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Query: UMLS:C0085584 (encephalopathy)
 18,178 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Whole body calcium, phosphorus and nitrogen have been measured by in vivo neutron activation analysis in patients with chronic renal failure, including 9 with dialysis encephalopathy. Aluminium was also activated by this procedure, but to the same radioactive product as that from phosphorus: its presence was therefore detected as an increase in the apparent total body phosphorus above that expected for a person with the same calcium content. Patients with dialysis encephalopathy had slightly more apparent phosphorus than others with chronic renal failure, although the difference was not statistically significant. This difference corresponded to an excess of aluminium not greater than 3.3 g(95% confidence limit) which places an upper limit on excess aluminium accumulation in this condition.
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PMID:Whole body aluminium in chronic renal failure and dialysis encephalopathy. 677 55

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 accumulation 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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PMID:Aluminum toxicity in relation to kidney disorders. 702 47

We compared the electroencephalograms (EEGs) of 17 patients with progressive dialytic encephalopathy with 17 chronic renal failure patients who did not have dialytic encephalopathy and who had been matched for age, type and duration of dialysis. The EEGs were analyzed in a semiquantitative fashion by counting the number of paroxysms of frontal intermittent rhythmic delta activity and frontocentral spike-waves, and by grading the amount of diffuse theta and delta waves during waking EEG on a 4-point scale. The two most important EEG predictors of dialytic encephalopathy in the present study consisted of synchronous and symmetrical frontal intermittent rhythmic delta waves and frontocentral spike-waves, confirming our previous observations.
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PMID:Electroencephalograms in patients with progressive dialytic encephalopathy. 709 54

Histochemical studies and electron probe x-ray microanalysis for aluminium have been performed on 16 samples of undecalcified bone from cases of renal osteodystrophy associated with a syndrome suggestive of dialysis encephalopathy (five cases), age and sex matched controls for these and a group of patients with chronic renal failure (six cases) who have never been on haemodialysis. Aluminium was detected only in the patients with a dialysis encephalopathy-like syndrome. This group had significant histological bone disease the features of which were broadly consistent with the so-called atypical renal osteomalacia which is thought to be due to a metal toxin. Aluminium was demonstrated at the interface between osteoid and mineralised tissue--that is, at the site of the calcification front, where it could interfere with the mineralisation process. In the group of patients who had never been subjected to haemodialysis there was also significant histological bone disease but no evidence of aluminium accumulation. In this group the bone disease was of a more typical pattern of osteomalacic changes coupled with those of hyperparathyroidism.
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PMID:Localisation of aluminium by histochemical and electron probe x-ray microanalytical techniques in bone tissue of cases of renal osteodystrophy. 714 36

The examination of five pediatric patients with encephalopathy secondary to chronic renal failure has indicated a stereotyped sequence of neurologic signs and symptoms including ataxia, loss of motor abilities, myoclonus, seizures, dementia, and bulbar dysfunction. Both the patients with CNS dysfunction and a control group selected for a similar degree of renal failure had increased levels of serum phosphate, alkaline phosphatase, and parathyroid hormone. Serial EEGs in the affected group revealed progressive slowing and an increase in paroxysmal features. No specific neuropathologic findings were noted in one patient.
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PMID:Encephalopathy in infants and children with chronic renal disease. 729 12

Progressive encephalopathy with characteristic clinical features and electroencephalographic findings has been reported many times in adult patients treated with maintenance hemodialysis. Two children with chronic renal failure developed a similar encephalopathy prior to their second birthdays and before the initiation of dialysis. Both children required parathyroidectomy for control of severe hyperparathyroidism with persistent hypercalcemia. Slight improvement followed this procedure in one patient. Selected biochemical abnormalities in serum and in brain tissue specimens were compared to those of neurologically unaffected children. Results of thes studies suggest that a direct toxic effect of either aluminum or calcium on the brain does not play an etiologic role in this disorder.
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PMID:Encephalopathy in children with chronic renal failure. 738 46

