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

The uremic syndrome is multifactorial, and affects most tissues and organs. Disturbances in protein and amino acid metabolism may play important roles, especially in chronic uremia, either directly or by production of toxic metabolites, with resultant negative nitrogen (N) balance, muscle wasting, reduced protein synthesis, and characteristically abnormal intracellular free amino acid concentrations. There are also grossly abnormal amino acid levels in the plasma of uremic patients, e.g., increases in conjugated amino acids, high levels of several nonessential and low levels of essential amino acids. The ratios of tyrosine/phenylalanine and of valine/glycine are decreased. The low tryptophan levels may contribute to encephalopathy as a result of an imbalance in neurotransmitter synthesis. Citrulline is found in excess; the explanation is unresolved. There are elevated concentrations of the sulfur-containing amino acids: cystine, taurine, cystathionine, and homocysteine. Excess of the latter is implicated in the atherogenesis of renal failure. Disturbed metabolism and interorgan exchange of amino acids in the uremic state explains some of the abnormalities in tissue and plasma concentrations of individual amino acids. Enzymatic defects are involved in the disturbed metabolism of branched chain amino acids (BCAA), with possible antagonism among them, which impairs growth and amino acid utilization. Carbohydrate intolerance, associated with insensitivity of peripheral tissues to insulin and hyperinsulinemia, elicits decreased plasma BCAA. Protein synthesis rates in normal and pathological conditions are more closely related to the intracellular amino acid pool than to plasma amino acid levels. Concentrations of individual amino acids in the plasma pool are poor indicators of their intracellular concentrations. Muscle contains the largest pool of protein and free amino acids in the body. In chronic renal failure patients, the intracellular concentrations of valine, threonine, lysine, and carnosine are low. With low protein diets and in hemodialysis, serine, tyrosine, and taurine often are also low. The low taurine may be related to fatigue and to uremic cardiomyopathies. The commonly used amino acid supplements generally fail to correct the intracellular amino acid deficits. A "New Formula" has been developed to correct these intracellular amino acid abnormalities, and to supplement a low protein diet. It provides more valine than leucine, increased tyrosine and threonine, and less histidine, leucine, isoleucine, lysine, methionine, and phenylalanine than in formulas customarily used for patients with chronic renal failure. It is uncertain whether other ap
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PMID:Amino acid metabolism in uremia. 267 58

Following the occurrence of aluminum encephalopathy in four patients with chronic renal failure, we studied 34 azotemic patients seen during the same year and five volunteers who took varying combinations of aluminum hydroxide and an alkalinizing citrate (Shohl's) solution. We found that the four encephalopathic cases were older than the 34 azotemic patients (68 years +/- 14 SD, vs 50 +/- 13, p less than 0.05), had a higher mean serum aluminum value (727 micrograms/l +/- 320 vs 92 +/- 73, p less than 0.005), had taken more aluminum hydroxide (5 g/day +/- 0.9 vs 1.6 +/- 1.8, p less than 0.01), and more Shohl's solution (64 ml/day +/- 19 vs 20 +/- 29, p less than 0.01). In all 38 patients the serum aluminum values correlated directly with age (p = 0.01), aluminum hydroxide (p = 0.001) and concomitant citrate intake (p = 0.004). In the five healthy volunteers the 24-hour urinary aluminum excretion increased from a baseline of 22 micrograms +/- 19 SD to 167 +/- 109 (p = 0.05) during aluminum hydroxide intake, rising to 580 +/- 267 (p = 0.01) during the simultaneous intake of citrate and aluminum hydroxide. Corresponding serum aluminum values were 11 micrograms/l +/- 2 SD, 44 +/- 34 (p = 0.1), and 98 +/- 58 (p less than 0.05). Thus citrate seems to enhance aluminum absorption and may cause encephalopathy in patients with chronic renal failure, especially the elderly.
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PMID:Hyperaluminemia in renal failure: the influence of age and citrate intake. 291 9

