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

Background: The association between aluminium anddialysis encephalopathy and deterioration of the neurological state duringdesferrioxamine treatment of dialysis patients is well established. Atpresent little is known about the speciation and the mechanisms underlyingthe element's neurotoxicity. Methods. Aluminium speciation was performed incerebrospinal fluid samples of acutely aluminium-intoxicated dialysispatients using a recently developed high-performance liquidchromatographic/electro-thermal atomic absorption spectrometric hybridmethod. Results: Baseline cerebrospinal fluidaluminium levels of samples taken shortly after the intoxication were lowbut elevated (5.0±2.0 &mgr;g/l, n=3) as compared to subjectswith normal renal function (<1 &mgr;g/l). In contrast to thesituation noted in serum and to the iron speciation in cerebrospinal fluid,aluminium was not bound to transferrin but appeared as two distinctcompounds, the main fraction eluting at the elution volume of aluminiumcitrate/silicate. The second compound was not identified. Forty-four hoursafter desferrioxamine administration the cerebrospinal fluid aluminiumlevels had increased up to a concentration of 10.3±2.5&mgr;g/l (n=3). This was accompanied by a change in the speciationprofile with aluminium appearing at the elution volume of aluminoxamine.Conclusion: Our findings may contribute to a betterunderstanding of the neurotoxic effects of aluminium and itsdesferrioxamine chelate in dialysis patients.