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

Elevated concentration of aluminum has been reported in serum, whole blood and tissue samples of patients with renal insufficiency. Evidence incriminating aluminum as a neurotoxin among the dialysis population is strong. The source of this aluminum has not been clearly defined, although both gastrointestinal and parenteral routes may be involved. Data from this laboratory suggest that an effect of parathyroid hormone on tissue aluminum burdens may, in part, explain why only certain patients exposed to high dialysate aluminum develop the dialysis encephalopathy syndrome and the occasional occurrence of this syndrome in the absence of dialysis or increased dialysate aluminum.
J Dial 1978
PMID:Factors affecting tissue aluminum concentration. 37 33

There is increasing evidence that aluminium accumulation in patients with impaired renal function has pathological consequences. The serum aluminium content of 45 patients with chronic renal failure was found to be significantly elevated when compared with normal subjects. A further rise in serum aluminium concentration was seen in patients with chronic renal failure when they were taking aluminium-containing phosphate binding agents. Patients with stable but moderately impaired renal function who are taking aluminium-containing phosphate binders for several years may be at risk from aluminium accumulation and the development of osteomalacia and encephalopathy as seen in patients on intermittent haemodialysis.
Proc Eur Dial Transplant Assoc 1979
PMID:Evidence for aluminium accumulation in renal failure. 54 3

The progressive encephalopathy observed in 5 children with chronic renal failure was clinically similar to the so-called dialysis encephalopathy of adults, except that it was not related to dialysis therapy. Renal osteodystrophy is more prevalent in children than in adults and often more severe. The attempt to control the crippling deformities of renal osteodystrophy in growing children with renal insufficiency has led to the use of large quantities of aluminum containing antacids. The encephalopathy observed in children with chronic renal failure may be related to the oral ingestion of aluminum containing compounds in the presence of persistent secondary hyperparathyroidism. We suggest that alternative methods for the adequate control of serum phosphorus levels should be sought and indications for parathyroidectomy in children reevaluated. During the past 18 mos we have lowered the dose of aluminum containing compounds to 50 to 100 mg/Kg/day in our patients with progressive renal failure and recommend parathyroidectomy. No new cases of the encephalopathy have occurred.
Proc Clin Dial Transplant Forum 1977
PMID:Encephalopathy in children with chronic renal failure. 61 6

The dialysis encephalopathy syndrome has a geographical distribution related to the aluminium content of the dialysis water supply. There is a close relationship between concentrations of water aluminium and serum aluminium, and patients with dialysis encephalopathy have serum aluminium concentrations greater than 400 microgram/litre. High serum aluminium is also associated with osteomalacic bone disease, and worsening anaemia. In dialysis encephalopathy, elevated concentrations of aluminium are found in CSF and in grey matter, and an aluminium burden of 2-8 g is calculated from whole body in vivo analysis. There is sufficient evidence for an aluminium toxicity syndrome to warrant specific removal of aluminium by water purification systems.
Proc Eur Dial Transplant Assoc 1978
PMID:Aluminium studies in dialysis encephalopathy. 74 Jun 62

The dialysis dementia syndrome was observed in eight of 21 patients dialyzed in a small center during a 22-month period in which dialysate contained aluminum levels of 618 microgram/liter. This incidence of 38% was significantly higher than the zero incidence of four prior years when no aluminum was added to city water (p less than 0.05) and also when compared to the zero incidence in the 2.5 years subsequent to deionization of dialysis water which lowered its aluminum content to less than 1 microgram/liter (p less than 0.0002). Since other factors were not altered, we conclude that aluminum intoxication from the dialysate was the cause for the outbreak of this progressive encephalopathy.
J Dial 1978
PMID:An outbreak of dialysis dementia due to aluminum in the dialysate. 75 Jun 12

In order to evaluate the CNS-function of uremic patients, the magnetic activity emitted from the brain of 20 pts (10 pts on CAPD and 10 on HD) was measured. MEG consisted of taking 32 consecutive records from the 32 equally spaced points chosen on the skull in uremic pts around our reference points T3, T4, P4, F3, F4 of the international 10-20 electrode placement point system. MEG data were converted using an AD-converter with sampling frequency 256 Hz and stored in a P/C. Our results showed significant differences between the two groups. In all HD pts there was abnormal magnetic brain activity with high spectral amplitudes (in the band 2-7 Hz) which was more prominent in pts in hemo for more than 4 years. The magnetic activity was within normal ranges in all CAPD pts. We conclude that: 1) There is high magnetic brain activity in HD pts, which in accordance with the EEG findings are signs of diffuse encephalopathy. 2) CAPD pts show a very low magnetic brain activity which must be interpreted as normal brain function, and 3) MEG can be useful in further measurement of adequacy of dialysis.
Adv Perit Dial 1992
PMID:Evaluation of CNS-function in CAPD patients using magnetoencephalography (MEG): comparison with hemodialysis patients. 136 82

