The Experts below are selected from a list of 876 Experts worldwide ranked by ideXlab platform
K Beyreuther - One of the best experts on this subject based on the ideXlab platform.
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aluminium accumulation in relation to senile plaque and neurofibrillary tangle formation in the brains of patients with renal failure
Journal of the Neurological Sciences, 1992Co-Authors: J M Candy, A E Oakley, F K Mcarthur, Geoffrey A Taylor, C P L H Chen, S Mountfort, J E Thompson, P R Chalker, H E Bishop, K BeyreutherAbstract:Abstract The effects of long-term exposure to aluminium on the development of Alzheimer-type neuropathological changes have been studied post-mortem in patients with chronic renal failure who did not have Dialysis Encephalopathy. Administration of aluminium-containing phosphate binding compounds appears to be a major factor in the accumulation of aluminium in the brain of Dialysis patients. The mean serum aluminium concentrations determined during life and brain aluminium concentrations determined post-mortem correlated with both the duration and total amount of aluminium hydroxide administered to these patients. No correlation was found between the presence of bone aluminium and either the mean serum or brain aluminium concentration. Longitudinal monitoring of serum aluminium concentrations may provide a more reliable index than bone biopsy of brain aluminium concentrations in Dialysis patients. Dynamic secondary ion mass spectrometry revealed focal accumulations of aluminium associated with cortical pyramidal neurones. The majority of patients also showed immunostaining in pyramidal neurones with an antibody to the N-terminal region of the β A 4 amyloid precursor protein, while staining was absent in age-matched control cases. One-third of the patients exhibited β A 4- positive amorphous senile plaques in the cerebral cortex. However, there was no clear correlation between either the presence and intensity of β A 4 amyloid precursor immunostaining or the presence of senile plaques and the concentration of aluminium in the cerebral cortex. Cortical neurofibrillary tangles were not observed in any of the Dialysis patients. These data suggest that it is unlikely that aluminium plays any major role in neurofibrillary tangle formation and that its putative role in senile plaque formation is likely to be only part of a complex cascade of changes.
John Savory - One of the best experts on this subject based on the ideXlab platform.
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Aluminum Toxicity in Relation to Kidney Disorders
2016Co-Authors: Steven W. King, John Savory, Ph D, R. WillsAbstract:Aluminum toxicity in patients with chronic renal failure has been related to renal osteodystrophy and Dialysis Encephalopathy (DES). The toxicity is associated with renal osteodystrophy in two ways. One association is the iatrogenic effect of excessive use of aluminum hydroxide gels resulting in hypophosphatemia which interferes with bone mineralization. The second association may involve deposition of aluminum in bone owing to aluminum being absorbed during hemoDialysis. Evidence for this second association has been gathered from epidemiological studies of hemoDialysis centers and their practices of using either tap water high in aluminum in the dialysate, or aluminum-free deionized water. In patients with DES, aluminum accumula tion in the brain has been clearly shown to come from either the ingestion of aluminum containing phosphate-binding gels, aluminum in the dialysate, or a combination of the two. The outbreak of the DES also has been well-correlated with the sudden elevation of aluminum in tap water owing to the use of large amounts of aluminum in water treatment plants. Whether aluminum itself or a combination of aluminum and other factors causes DES is not understood at this time
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Aluminum and chronic renal failure: sources, absorption, transport, and toxicity
Critical Reviews in Clinical Laboratory Sciences, 2008Co-Authors: Michael R. Wills, John SavoryAbstract:In normal subjects the gastrointestinal tract is a relatively impermeable barrier to aluminum with a low fractional absorption rate for this metal ion. Aluminum absorbed from the gastrointestinal tract is normally excreted by the kidneys; in the presence of impaired renal function aluminum is retained and accumulates in body tissues. Aluminum-containing medications are given, by mouth, to patients with chronic renal failure as phosphate-binding agents for the therapeutic control of hyperphosphatemia. Patients with chronic renal failure are also exposed to aluminum in domestic tap-water supplies used either for drinking or, in those on Dialysis treatment, in the preparation of their dialysate. In patients with end-stage chronic renal failure, particularly in those on treatment by hemoDialysis, the accumulation of aluminum in bone, brain, and other tissues is associated with toxic sequelae. An increased brain content of aluminum appears to be the major etiological factor in the development of a neurological syndrome called either "Dialysis Encephalopathy" or "Dialysis dementia"; an increased bone content causes a specific form of osteomalacia. An excess of aluminum also appears to be an etiological factor in a microcytic, hypochromic anemia that occurs in some patients with chronic renal failure on long-term treatment with hemoDialysis. The various mechanisms involved in the toxic phenomena associated with the accumulation of aluminum in body tissues have not been clearly defined but are the subject of extensive investigations.
J M Candy - One of the best experts on this subject based on the ideXlab platform.
