Relative roles of intestinal absorption and dialysis-fluid-related exposure in the accumulation of aluminium in haemodialysis patients.

BACKGROUND

A recent retrospective study has clearly demonstrated a reduction of cases with positive bone aluminium (Al) staining in the Italian dialysis population, which in general has had a low prevalence of bone Al toxicity. In the present study we tried to better address the relative role played, in our study population, by enteral and parenteral exposure to Al in reducing bone accumulation.

METHODS

We retrospectively examined the data of 105 DFO tests and bone Al determinations performed in dialysis patients from 1984 to 1995. Enternal exposure was analysed by accurate anamnestic records, while parenteral exposure was evaluated by the determination of Al content in dialysis fluids. Bone Al content was assayed chemically and histochemically, while serum Al was assayed spectrophotometrically. Data pertinent to the patients were allotted into three period groups: 1984-1987; 1988-1991; 1992-1995. As for Al concentrations in dialysis fluids, the interval 1980-1983 (immediately before the start of our study), which could clearly have influenced bone Al content, was also considered.

RESULTS

Basal serum Al showed some fluctuations (42.7 +/- 34.1; 24.8 +/- 21.9 and 38.9 +/- 34.9 micrograms/l respectively in the three groups, ANOVA P < 0.01) but only values of the period 1988-1991 were significantly lower than those of the period 1984-1987 (P < 0.05). Increments after DFO did not differ in the three periods (136.5 +/- 105.7; vs 98.7 +/- 91.7 and 106.1 +/- 96.2 micrograms/l respectively, P = n.s.). Enteral exposure to drugs containing Al was comparable (4.1 +/- 2.9 vs 4.0 +/- 4.6 and 5.8 +/- 7.9 total kg ingested respectively; P = n.s.), but bone Al was dramatically reduced (from 60.7 +/- 43.0 to 29.0 +/- 24.4 and 31.9 +/- 29.9 mg/kg/dw respectively; P < 0.0001), along with the definite disappearance of Aluminon-positive cases and Al-related bone disease (ARBD) after 1991. Parenteral exposure through the dialysate dropped from a mean of 26 +/- 14 micrograms/l in the 4-year period prior the start of the study (1980-1983) to 9 +/- 6 micrograms/l in the period 1984-1987 and to 4.9 +/- 2.1 micrograms/l and 5.0 +/- 2.0 micrograms/l respectively thereafter (P < 0.0001).

CONCLUSIONS

Despite the persistence of oral exposure to Al, responsible for the observed stability of serum Al levels, a definite reduction of bone Al content has been recorded in our dialysis population, and ARBD has disappeared. This result has to be referred essentially to the optimal control of Al content in dialysis fluids, which is confirmed as a major factor for Al intoxication.