Aluminum excretion

Bile excretion was >0. 1% of the aluminum load. When aluminum was administered via the external jugular vein, aluminum excretion was found to occur in the distal tubule of the kidney in pigs (Monteagudo et al. 1988). Yokel and McNamara (1985) did not find any age-related differences in the systemic clearance or half-time of aluminum in rabbits following parenteral administration of aluminum lactate. 

Monteagudo FSE, Isaacson LC, Wilson G, et al. 1988. Aluminum excretion by the distal tubule of the pig kidney. Nephron 49 245-250. 

E. Delhaize, P. R. Ryan, and P. J. Randall, Aluminum tolerance in wheat (Triticum aestivum L.) 11. Aluminum-stimulated excretion of malic acid from root apices. Plant Physiol. 103 695 (1993). 

Factors that can predispose patients to developing metabolic bone disease include deficiencies of phosphorus, calcium, and vitamin D vitamin D and/or aluminum toxicity amino acids and hypertonic dextrose infusions chronic metabolic acidosis corticosteroid therapy and lack of mobility.35,39 Calcium deficiency (due to decreased intake or increased urinary excretion) is one of the major causes of metabolic bone disease in patients receiving PN. Provide adequate calcium and phosphate with PN to improve bone mineralization and help to prevent metabolic bone disease. Administration of amino acids and chronic metabolic acidosis also appear to play an important role. Provide adequate amounts of acetate in PN admixtures to maintain acid-base balance. 

Chronic renal failure/dialysis During sucralfate administration, small amounts of aluminum are absorbed. Concomitant use with other aluminum-containing products may increase the total body burden of aluminum. Patients with chronic renal failure or receiving dialysis have impaired excretion of absorbed aluminum, and aluminum is not dialyzed. Aluminum accumulation and toxicity have occurred. 

Gerke, J. Romer, W. [ungk, A. (1994) The excretion of citric and malic acid by proteoid roots of Lupinus albus L. effects on soil solution concentrations of phosphate, iron, and aluminum in the proteoid rhizospere in samples of an oxisol and a luvisol. Z. Pflanzener-nahr. Bodenk. 157 289-294 Gerlach, R. Cunningham, A.B. Caccavo Jr.,... 

Mechanism of Action An antacid that reduces gastric acid by binding with phosphate in the intestine, and then is excreted as aluminum carbonate in feces. Aluminum carbonate may increase the absorption of calcium due to decreased serum phosphate levels. The drug also has astringent and adsorbent properties. Therapeutic Effect Neutralizes or increases gastric pH reduces phosphates in urine, preventing formation of phosphate urinary stones reduces serum phosphate levels decreases fluidity of stools. 

Sucralfate is a salt of sucrose complexed to sulfated aluminum hydroxide. In water or acidic solutions it forms a viscous, tenacious paste that binds selectively to ulcers or erosions for up to 6 hours. Sucralfate has limited solubility, breaking down into sucrose sulfate (strongly negatively charged) and an aluminum salt. Less than 3% of intact drug and aluminum is absorbed from the intestinal tract the remainder is excreted in the feces. 

Deferoxamine is isolated from Streptomycespilosus. It binds iron avidly but essential trace metals poorly. Furthermore, while competing for loosely bound iron in iron-carrying proteins (hemosiderin and ferritin), it fails to compete for biologically chelated iron, as in microsomal and mitochondrial cytochromes and hemoproteins. Consequently, it is the chelator of choice for iron poisoning (Chapters 33 and 59). Deferoxamine plus hemodialysis may also be useful in the treatment of aluminum toxicity in renal failure. Deferoxamine is poorly absorbed when administered orally and may increase iron absorption when given by this route. It should therefore be administered intramuscularly or, preferably, intravenously. It is believed to be metabolized, but the pathways are unknown. The iron-chelator complex is excreted in the urine, often turning the urine an orange-red color. 

Aluminum can form complexes with many molecules in the body (organic acids, amino acids, nucleotides, phosphates, carbohydrates, macromolecules). Free aluminum ions (e.g., A1(H20)63+) occur in very low concentrations. The toxicokinetics of aluminum can vary, depending on the nature of these complexes. For example, aluminum bound in a low-molecular-weight complex could be filtered at the renal glomeruli and excreted, while aluminum in a high-molecular-weight complex would not. 

Most of the estimates of aluminum uptake summarized above are based on the assumption that urinary excretion represents absorption, although a few values were determined using the anthropogenic radioactive isotope 26Al in combination with a sophisticated analytical technique (accelerator mass... 

The kidney is the major route of excretion of absorbed aluminum after inhalation exposure in humans. 

No studies were located regarding excretion in animals after inhalation exposure to aluminum or its compounds. 

Excretion of aluminum may be lower in premature compared to full-term infants (Bougie et al. 1991). Plasma levels of aluminum in premature infants were 14.6 g/L compared to 7.8 g/L in full-term infants, and absolute urinary excretion was reduced. The aluminum-creatinine ratio in the urine was similar in both groups, indicating that the lower excretion in the premature infants may be due to a lower glomerular fdtration rate, thus increasing the risk of aluminum accumulation in this group. 

Aluminum can be measured in the blood, urine, and feces (see Chapter 6 for description of available methods). Since aluminum is found naturally in a great number of foods, it is found in everyone. Unfortunately, exposure levels cannot be related to serum or urine levels very accurately, primarily because aluminum is very poorly absorbed by any route and its oral absorption in particular can be quite affected by other concurrent intakes. There is an indication that high exposure levels are reflected in urine levels, but this cannot be well quantified as much of the aluminum may be rapidly excreted. Aluminum can also be measured in the feces, but this cannot be used to estimate absorption. 

A susceptible population will exhibit a different or enhanced response to aluminum than will most persons exposed to the same level of aluminum in the environment. Reasons may include genetic makeup, age, health and nutritional status, and exposure to other toxic substances (e.g., cigarette smoke). These parameters may result in reduced detoxification or excretion of aluminum, or compromised function of target organs affected by aluminum. Populations who are at greater risk due to their unusually high exposure to aluminum are discussed in Section 5.7, Populations With Potentially High Exposure. 

The major population at risk for aluminum loading and toxicity consists of individuals with renal failure. In a study by Alfrey (1980), 82% of nondialyzed uremic patients and 100% of dialyzed uremic patients had an increased body burden of aluminum. The decreased renal function and loss of the ability to excrete aluminum, ingestion of aluminum compounds to lessen gastrointestinal absorption of phosphate, the aluminum present in the water used for dialysate, and the possible increase in gastrointestinal absorption of aluminum in uremic patients can result in elevated aluminum body burdens. The increased body burdens in uremic patients has been associated with dialysis encephalopathy (also referred to as dialysis dementia), skeletal toxicity (osteomalacia, bone pain, pathological fractures, and proximal myopathy), and hematopoietic toxicity (microcytic, hypochromic anemia). Pre-term infants may also be particularly sensitive to the toxicity of aluminum due to reduced renal capacity (Tsou et al. 1991)... 

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