Patients with chronic renal failure (CRF) on periodical hemodialysis may accumulate aluminum in tissues and show typical disorders such as dialysis encephalopathy, osteodystrophy, and microcytic anemia. Aluminum contamination of the water used to prepare the dialysis solution (dialysate) is one of the metal sources that may affect people under hemodialysis, especially in units in which untreated water is used. Graphite furnace atomic absorption spectrometric methods for aluminum determination in whole blood, dialysis solution, and tap water samples from CRF patients were developed, based upon the use of the same furnace temperature program. Samples were diluted 4-fold with 0.6% triton X-100 (whole blood) or with 0.01 mol/L nitric acid (dialysis solution and tap water) and analyzed by aqueous standard (blood and tap water) or matrix-matching standard (dialysis solution) calibration curves. The characteristic masses were 33.8, 11.3, and 19.5 pg Al/0.0044 A.s for whole blood, dialysate, and tap water, respectively. In the diluted solutions, the detection limits (2 sigma) for the described methods were 0.5 microgram/L Al (whole blood), 0.4 microgram/L Al (dialysate), and 0.4 microgram/L Al (tap water). The methods were applied to samples from several CRF patients under hemodialysis at Maracaibo University hospital. The data revealed extremely high aluminum levels, which corresponded to the symptoms of dialysis encephalopathy and/or osteodystrophy showed by some of them. The proposed methods are reliable and reproducible.
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PMID:Aluminum determination in whole blood, dialysis solution, and tap water samples from Maracaibo dialysis units (Venezuela) by graphite furnace atomic absorption spectrometry. 298 Jul 89

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.
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PMID:The role of parathyroid function and parathyroidectomy in the outcome of aluminium-related dialysis encephalopathy. 311 Jun 73

Aluminum has been proposed as the causative agent in dialysis encephalopathy syndrome. We prospectively assessed whether other, less severe, neuropsychologic abnormalities were also associated with aluminum. A total of 16 patients receiving chronic dialytic therapy were studied. The deferoxamine infusion test (DIT) was used to assess total body aluminum burden. Neurologic function was evaluated by quantitative measures of asterixis, myoclonus, motor strength, and sensation. Cognitive function was assessed by measures of dementia, memory, language, and depression. There were four patients with a positive DIT (greater than 125 micrograms/L increment in serum aluminum) that was associated with an increase in the number of neurologic abnormalities observed, as well as an increase in severity of myoclonus, asterixis, and lower extremity weakness. Patients with a positive DIT also showed significant impairment in memory; however, no differences were noted on tests of dementia, depression, or language. There was no significant correlation between sex, age, presence of diabetes, mode of dialysis, years of chronic renal failure, years of dialysis or years of aluminum ingestion and any neurologic or neurobehavioral measurement, serum aluminum level, or DIT. These changes may represent early aluminum-associated neurologic dysfunction.
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PMID:Relationship of aluminum to neurocognitive dysfunction in chronic dialysis patients. 317 74

There are reports that patients with renal failure have elevated circulating concentrations of parathyroid hormone (PTH), which is suspected to be a causal factor of the cerebral symptoms of these patients. A positive correlation between the circulating level of immunoreactive PTH and the extent of abnormality in the electroencephalogram (EEG) in humans has been reported. Moreover, in uremic dogs normalization of the EEG was observed after parathyroidectomy, and increased abnormality of the EEG was observed on infusion of PTH. If PTH is really a causal factor of uremic encephalopathy and abnormality of the EEG in patients with renal failure, the question arises as to whether PTH acts on the brain after penetrating through the blood-brain barrier or in some other way. In this work, we measured PTH by both C-terminal-specific RIA (C-PTH) and N-terminal-specific RIA (N-PTH) in the circulation and cerebrospinal fluid (CSF) of normal subjects and patients with renal failure. Blood and CSF samples were obtained from 7 normal volunteers (31 approximately 81 years old: 4 males and 3 females) and 22 patients with chronic renal failure (25 approximately 87 years old: 12 males and 10 females). No patients had a psychotic disease or endocrinopathy other than secondary hyperparathyroidism. Samples of venous blood were collected from the subjects after an overnight fast at the time of lumbar puncture for CSF sampling. C-terminal-specific RIA for measurement of the plasma and CSF concentrations of C-PTH was carried out using a commercially available RIA kit (Eiken Laboratory Inc., Tokyo, Japan).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Immunoreactive parathyroid hormones in the circulation and cerebrospinal fluid from patients with renal failure: possible restriction of parathyroid hormone by the blood-brain barrier]. 322 22

