Aluminum, Serum, Plasma

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Turnaround Time: 2 -4 days
CPT Code:


Test Type: 7 mL, Serum, plasma
Stability Time:



Room temperature

14 days


14 days


14 days

Freeze/thaw cycles

Stable x3

Reference Range:

Environmental exposure: 0−9 μg/L; patients on dialysis: <40 μg/L

Potentially toxic: >60 μg/L


Monitor patients for prior and ongoing exposure to aluminum. Patients at risk include:

• Infants on parenteral fluids, particularly parenteral nutrition

• Burn patients through administration of intravenous albumin, particularly with coexisting renal failure

• Adult and pediatric patients with chronic renal failure who accumulate aluminum readily from medications and dialysate

• Adult parenteral nutrition patients (less so, recently)

• Patients with industrial exposure

Monitor dialysate and water to prepare dialysate to prevent aluminum toxicity in dialysis patients.

Serum levels rise and fall after each dose of aluminum-containing phosphate binder or sucralfate. If renal function is normal, renal clearance of aluminum is prompt, with urine levels rising quickly after a course of aluminum-containing antacid is begun, and with levels persisting elevated for over a week. Urine levels rise after a dose of deferoxamine given for any reason. The degree of rise in serum aluminum after deferoxamine is regarded as reflecting total body aluminum burden.

This test was developed and its performance characteristics determined by LabCorp. It has not been cleared or approved by the Food and Drug Administration.

Aluminum toxicity has been recognized in many settings where exposure is heavy or prolonged, where renal function is limited, or where a previously accumulated bone burden is released in stress or illness. Toxicity may include:

• Encephalopathy (stuttering, gait disturbance, myoclonic jerks, seizures, coma, abnormal EEG)

• Osteomalacia or aplastic bone disease (associated with painful spontaneous fractures, hypercalcemia, tumorous calcinosis)

• Proximal myopathy

• Increased risk of infection

• Increased left ventricular mass and decreased myocardial function

• Microcytic anemia

• With very high levels, sudden death

Aluminum is ubiquitous in our environment; it is the third most prevalent element in the earth's crust. The gastrointestinal tract is relatively impervious to aluminum, absorption normally being only about 2%. Aluminum is absorbed by a mechanism related to that for calcium. Gastric acidity and oral citrate favors absorption, and H2-blockers reduce absorption. As is true for several trace elements, transferrin is the primary protein binder and carrier for aluminum in the plasma, where 80% is protein bound and 20% is free or complexed to small molecules such as citrate. Cells appear to take up aluminum from transferrin rather than from citrate. Purified preparations of ferritin from brain and liver have been found to contain aluminum. It is not known if ferritin has a specific binding site for aluminum. Factors regulating the migration of aluminum across the blood-brain barrier are not well understood. Serum aluminum correlates with encephalopathy; red cell aluminum correlates with microcytic anemia;1 and bone aluminum correlates with aluminum bone disease. Basal PTH when elevated appears to protect bone and thereby favor CNS toxicity. Other factors favoring one form of toxicity over another are not well understood. Aluminum toxicity has been reported to impair the formation and release of parathyroid hormone. The parathyroid glands concentrate aluminum above levels in surrounding tissues. Treatment of aluminum toxicity in renal failure patients often reactivates hyperparathyroidism, which to a certain extent is helpful for bone remodeling and healing.

1. Abreo K, Brown ST, Sella M, Trapp G. Application of an erythrocyte aluminum assay in the diagnosis of aluminum-associated microcytic anemia in patients undergoing dialysis and response to deferoxamine therapy. J Lab Clin Med. 1989 Jan; 113(1):50-57. PubMed 2909650

Alfrey AC, LeGendre GR, Kaehny WD. The dialysis encephalopathy syndrome: Possible aluminum intoxication. N Engl J Med. 1976 Jan 22; 294(4):184-188. PubMed 1244532

Chappuis P, Poupon J, Rousselet F. A sequential and simple determination of zinc, copper and aluminium in blood samples by inductively coupled plasma atomic emission spectrometry. Clin Chim Acta, 1992 Mar 31; 206(3):155-165. PubMed 1606703

Ellenberg R, King AL, Sica DA, et al. Cerebrospinal fluid aluminum levels following deferoxamine. Am J Kidney Dis. 1990 Aug; 16(2):157-159. PubMed 2382654

Gruskin AB. Aluminum: A pediatric overview. Adv Pediatr, 1988; 35:281-330. PubMed 3055861

Klein GL. Aluminum in parenteral products: medical perspective on large and small volume parenterals. J Parenter Sci Technol. 1989 May-Jun; 43(3):120-124. PubMed 2499667

Monteagudo FS, Cassidy MJ, Folb PI, Recent developments in aluminum toxicology. Med Toxicol Adverse Drug Exp. 1989 Jan-Feb; 4(1):1-16. PubMed 2651849

Tzamaloukas AH. Diagnosis and management of bone disorders in chronic renal failure and dialyzed patients. Med Clin North Am. 1990 Jul; 74(4):961-974. PubMed 2195265

Wills MR, Savory J. Aluminum and chronic renal failure: Sources, absorption, transport, and toxicity. Crit Rev Clin Lab Sci. 1989; 27(1):59-107. PubMed 2647415

Collection Details:

Collection Instructions:

Royal blue-top (EDTA) tube or royal blue-top without EDTA.

Separate serum or plasma immediately after the collection, and transfer to a certified metal-free transport tube

Maintain specimen at room temperature.