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aluminium accumulation in relation to senile plaque and neurofibrillary tangle formation in the brains of patients with renal failure
Journal of the Neurological Sciences, 1992Co-Authors: J M Candy, A E Oakley, F K Mcarthur, Geoffrey A Taylor, C P L H Chen, S Mountfort, J E Thompson, P R Chalker, H E Bishop, K BeyreutherAbstract:Abstract The effects of long-term exposure to aluminium on the development of Alzheimer-type neuropathological changes have been studied post-mortem in patients with chronic renal failure who did not have Dialysis Encephalopathy. Administration of aluminium-containing phosphate binding compounds appears to be a major factor in the accumulation of aluminium in the brain of Dialysis patients. The mean serum aluminium concentrations determined during life and brain aluminium concentrations determined post-mortem correlated with both the duration and total amount of aluminium hydroxide administered to these patients. No correlation was found between the presence of bone aluminium and either the mean serum or brain aluminium concentration. Longitudinal monitoring of serum aluminium concentrations may provide a more reliable index than bone biopsy of brain aluminium concentrations in Dialysis patients. Dynamic secondary ion mass spectrometry revealed focal accumulations of aluminium associated with cortical pyramidal neurones. The majority of patients also showed immunostaining in pyramidal neurones with an antibody to the N-terminal region of the β A 4 amyloid precursor protein, while staining was absent in age-matched control cases. One-third of the patients exhibited β A 4- positive amorphous senile plaques in the cerebral cortex. However, there was no clear correlation between either the presence and intensity of β A 4 amyloid precursor immunostaining or the presence of senile plaques and the concentration of aluminium in the cerebral cortex. Cortical neurofibrillary tangles were not observed in any of the Dialysis patients. These data suggest that it is unlikely that aluminium plays any major role in neurofibrillary tangle formation and that its putative role in senile plaque formation is likely to be only part of a complex cascade of changes.
Michael R. Wills - One of the best experts on this subject based on the ideXlab platform.
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Savory
2015Co-Authors: Roger L. Bertholf, Jorge M. Roman, Sue Brown John, Michael R. WillsAbstract:We present the clinical course of a patient who has been treated with CAPD since 1979. He developed Dialysis Encephalopathy and fracturing osteomalacia, and was found to have a serum aluminum concentration of 560 μg/L. Treatment with desferrioxamine over a six month's period reduced his serum aluminum concentration to a non-toxic level, and his symptoms abated. One year after his initial Encephalopathy this patient has a normal EEG, the bone fractures have healed, and serum aluminum concentration is 38 μg / L. Apparently the hyperaluminemia was due to the ingestion of prescribed aluminum hydroxide. Aluminum has been recognized as a major, if not the primary, etiological agent in Dialysis Encephalopathy and osteomalacia (1). Most patients with these complications are on long-term intermittent hemoDialysis and there are relatively few reports of this syndrome in patients on peritoneal Dialysis. This paper describes Dialysis encephalopath
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Aluminum and chronic renal failure: sources, absorption, transport, and toxicity
Critical Reviews in Clinical Laboratory Sciences, 2008Co-Authors: Michael R. Wills, John SavoryAbstract:In normal subjects the gastrointestinal tract is a relatively impermeable barrier to aluminum with a low fractional absorption rate for this metal ion. Aluminum absorbed from the gastrointestinal tract is normally excreted by the kidneys; in the presence of impaired renal function aluminum is retained and accumulates in body tissues. Aluminum-containing medications are given, by mouth, to patients with chronic renal failure as phosphate-binding agents for the therapeutic control of hyperphosphatemia. Patients with chronic renal failure are also exposed to aluminum in domestic tap-water supplies used either for drinking or, in those on Dialysis treatment, in the preparation of their dialysate. In patients with end-stage chronic renal failure, particularly in those on treatment by hemoDialysis, the accumulation of aluminum in bone, brain, and other tissues is associated with toxic sequelae. An increased brain content of aluminum appears to be the major etiological factor in the development of a neurological syndrome called either "Dialysis Encephalopathy" or "Dialysis dementia"; an increased bone content causes a specific form of osteomalacia. An excess of aluminum also appears to be an etiological factor in a microcytic, hypochromic anemia that occurs in some patients with chronic renal failure on long-term treatment with hemoDialysis. The various mechanisms involved in the toxic phenomena associated with the accumulation of aluminum in body tissues have not been clearly defined but are the subject of extensive investigations.
E Reusche - One of the best experts on this subject based on the ideXlab platform.
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argyrophilic inclusions distinct from alzheimer neurofibrillary changes in one case of Dialysis associated Encephalopathy
Acta Neuropathologica, 1997Co-Authors: E ReuscheAbstract:A 72-year-old female demonstrated neurofibrillary changes of Alzheimer's disease (AD) as well as morphological features of Dialysis-associated Encephalopathy (DAE). This unique autopsy case was selected from a group of 127 patients with a history of long-term hemoDialysis. Silver-stained paraffin sections revealed hall-marks of DAE with characteristic fine-granular aluminium-containing inclusions in the cytoplasm of plexus epithelia, cortical glia and neurons. Additionally, neurofibrillary tangles (NFT) and neuropil threads of the AD-type were demonstrated, consisting of paired helical filaments. No beta/A4 amyloid deposits were present. AD changes have been interpreted as age-related phenomena. Concerning the role of aluminium (Al) in AD, our morphological findings indicate that Al-induced DAE changes develop via different pathogenetic pathways compared to AD. Transferrin receptors stained positively in choroid plexus and neurons, in glial cells of the gray and white matter, in cerebellar (DAE-negative) Purkinje and granule cells as well as in AD-type NFT (and additionally in NFT of AD controls). This points to the ubiquitous distribution of transferrin receptors rather than to specific patterns in DAE and/or AD. Laser microprobe mass analysis indicated high Al-related signals at m/z 27, confirming the increase of Al in neurons with DAE. In contrast to the former clinically endemic and lethal Dialysis Encephalopathy, caused by massive Al-uptake by non-deionized dialysates, the term DAE comprises a morphological description in psychiatrically mostly unconspicious patients. It is characterized by the storage of argyrophilic degradation products of lysosomal-derived exclusively intracytoplasmic Al-containing inclusions, nowadays predominantly caused by long-term ingestion of Al-containing drugs in hemoDialysis.