Aluminum | Al (blood)

General Information

Aluminum is a fairly widespread element in our surrounding world.

Absorption of aluminum from the gastrointestinal tract normally does not exceed 2%. The acidic environment of the stomach and oral citrates (acids) increase absorption, although gastric mucosal H2 receptor blockers (eg, antacid medications, proton pump inhibitors) decrease absorption. Physiologically accepted daily dose (5-10mg) is completely excreted from the body. Filtration is carried out in the kidney glomeruli. In patients with kidney glomeruli damage, the process of aluminum excretion is disrupted and it accumulates in the body. Aluminum accumulates in the blood, binds to blood serum proteins, and is quickly distributed in the tissues, especially in the brain and bones. As with other elements, the main transporter of aluminum is the protein transferrin, through which cells absorb microelements more easily.

The mechanism of how aluminum will pass through the blood-brain barrier is not fully understood.

In patients with kidney failure, the toxic effect of aluminum is enhanced by factors such as: dialysis fluid, albumin (protein) molecules containing excess aluminum, and the dialysis process, which is not very effective in removing aluminum from the blood.

The toxic effect of aluminum is caused by its long-term exposure (exposure) to a large dose. Effects of toxic exposure to aluminum include: Encephalopathy (impairment of walking, speech, consciousness, abnormal encephalographic data)

Osteomalacia or aplastic bone disease (disruption of bone tissue formation, resulting in pathological fractures, leaching of calcium from the bone)

Myopathies (muscle damage)

resistance to infections Impairment (due to damage to the immune system)

Hypertrophy of the left ventricle of the heart (as a result of damage to the heart muscle)

Microcytic anemia (reduction in the size of erythrocytes - red blood cells, due to a violation of hemoglobin synthesis)

Sudden death too Yes.

When it accumulates in the bones, calcium is replaced by aluminum during the bone mineralization process, which prevents the formation of normal bone cells. Under the influence of parathyroid hormone, the resorption (release) of calcium from the bones into the blood is disturbed, which also disrupts the secretion of parathyroid hormone and causes secondary and sometimes tertiary hyperparathyroidism (increased hormone secretion).

In acute toxic effects of aluminum, metal chelators or binding drugs are used for treatment, which bind and expel the mineral (in this case, aluminum) from the body.

When is the survey conducted?

in dialysis patients

in patients with metal prostheses

In patients with an excess of aluminum

In patients with parenteral nutrition (feeding by tube or other means)

In patients receiving regular intravenous albumin transfusions

In case of chronic kidney diseases and failure

Preparation of the patient: The study is conducted on an empty stomach

Material for examination: Venous blood

Referral norm:  <11.4 ng/ml

In dialysis patients:      Acceptable level is: <60 ng/ml

The cutoff is: <100 ng/mL

The toxic level is: <200 ng/ml

Interpretation of results:

Patients with renal failure have serum aluminum levels above 60 ng/ml.

Dialysis patients with high aluminum concentrations have a specific biochemical profile:

• In patients, without signs of osteomalacia (bone "softening", due to impaired mineralization processes) or encephalopathy, the level of aluminum in the blood is less than 20 ng/ml and parathyroid hormone is more than 16 pmol/ml, which is a sign of secondary hyperparathyroidism.
• Patients with symptoms of osteomalacia and encephalopathy typically have serum aluminum levels >60 ng/mL and parathyroid hormone levels <16 picomoles/mL.
• When the level of plasma aluminum is 60-100 ng/ml, the clinical manifestations of the toxic effect of aluminum begin, which requires intervention.

Limitation:

An increased concentration of gadolinium or iodine in the serum prevents the determination of an accurate indicator of aluminum. At least 96 hours should pass after the administration of gadolinium and iodine-containing contrast material in order to obtain a correct reading for aluminum determination.