Two haemodialysis patients with aluminium encephalopathy developed dramatic deteriorations of their neurological symptoms after initiation of desferrioxamine (DFO) therapy. Both patients were treated with relatively large doses of DFO (1 g and 2 g per treatment). In the first case, paranoid delusions, visual hallucinations, seizures and deteriorating speech followed each dialysis treatment with DFO. The second patient experienced increasing confusion, decreasing short-term memory, and deterioration in speech. In both cases the neurological symptoms regressed after decreasing or discontinuing the DFO. These patients demonstrate the potential dangers of using high doses of DFO. The pathogenesis of the exacerbation is not well understood but, may not simply be due to the result of elevated plasma aluminium levels after DFO therapy. We argue in this communication for reducing DFO in patients with aluminium encephalopathy to doses of 1 g three times per week to ensure adequate treatment of aluminium encephalopathy while minimising the risk of exacerbation from overzealous DFO administration.
Nephrol Dial Transplant 1989
PMID:Exacerbation of aluminium encephalopathy after treatment with desferrioxamine. 249 51

This study records our experience with 40 infants who developed acute renal failure in a tropical environment over a period of 2 years. All the patients required intermittent peritoneal dialysis. Septicaemia (88%) and acute gastroenteritis (55%) constituted the leading causes of acute renal failure. Haemolytic uraemic syndrome was present in six (18%) patients. An elevated serum creatinine (85%), metabolic encephalopathy (75%), uncompensated metabolic acidosis (75%) and hyperkalaemia (48%) were the major indications for dialysis, while fluid overload was present in only 18% of the infants. Intermittent peritoneal dialysis was used in all the patients and was found to be effective. Procedural complications were minor and infrequently encountered. The clinical course and laboratory data consistent with haemolytic uraemic syndrome was observed in six patients, and acute tubular necrosis was the predominant renal lesion in the remainder. Mortality was 75%. The aetiology of acute renal failure in infants in the tropics differs significantly from that in the West, and even within a given country marked regional variations exist.
Nephrol Dial Transplant 1989
PMID:Acute renal failure in infants in the tropics. 250 74

Closed-circuit dialysis using the Redy sorbent cartridge to regenerate the dialysate has been incriminated in previous reports as a cause of severe fracturing osteomalacia and fatal encephalopathy in several patients treated with this procedure for 15-36 months. In a retrospective study, we compared 15 unselected patients who had received Redy dialysis for 66 +/- 14 months with 15 control patients dialysed with single passage of dialysate. Redy and control patients were matched for age, sex, and duration of dialysis. They belonged to two dialysis centres, situated in the same geographical area and having a common water supply. Mean serum and bone aluminium concentrations were slightly greater in the Redy group but the differences were not significant. Pathological fractures had occurred in two Redy patients and in one control, but could not be attributed to aluminium-induced bone disease. Although the histochemical staining for aluminium in bone was positive in six patients, diagnosis of aluminium-induced bone disease was made in one case only. The results of bone histomorphometry did not differ significantly between the two groups. Our findings may be explained by the strict application of the measures required to avoid aluminium contamination of the Redy dialysate, i.e. sufficient rinsing before dialysis, use of almost aluminium-free water, and of acetate-buffered dialysate.
Nephrol Dial Transplant 1989
PMID:Risk of aluminium intoxication in long-term acetate Redy dialysis. 250 78

Aluminium (Al) intoxication in patients with chronic renal failure may lead to osteomalacia, microcytic anaemia, and encephalopathy. It has been suggested that the expression of Al toxicity may be related to the function of the parathyroid glands. The purpose of this study was to determine whether the functional state of the parathyroids influenced the evolution of Al-related encephalopathy in Al-intoxicated haemodialysed patients. The patients were subdivided into two groups according to outcome: group I patients (n = 6) had died with the clinical feature of severe cerebral dysfunction; group II patients (n = 15) had a favourable outcome with partial or complete recovery. The degree of hyperparathyroidism, as evaluated by plasma biochemistry and bone histology, was comparable in both groups. Three patients of group I and five of group II underwent parathyroidectomy. Before the clinical onset of encephalopathy the duration of Al overload in group I was not different from group II, but after its onset patients of group I were intoxicated significantly longer (8 months +/- 6.6) than those of group II (1.5 months +/- 1.9). This study shows that, in uraemic patients with Al-related encephalopathy, parathyroid function and parathyroidectomy do not play an essential role in clinical outcome. The duration of Al intoxication following the first signs of encephalopathy appears to be the major prognostic element.
Nephrol Dial Transplant 1986
PMID:The role of parathyroid function and parathyroidectomy in the outcome of aluminium-related dialysis encephalopathy. 311 Jun 73


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