Aluminum, Serum or Plasma

Serum or plasma

7 mL

0.6 mL

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

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.

Inductively coupled plasma/mass spectrometry (ICP/MS)

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

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.