Nephrology Dialysis Transplantation, Vol 12, Issue 12 2679-2682, Copyright © 1997 by Oxford University Press
S Mazzaferro, I Perruzza, S Costantini, M Pasquali, L Onorato, D Sardella, R Giordano, L Ciaralli, P Ballanti, E Bonucci, G Cinotti and G Coen
Background: A recent retrospective study has clearly
demonstrated a reduction of cases with positive bone aluminium (A1)
staining in the Italian dialysis population, which in general has had a low
prevalence of bone A1 toxicity. In the present study we tried to better
address the relative role played, in our study population, by enteral and
parenteral exposure to A1 in reducing bone accumulation.
Methods: We retrospectively examined the data of 105
DFO tests and bone A1 determinations performed in dialysis patients from
1984 to 1995. Enteral exposure was analysed by accurate anamnestic records,
while parenteral exposure was evaluated by the determination of A1 content
in dialysis fluids. Bone A1 content was assayed chemically and
histochemically, while serum A1 was assayed spectrophotometrically. Data
pertinent to the patients were allotted into three period groups:
1984-1987; 1988-1991; 1992-1995. As for A1 concentrations in dialysis
fluids, the interval 1980-1983 (immediately before the start of our study),
which could clearly have influenced bone A1 content, was also considered.
Results: Basal serum A1 showed some fluctuations
(42.7±34.1; 24.8±21.9 and 38.9±224.9
&mgr;g/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 the DFO did not
differ in the three periods (136.5±105.7; vs
98.7±91.7 and 106.1±96.2 &mgr;g/l respectively,
P=n.s). Enteral exposure to drugs containing A1 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 A1 was dramatically reduced (from
60.7±43.0 to 29.0±24.4 and 31.9±29.9
mg/dg/dw respectively; P <0.0001), along with the definite
disappearance of Aluminon-positive cases and A1-related bone disease (ARBD)
after 1991. Parenteral exposure through the dialysate dropped from a mean
26±14 &mgr;g/l in the 4-year period prior the start of the
study (1980-1983) to 9±6 &mgr;g/l in the period 1984-1987
and to 4.9±2.1 &mgr;g/l and 5.0±2.0 &mgr;g/l
respectively thereafter (P <0.0001).
Conclusions: Despite the persistence of oral exposure
to A1, responsible for the observed stability of serum A1 levels, a
definite reduction of bone A1 content has been recorded in our dialysis
population, and ARBD has disappeared. This result has to be referred
essentially to the optimal control of A1 content in dialysis fluids, which
is confirmed as a major factor for A1 intoxication. Key
words: aluminium hydroxide; aluminium toxicity; bone aluminium;
desferrioxamine test; dialysate aluminium; dialysis fluids; haemodialysis
BRIEF REPORTS
Relative roles of intestinal absorption and dialysis-fluid-related exposure in the accumulation of aluminium in haemodialysis patients
Division of Nephrology and Dialysis, Renal Pathophysiology and Hypertension Unit, and Department of Experimental Medicine and Pathology of the University La Sapienza, Italy; Istituto Superiore di Sanita, Rome, Italy; Corresponding author at; 2nd Medical Clinic, Policlinico Umberto I, Viale del Policlinico, I-00161 Rome, Italy
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