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NDT Advance Access originally published online on August 16, 2005
Nephrology Dialysis Transplantation 2005 20(11):2581-2582; doi:10.1093/ndt/gfi072
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© The Author [2005]. Published by Oxford University Press on behalf of ERA-EDTA. All rights reserved. For Permissions, please email: journals.permissions@oxfordjournals.org


Letter

Dialysis encephalopathy secondary to aluminum toxicity, diagnosed by bone biopsy

Sir,

Dialysis encephalopathy is a syndrome observed in chronic renal insufficiency patients on dialysis, characterized by dementia, speech alterations, myoclonias, asterixis and convulsions, associated with typical electroencephalogram alterations. These clinical findings show a poor prognosis, resulting in death in the majority of cases. The association with aluminum toxicity is indicated frequently as the underlying cause and described in the majority of the reports in the literature, although other etiologies cannot be discarded [1–5].

Case. A 40-year-old black male patient had chronic renal failure of undetermined aetiology, and was on haemodialysis for 5 years and without personal antecedents of aluminum use or exposure to heavy metals. After 3 years of dialysis therapy, he began to present clinical findings of slight mental confusion and shivering in his extremities after haemodialysis sessions, showing spontaneous improvement, but with a repetitive and progressive character. Hospitalized 30 days after the onset of symptoms, he presented an intense state of mental confusion, speech apraxia and myoclonias, evolving into a diminished level of consciousness (Glasgow <8) and the need for mechanical ventilation. On this occasion he presented the following serum biochemical results: serum creatinine, 10.3 mg/dl; blood urea nitrogen, 57 mg/dl; serum potassium, 4.0 mEq/l; serum calcium, 4.4 mEq/l and anaemia, with no signs of an infectious process (haematocrit, 27%; haemoglobin, 8.5 g/dl). A cerebral computed tomography scan was performed, which was normal. He had a normal liquor and negative toxicological exams. The electroencephalogram showed wide {theta} and {theta}-{delta} waves, often in a triphasic fashion, and diffuse slow spikes. Following support, clinical improvement was observed on the second day of treatment and the patient was discharged from hospital in good clinical condition. However, from this period onward, he began to present similar symptoms with variable intensity, always after haemodialysis sessions. An investigation for aluminum toxicity was begun. The dialysis unit presented reverse osmosis-treated water with normal levels of aluminum (<10 µg/l); the same occurred with the patient's serum aluminum (47 µg/l, an exam confirmed twice on other occasions, normal up to 30 µg/l), as well as ferritin at 150 ng/ml (15–200 ng/ml) and parathormone at 100 pg/ml (7–53 pg/ml). The test for desferoxamine was not suggestive of aluminum toxicity. In spite of the lack of evidence, a bone biopsy was performed which showed numerous deposits of aluminum. Desferoxamine treatment was then initiated, with a progressive improvement in the symptoms until disappearance and normalization of the electroencephalogram.

Comment. Many studies have shown good results with desferoxamine following dialysis encephalopathy by aluminum toxicity, as well as treatment of the dialysis water by reverse osmosis, with electroencephalogram normalization [6,7]. However, in all the cases described, diagnosis was based on the verification of a serum aluminum level increase or a positive desferoxamine test. In our case, it was necessary to perform a bone biopsy for confirmation of the diagnosis.

The data presented here suggest that a bone biopsy should be performed when investigating dialysis encephalopathy, principally in cases where the etiology remains undefined after less invasive examination.

Conflict of interest statement. None declared.

Luis Gustavo Modelli Andrade, Fábio Duarte Garcia, Vanessa Santos Silva, Daniela Ponce Gabriel, Antonio Gonçalves Rodrigues, Jr, Ginivaldo Victor R. Nascimento, Jacqueline Teixeira Caramori, Luis Cuadrado Martin, Pasqual Barretti and André Luis Balbi

Department of Internal Medicine Hospital das Clínicas da Faculdade de Medicina de Botucatu UNESP Rubião Jr PO Box 584 CEP 18618970 São Paulo Brazil Email: gustavomodelli{at}yahoo.com.br

References

  1. Rozas VV, Port FK, Rutt WM. Progressive dialysis encephalopathy from dialysate aluminum. Arch Int Med 1978; 138: 1375–1377[Abstract/Free Full Text]
  2. Alfrey AC, LeGendre GR, Kaehny WD. The dialysis encephalopathy syndrome. N Engl J Med 1976; 294: 184–188[Abstract]
  3. Alfrey AC. Dialysis encephalopathy. Kidney Inter 1986; 29S18: 53–57
  4. Alfrey AC. Dialysis encephalopathy. Clinical Nephrol 1985; 24S1: 15–19
  5. Zatta P, Zambenedetti P, Reusche E et al. A fatal case of aluminium encephalopathy in a patient with severe chronic renal failure not on dialysis. Nephrol Dial Transplant 2003; 19: 2929–2930
  6. Milne FJ, Sharf B, Bell P, Meyers AM. The effect of low aluminum water and desferrioxamine on the outcome of dialysis encephalopathy. Clin Nephrol 1983; 20:202–207[Web of Science][Medline]
  7. Ackrill P, Ralston AJ, Day JP, Hodge KC. Successful removal of aluminium from patient with dialysis encephalopathy. Lancet 1980; 27: 692–693

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This Article
Right arrow Extract Freely available
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Right arrow All Versions of this Article:
20/11/2581    most recent
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