|Values are valid only on day of printing.|
Under normal physiologic conditions, the usual daily dietary intake of aluminum (5-10 mg) is completely eliminated. Excretion is accomplished by avid filtration of aluminum from the blood by the glomeruli of the kidney. Patients in renal failure (RF) lose the ability to clear aluminum and are candidates for aluminum toxicity. Many factors increase the incidence of aluminum toxicity in RF patients:
-Aluminum-laden dialysis water can expose dialysis patients to aluminum.
-Aluminum-laden albumin can expose patients to an aluminum burden they cannot eliminate.
-The dialysis process is not highly effective at eliminating aluminum.
-Aluminum-based phosphate binder gels are administered orally to minimize phosphate accumulation; a small fraction of this aluminum may be absorbed and accumulated.
If it is not removed by renal filtration, aluminum accumulates in the blood where it binds to proteins such as albumin and is rapidly distributed through the body. Aluminum overload leads to accumulation of aluminum at 2 sites: brain and bone. Brain deposition has been implicated as a cause of dialysis dementia. In bone, aluminum replaces calcium at the mineralization front, disrupting normal osteoid formation.
Urine aluminum concentrations are likely to be increased above the reference range in patients with metallic joint prosthesis. Prosthetic devices produced by Zimmer Company and Johnson and Johnson typically are made of aluminum, vanadium, and titanium. This list of products is incomplete, and these products change occasionally; see prosthesis product information for each device for composition details.
Monitoring aluminum exposure
Monitoring metallic prosthetic implant wear
Daily excretion >20 mcg/specimen indicates exposure to excessive amounts of aluminum. In renal failure, the ability of the kidney to excrete aluminum decreases, while the exposure to aluminum increases (aluminum-laden dialysis water, aluminum-laden albumin, and aluminum-laden phosphate binders).
Patients receiving chelation therapy with desferrioxamine (for iron- or aluminum-overload states) also excrete considerably more aluminum in their urine than normal.
Prosthesis wear is known to result in increased circulating concentration of metal ions.(1,2) Modest increase (10-20 mcg/specimen) in urine aluminum concentration is likely to be associated with a prosthetic device in good condition. Urine concentrations >50 mcg/specimen in a patient with an aluminum-based implant, not undergoing dialysis, suggest significant prosthesis wear. Increased urine trace element concentrations in the absence of corroborating clinical information do not independently predict prosthesis wear or failure.
This test is not an acceptable substitute for serum aluminum measurements and is not recommended for routine aluminum screening.
Falsely increased results may be obtained if the specimen is collected in nonacid-washed polypropylene collection vessels or if metal caps are used to seal the container.
High concentrations of gadolinium and iodine are known to interfere with most metals tests. If either gadolinium- or iodine-containing contrast media has been administered, a specimen should not be collected for 96 hours.
Reference values apply to all ages.
1. O’Shea S, Johnson DW: Review article: addressing risk factors in chronic kidney disease mineral and bone disorder: can we influence patient-level outcomes? Nephrology 2009;14:416–427
2. Meyer-Baron M, Schuper M, Knapp G, van Thriel C: Occupational aluminum exposure: evidence in support of its neurobehavioral impact. Neurotoxicology 2007;28:1068–1078