Aluminium kinetics in CAPD patients
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概要
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Accumulation of aluminium (Al) in the blood and body tissue of patients on maintenance hemodialysis (HD) may cause dialysis encephalopathy, fracturing osteomalacia or microcytic anemia. The Al contents of dialysate or the aluminium-containing phosphate binder (ACPB) are responsible for the Al intoxication. We studied Al kinetics in 18 CAPD patients. They required the same amount of ACPB as HD patients to control their serum phosphate levels. The absorption of Al from CAPD solution seemed to be negligible because the Al content of CAPD solution was very low. The sequential serum Al level over three to 36 months of CAPD treatment was relatively high, with a mean value of 50μg/l, which did not differ from that of HD patients. The increment of serum Al by desferrioxamine (DFO) loading, which might reflect the Al accumulation in the tissue, was larger in the patients dialyzed for longer periods. The protein binging rate with Al decreased from 86% to 30% by the administration of DFO, and DFO treatment could enhance the clearance of Al to 30l/week. The DFO concentration in plasma and dialysate was analyzed by HPLC using a reversed-phase column, and the mode of complex formation betwees Al and DFO was discussed. The intravenous administration of DFO, 30mg/kg BW, once a week, seemed to be safe and effective in CAPD patients with Al intoxication. The discontinuance of ACPB for 12 months reduced the tissue accumulation of Al in CAPD patients, judging from the DFO loading test, and calcium carbonate could be a good alternative to control the serum inorganic phosphate level.