We studied three boys who had a similar encephalopathy develop during moderate chronic renal failure. The features included cerebellar system dysfunction, seizures, and intellectual and motor retardation. Extensive laboratory investigation failed to disclose an etiology other than chronic azotemia. These cases suggest that the developing nervous system is particularly sensitive to the effects of chronic azotemia. Early dialysis and/or transplantation should be considered in such children in an attempt to modify the serious nervous system abnormalities.
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PMID:Encephalopathy in young children with moderate chronic renal failure. 738 32

In order that better therapeutic approaches to disorders in man characterized by aluminium (Al) overload might be developed it is essential to have an appropriate animal model. Chronic oral administration of Al citrate to male Wistar rats leads to an Al overload in a relatively short period of time when compared to previous published animal models. Liver and brain Al levels are increased by 25 and 30-fold respectively compared to control rats after 6 months of loading. Al tissue content was significantly greater when the Al citrate was administered in an iron-free diet. The distribution of Al in brain was similar to that in the Al encephalopathy of patients with chronic renal failure or Alzheimer's disease and is in accord with observations that areas of brain that accumulate greatest amounts of Al have highest concentrations of transferrin receptors. In the brain, the toxic effect of Al at the cellular level was characterized by an extensive cytoplasmic vacuolation in astrocytes (especially) and neurones. These changes are reminiscent of those observed in certain human neurodegenerative diseases.
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PMID:An experimental animal model of aluminium overload. 784 2

Progressive encephalopathy, developmental delay, microcephaly, electroencephalogram (EEG) and computed tomographic (CT) scan abnormalities have been reported in 80% of children with chronic renal failure (CRF) in infancy. Malnutrition, aluminium intoxication and psychosocial deprivation are proposed as causes. In 15 children with CRF from infancy we evaluated the effect of no aluminium salts and early vigorous nutritional and psychosocial support, in addition to the standard therapy, on neurological development. Six patients underwent dialysis (2 at birth) and 3 received transplants. None of our patients were given aluminium therapy. The nutritional status of the patients in the first 2 years of life was assessed with the waterlow classification. At the end of the follow-up period (mean 50 months range 14-148 months), patients underwent neurodevelopmental assessment, head CT scan, EEG, nerve conduction velocity (NCV) and auditory brain stem evoked response (ABER). None of our patients developed progressive encephalopathy or recurrent seizures. All have a normal neurological examination apart from hypotonia. Microcephaly was present in 5 patients. There was a good correlation between malnutrition in the first 2 years of life and microcephaly. Developmental delay was present in 3 patients; all 3 were microcephalic. There was evidence of brain atrophy on CT scan in only 3 patients. EEG was abnormal in 6 patients, but only severe in 1 patient. Only 1 patient had diminished NCV; all patients had a normal ABER. We conclude that a policy of no oral aluminium therapy and early nutritional support leads to better neurological outcome in children with CRF from infancy.
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PMID:Improved neurological outcome in children with chronic renal disease from infancy. 801

In the paper below are presented the undesirable effects of aluminium in patients with chronic renal failure. Until now aluminum treatment has been used to reduce the level of phosphates in blood serum or in haemodialysis a this group of patients. The toxic activity is a result of cumulation of the element in organism, mainly owing to limited elimination through kidneys, but also as a consequence of disturbed absorption in digestive tract or intravenous infusion of blood serum and albumins. It can be expressed by several clinical syndromes, especially dialysis, encephalopathy, osteomalacia, microcystic++ anaemia, more rarely calcinosis and increased general morbidity and mortality rate. The diagnosis of suspected toxic activity of aluminium in patients with uraemia is based mainly on estimation of concentration of this ion in blood serum and aluminium deposits in skeletal system and skin. The effective treatment consist in intravenous infusions of deferoxamine in a dose 2 g 3 times a week for a long time.
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PMID:[Aluminum in chronic renal failure]. 823 41


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