The dialysis encephalopathy syndrome is at once the most widely recognized and most severe manifestation of aluminum toxicity. Evidence linking this syndrome and aluminum intoxication is virtually incontrovertible. The syndrome is characterized by speech and motor difficulties, dementia, and seizures. Less widely recognized symptoms include subtle changes in cognition and personality and directional disorientation. Since the widespread use of water treatment, aluminum exposure in the dialysis population has been primarily via intravenous (IV) medications and oral aluminum-containing, phosphate-binding antacid gels. In addition to the encephalopathy syndrome, aluminum has been linked to toxicity in bone, parathyroid gland, RBC, and kidney. These organ toxicities seem to be the result of specific protein enzyme inhibition. Currently identified factors that affect aluminum accumulation and modulate aluminum balance include uremia, renal function, parathyroid hormone withdrawal and suppression, 1,25-dihydroxycholecalciferol, and serum aluminum binding. Impaired renal function is not a prerequisite for increased tissue aluminum burdens. It is likely that aluminum-related disease will be increasingly observed in populations other than those with chronic renal failure.
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PMID:The metabolism of aluminum and aluminum-related encephalopathy. 329 87

The brain changes in patients with chronic renal failure treated by chronic hemodialysis were studied with the help of computed tomography. The results showed the development of internal hydrocephalus in the patients in whose treatment "hard" water was used. In some of these patients the hydrocephalus was accompanied by clinical manifestations of the "disequilibrium" syndrome and the "hard water" syndrome. The patients dialyzed with "soft" water showed no brain changes and clinical signs. Hydrocephalus is probably the main pathogenetic factor for the development of the "hard water" syndrome which later develops in dialysis encephalopathy.
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PMID:[Brain changes in patients on chronic hemodialysis recorded by computed axial tomography]. 341 93

We treated a Japanese man with Rendu-Osler-Weber disease and a recurrent encephalopathy with hyperammonemia concomitant with recurrent epistaxis, G-I bleeding, congestive heart failure with aortic and mitral regurgitation, and chronic renal failure. At peritoneoscopy, several telangiectasia were noted on the surface of the liver. Angiographical studies revealed widened and tortuous hepatic arteries with early filling of hepatic veins and small pools of contrast medium scattered throughout the parenchyma. The recurrent encephalopathy was attributed to the porto-systemic shunt formed in the liver.
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PMID:Rendu-Osler-Weber disease with portosystemic encephalopathy. 369 24

A number of factors affect the concentration and distribution of magnesium in patients with chronic renal failure (CRF). Poor nutritional intake, impaired absorption from the intestine, vomiting, diarrhea, the use of diuretics and acidosis may result in a negative balance. More commonly, accumulation of magnesium may be the consequence of reduced renal excretion. Magnesium concentrations are increased in serum and red cells in CRF patients. Bone concentrations and total body magnesium also appear to be increased; muscle magnesium does not appear to be increased. Use of magnesium hydroxide-containing antacids as phosphate binders in patients with CRF was largely discontinued 2 decades ago after reports described increases in serum magnesium concentrations to toxic levels. More recently, the undesirable effects of aluminum-containing phosphate binders (encephalopathy, osteomalacia) have led several investigators to report favorable experiences using low concentrations of magnesium in dialysate and a combination of magnesium and aluminum-containing antacids, as phosphate binders, while closely monitoring serum magnesium concentrations.
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PMID:Chronic renal failure and magnesium metabolism. 380 22


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