Aluminium speciation in cerebrospinal fluid of acutely aluminium-intoxicated dialysis patients before and after desferrioxamine treatment; a step in the understanding of the element's neurotoxicity

• Published in: Nephrology, dialysis, transplantation dialysis, transplantation, 1997-08, Vol.12 (8), p.1692-1698
• Main Authors: VAN LANDEGHEM, G. F, D'HAESE, P. C, LAMBERTS, L. V, BARATA, J. D, DE BROE, M. E
• Format: Article
• Language: English
• Subjects: Adult; Aluminum - cerebrospinal fluid; Aluminum - poisoning; Anesthesia. Intensive care medicine. Transfusions. Cell therapy and gene therapy; Biological and medical sciences; Citric Acid - cerebrospinal fluid; Deferoxamine - cerebrospinal fluid; Deferoxamine - therapeutic use; Emergency and intensive care: renal failure. Dialysis management; Female; Humans; Intensive care medicine; Kidney - physiology; Male; Medical sciences; Middle Aged; Organometallic Compounds - cerebrospinal fluid; Reference Values; Renal Dialysis; Transferrin - cerebrospinal fluid; Transferrin - metabolism
• ISSN: 0931-0509; 1460-2385
• DOI: 10.1093/ndt/12.8.1692

The association between aluminium and dialysis encephalopathy and deterioration of the neurological state during desferrioxamine treatment of dialysis patients is well established. At present little is known about the speciation and the mechanisms underlying the element's neurotoxicity. Aluminium speciation was performed in cerebrospinal fluid samples of acutely aluminium-intoxicated dialysis patients using a recently developed high-performance liquid chromatographic/electrothermal atomic absorption spectrometric hybrid method. Baseline cerebrospinal fluid aluminium levels of samples taken shortly after the intoxication were low but elevated (5.0 +/- 2.0 micrograms/l, n = 3) as compared to subjects with normal renal function (< 1 microgram/l). In contrast to the situation noted in serum and to the iron speciation in cerebrospinal fluid, aluminium was not bound to transferrin but appeared as two distinct compounds, the main fraction eluting at the elution volume of aluminium-citrate/silicate. The second compound was not identified. Forty-four hours after desferrioxamine administration the cerebrospinal fluid aluminium levels had increased up to a concentration of 10.3 +/- 2.5 micrograms/l (n = 3). This was accompanied by a change in the speciation profile with aluminium appearing at the elution volume of aluminoxamine. Our findings may contribute to a better understanding of the neurotoxic effects of aluminium and its desferrioxamine chelate in dialysis patients.