis dementia), skeletal toxicity (osteomalacia, bone pain, pathological fractures, and proximal myopathy), and hematopoietic toxicity (microcytic, hypochromic anemia). Pre-term infants may also be particularly sensitive to the toxicity of aluminum due to reduced renal capacity (Tsou et al. 1991)... 

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. 

Ackrill P, Ralston A], Day JP, et al Successful removal of aluminium from patient with dialysis encephalopathy (letter). Lancet 2 692-693,1980 Altmann P, Hamon C, Blair JA, et al Disturbance of cerebral function by aluminium in haemodialysis patients without overt aluminium toxicity. Lancet 2 7-12,1989 Arieff Al, Cooper JD, Armstrong D, et al Dementia, renal failure, and brain aluminum. Ann Intern Med 90 741-747, 1979... 

The aforementioned findings involve studies in less than 20 patients with dialysis dementia (Farrar et al., 1990) and five with chronic renal failure treated with hemodialysis. More such studies are needed before it can be conclusively stated that the distribution of aluminum in brains of patients with dialysis dementia is not similar to that in patients with Alzheimer s disease. In patients with chronic renal failure without dialysis dementia, neurofibrillary changes have not been found. 

The evidence available thus far indicates that aluminum is elevated in the brain (cortical gray matter) of patients with dialysis dementia. However, the actual contribution of aluminum to the encephalopathy remains unclear. Aluminum content has been reported to be elevated in the brains of patients with other disorders, including senile dementia and Alzheimer s syndrome, and might actually be a nonspecific finding associated with dementia. Aluminum is also elevated in the brains of patients who have other disorders associated with altered blood-brain barrier. Such disorders include renal failure, hepatic encephalopathy and metastatic cancer. Other evidence suggests that brain aluminum content may also increase as a function of the aging process.Blood-brain barrier abnormalities can result in increased brain aluminum content (Banks Kastin, 1983). 

Shoop et al. (1998) studied the behavior of aluminum in urine to understand the role of Al in diseases, such as dialysis, dementia, and osteomalacia, which are of major concern to patients with end-stage renal failure. Non-protein- and protein-bound Al species were separated using a cation-exchange resin followed by NAA of Al. The total Al content was determined by RNAA. It was concluded that the majority of Al is bound to protein. 

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. 

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