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Progressive dialysis encephalopathy. Prevention through control of aluminum levels in water
Author(s) -
Rozas Victor V.,
Port Friedrich K.
Publication year - 1979
Publication title -
annals of neurology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 4.764
H-Index - 296
eISSN - 1531-8249
pISSN - 0364-5134
DOI - 10.1002/ana.410060130
Subject(s) - annals , citation , port (circuit theory) , medicine , library science , history , classics , computer science , engineering , mechanical engineering
In the article "Progressive dialysis encephalopathy" (Ann Neurol ~ 4 : 199-204, 1978) , Drs Lederman and Henry considered the role of aluminum in the origin of dialysis encephalopathy 3s speculative. W-e were astonished that aluminum blood levels were not reported for their 9 patients. Like other authors 11, 31, we believe that aluminum toxicity probabl\, plays a role in the production of dialysis encephalopathv, at least in some cases. T h e following arguments favor o u r belief. First, neuropathological studies have not shown major lesions even under electron microscopy 12 I , which suggests a metabolic mechanism. Second, demographically, dialysis encephalopathy has a higher incidence in regions where the aluminum dialysate content is increased 1'11. Third, early interruption of aluminum intake has been reported to reverse the encephalopathy 151. Recently we have observed 6 patients i n whom the clinical and electroencephalographic findings were identical to those reporreti elsewhere in dialysis encephalopathy and to the 9 cases reporteci by Drs Lederman and Henry. In our 6 patients, psychic troubles and repeated somnolence were present in all, dysarthria in 5 , myoclonic jerks in 4 , and epileptic seizures in 1 . In all 6 patients the EEG was disturbed and showed bilateral symmetrical, periodic, monomorphic, slow activity; in 3 patients, biphasic and triphasic spike conhgurations were noted. The average serum aluminum level was 407 pg per liter in the acute phase, 161 pg per liter in the remission phase with an average delay of six weeks, and 123 pg per liter three months later with maintained remission. (The normal serum aluminum level i s 4 0 pg per liter as determined by flameless-oven atomic sl-'ectrophotometry. ) Following interruption of the oral and ilidysate aluminum intake, remissions were permanently mainrained. In 2 cases, transient oral readministration o f aluminum to treat hyperphosphatemia was followed 13, recurrent encephalopathy, reversed only when aluminum intake was stopped again.