Ca. Caramelo et al., MECHANISMS OF ALUMINUM-INDUCED MICROCYTOSIS - LESSONS FROM ACCIDENTALALUMINUM INTOXICATION, Kidney international, 47(1), 1995, pp. 164-168
Twenty-three hemodialysis patients exposed to an accidental aluminum o
verload, showed increased erythropoietin requirements and decreased er
ythrocyte mean corpuscular volume (MCV). At the peak of the intoxicati
on, MCV and plasma aluminum levels changed from unrelated (r = 0.02) t
o strongly related (r = 0.425) variables. The molar proportion of plas
ma aluminum to plasma iron increased dramatically (from 1:13.8 to 1:2.
4). This significant increment in the aluminum/iron ratio made higher
the relative offer of aluminum with respect to iron to the erythroid p
recursor cells. Accordingly, in a subset of 13 randomly selected alumi
num-intoxicated patients we found increased intraerythrocytic aluminum
, which paralleled the increase in plasma aluminum. Furthermore, in th
e aluminum-intoxicated group, intraerythrocytic ferritin, a marker of
iron content, and the ratio between erythrocyte and plasma ferritin we
re lower (P < 0.01 and <0.001, respectively), than in the control grou
p. These findings support the hypothesis that in some cases of aluminu
m-related microcytosis, a ferropenic mycrocitosis, as expression of er
ythroid ferropenia, may exist in spite of the presence of normal body
iron stores.