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

Iliac bone aluminium was determined by neutron activation analysis in 34 patients with chronic renal failure and in eight control subjects. In 17 patients treated by haemodialysis there was a significant increase in the amount of aluminium (mean +/- SE = 152 +/- 30 ppm bone ash). In eight patients treated by haemodialysis and subsequent renal transplantation, bone aluminium was still significantly increased (92 +/- 4.5 ppm bone ash) but was less than in the haemodialysed patients. In some patients aluminium persisted in bone for many years after successful renal transplantation. There was no relationship between hyperparathyroidism and bone aluminium. Although no statistically significant relationship was found between the mineralisation status of bone and bone aluminium, patients dialysed for the longest periods tended to be those with the highest levels of aluminium, osteomalacia, and dialysis encephalopathy. In 20 rats given daily intraperitoneal injections of aluminium chloride for periods of up to three months, there was accumulation of aluminium in bone (163 +/- 9 ppm ash) to levels comparable to those obtained in the dialysis patients, and after about eight weeks osteomalacia developed. The increased bone aluminium and osteomalacia persisted after injections had been stopped for up to 49 days, although endochondral ossification was restored to normal. As a working hypothesis it is suggested that aluminium retained in the bone of the dialysis patients and the experimental animals interferes with normal mineralisation.
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PMID:Bone aluminium in haemodialysed patients and in rats injected with aluminium chloride: relationship to impaired bone mineralisation. 38 58

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.
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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.
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PMID:Encephalopathy in children with chronic renal failure. 61 6

The consequences of chronic renal insufficiency relevant to hepatic failure are not well appreciated. We describe a patient with chronic cirrhosis and marked porto-systemic shunting who, after the onset of chronic renal failure, developed intractable encephalopathy which improved markedly during an eight month period of maintenance hemodialysis.
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PMID:Exacerbation of hepatic encephalopathy by chronic renal failure: response to maintenance hemodialysis. 66 27

This is a prospective study on 24 patients with chronic renal failure. Thirteen of them had evidence of acute uraemic encephalopathy. Of those 9 patients were found to have dilutional hyponatraemia, two patients severe salt and water depletion and one patient septicaemia. Hyponatraemia was associated with pulmonary oedema in 3 patients. Correction of salt and water disturbances and treatment of heart failure improved cerebral functions in 10 (77%) patients. It is therefore concluded that dilutional hyponatraemia probably leading to cerebral oedema is a reversibe major factor in the development of acute uraemic encephalopathy. This, if left uncorrected, may prove fatal especially in tropical countries.
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PMID:Acute uraemic encephalopathy in tropical countries. 70 18

The dialysis encephalopathy syndrome (DES) consists of altered mental status, communication difficulty, seizures and myoclonus. It has been attributed to elevated serum aluminium (A1) levels. Two undialysed patients with chronic renal failure who presented with the characteristic syndrome are reported. The first, a 48 year old female, had used A1 containing phosphate binders for two years. Her serum A1 level was 25.34 mumol/L. Despite treatment with desferoximine and dialysis, she died. Necropsy revealed elevated A1 levels in the cerebral cortex (19 mcg/gm) and spongioform change in the outer three cortical layers. The second patient, a 46 year old woman, had a serum A1 of 8.70 mumol/L. She had never taken A1 containing phosphate binders but had taken several grams/day of citrate for at least six months. Treatment with haemodialysis and discontinuation of the citrate produced a resolution of symptoms and return of the A1 level to normal. During two years of haemodialysis there has been no recurrence.
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PMID:Aluminium intoxication in undialysed adults with chronic renal failure. 152 41

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 beta/A4 amyloid precursor protein, while staining was absent in age-matched control cases. One-third of the patients exhibited beta/A4-positive amorphous senile plaques in the cerebral cortex. However, there was no clear correlation between either the presence and intensity of beta/A4 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.
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PMID:Aluminium accumulation in relation to senile plaque and neurofibrillary tangle formation in the brains of patients with renal failure. 156 20

The uremia of chronic renal failure (CRF) can alter brain electrophysiology and cognitive function, even in the well-dialyzed patient. The effect of uremia on brain function can be assessed by electrophysiologic techniques such as electroencephalogram (EEG), sensory-evoked potentials (EPs), and cognitive event-related potentials (ERPs), and through a series of neuropsychologic tests. Five tests have been used clinically to measure the speed and efficiency of cognitive functioning and include the following: Number Cancellation, Trailmaking Test, Symbol Digit Modalities Test, Rey Auditory Verbal Learning Test, and Controlled Oral Word Association Test. Test performance by patients with CRF is often below that of healthy controls. Auditory ERPs, a sensitive indicator of subtle changes in central nervous system (CNS) function in uremia, result in the generation of a P300 component wave that varies in amplitude and latency with patient variables such as attention and effort. Although dialysis tends to normalize P300 latencies, the waves remain somewhat prolonged in most patients. The anemia often observed in patients receiving chronic dialysis appears to aggravate uremic encephalopathy. This effect can be reversed when anemia is corrected following administration of recombinant human erythropoietin (epoetin). Improvement in P300 amplitudes, and, in some cases, decreases in P300 latencies correlated well with epoetin-induced increases in hematocrit levels. With the correction of anemia, that component of brain dysfunction not attributable to retention of uremic toxins can largely be reversed.
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PMID:Epoetin and cognitive function. 162 53

Two patients on dialysis because of chronic renal failure who developed herpes zoster associated encephalitis are reported. Both developed overt encephalopathy despite treatment with oral acyclovir for the preceding herpes zoster eruption. The encephalopathy responded rapidly to intravenous acyclovir.
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PMID:Herpes zoster associated encephalitis in dialysis patients. 175 16

Elevated levels of aluminum in brain tissue have been found in demented patients with Alzheimer's disease, with ALS-PD complex of Guam and with dialysis encephalopathy. A possible etiological relationship between enhanced aluminum exposure and impaired mental function was suggested both for ALS-PD of Guam (a region where high contents of aluminum in water are found) and for dialysis encephalopathy which appears in dialyzed patients exposed to high doses of aluminum in medications and in dialysate fluid. The role of aluminum in Alzheimer's disease is not known as is the question of life-long aluminum accumulation in healthy human beings. In this review we have limited ourselves to the issue of oral aluminum ingestion and the possible neurotoxic consequences of such exposure. The following topics are summarized: 1. Physiological mechanisms involved in ingestion and intestinal absorption of aluminum and the influences of pH and available organic complexing agents on these processes. 2. Effects of an aluminum-enriched diet on behavior and on brain metabolism. 3. Dietary sources of aluminum and elevated loads of this substance due to prolonged intake of aluminum-containing medications. The main conclusion of this summary is that aluminum is absorbed and may accumulate in different organs in both adults and infants. Two groups seem to be at particular risk for aluminum related toxicity: people with chronic renal failure treated with aluminum-containing medications and pre-term infants fed on aluminum containing formulate. It seems probable that at least upon short term exposure the healthy human body can defend itself adequately from aluminum's toxic effects. However, not enough information is available on possible effects of life-long exposure to aluminum in the environment, diet and medications, which over decades may lead to accumulation of this substance with expressions of toxicity. Therefore, the question of aluminum's relevance to dementive diseases cannot yet be adequately answered.
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PMID:Aluminum ingestion--is it related to dementia? 184 54


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