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Assays / Trace
Metals/ Aluminium
Specimen requirements
Aluminium is a non-essential trace element
of ubiquitous distribution. Until relatively recently it was assumed
to be biologically innocuous apart from rare cases of toxicity due
to industrial exposure. The recognition of its role as an iatrogenic
complication of chronic renal failure has radically altered our
appreciation of its clinical importance.
Toxicity
Occupational exposure to dust containing finely
divided aluminium may cause pulmonary fibrosis. It has been suggested
that uptake of aluminium into brain may be responsible for the symptoms
of Alzheimer's disease. These situations apart, aluminium toxicity
mainly arises in patients with chronic renal failure who are undergoing
treatment either by conservative means or by maintenance haemo or
peritoneal dialysis. Greatly elevated serum aluminium concentrations
in these patients are clearly associated with the symptoms of dialysis
encephalopathy (speech disorder, dementia, convulsions and death)
and dialysis osteodystrophy (osteomalacia frequently resistant to
treatment with vitamin D or its active metabolites). Aluminium accumulation
may be responsible, in part at least, for the anaemia and soft tissue
calcification of chronic renal failure. High concentrations may
also be cardiotoxic.
The increased body burden comes from two sources. Firstly,
oral aluminium hydroxide is widely used as a phosphate binder, and
the normal intestinal absorption may be enhanced in chronic renal
failure. Secondly, dialysis fluid may have a high aluminium content
arising from impurities in the salts used in its manufacture or
from the containers in which it is stored. A more significant cause
is from the preparation of the fluid by dilution of a concentrate
with water having a naturally high aluminium concentration, or to
which aluminium has been added by the local Water Authority as a
flocculent to remove coloured matter. Conventional water softening
devices or deionizers are not efficient in removing the aluminium
present in the supply, but the increasing use of reverse osmosis
for water purification has greatly reduced intake from this source,
leaving oral aluminium as the main hazard.
The aluminium content of certain blood products and
intravenous fluids may pose a considerable risk to individuals receiving
them on a long term basis, particularly premature infants in whom
renal function may be impaired.
Laboratory Indices of Aluminium Status
Aluminium is transported in the blood bound
to transferrin, and aluminium status is best assessed by measurement
of the plasma aluminium concentration. In addition, the aluminium
content of the dialysis solutions and of the water used for dilution
may also require measurement. Concern regarding the risk to dialysis
patients resulted in the issue of a CEC Resolution establishing
a protocol for the regular monitoring of such patients and setting
criteria necessary for the analytical techniques. In summary, this
recommends that patients at risk be monitored at least quarterly
by measurement of the plasma aluminium; that concentrations greater
than 2.2 µmol/L (60 µg/L) indicate an increased aluminium
body burden; that concentrations greater than 3.7 µmol/L (100µg/L)
indicate the need for an increased monitoring frequency and health
surveillance; that all steps should be taken to ensure that a concentration
of 7.4 µmol/L (200 µg/L) is never exceeded; that the aluminium
concentration in dialysis fluids should not exceed 1.1 µmol/L
(30 µg/L).
Many renal units now impose their own lower action
limits for plasma aluminium and it is unusual to see concentrations
greater than 3.0 µmol/L (71µg/L)
It must be stressed that regular monitoring of plasma
aluminium concentrations is also appropriate in patients with any
degree of renal failure who are being treated with oral aluminium.
The concentration should also be regularly determined in patients
receiving large amounts of blood products or on long term intravenous
therapy.
References:
Stokinger HE Chapter 29 - Metals, in Patty's
Industrial Hygiene and Toxicology, 3rd Revised Edition, Volume 2A.
Eds Clayton GD and Clayton FE. Wiley Interscience, 1981.
Savory J, Wills MR. Aluminium and chronic renal failure,
sources, absorption, transport and toxicity. Crit Rev Clin Lab Sci
1989; 27: 59-107
Eastwood JB, Levin GE, Pazianas M, Taylor A, Denton
J and Freemont AJ. Aluminium deposition in bone after contamination
of a drinking water supply. Lancet 1990; ii: 462-466
Nicolini M, Zatta PF, Corain B. eds, Aluminum in Chemistry,
Biology and Medicine. Life Chemistry Reports, Volume 2. Harwood
Academic Publishers, Switzerland, 1994
Yokel RA, Golub MS. eds, Research Issues in Aluminum
Toxicity. J Toxicol Environm Health 1996; 48 (6): 527-686
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