In the case of renal disease, the use of aluminum-containing drugs is often suggested. The conservative management of intrinsic renal failure requires careful attention to fluid balance, maintenance of adequate nutrition and prevention or correction of disorders like hyperphosphatemia. Hyperphospha-temia is a disorder responsible for osteodystrophy commonly seen in patients with end-stage renal disease.33 It requires medication, commonest of which are pharmaceutical preparations of aluminum, promoting efficient phosphate binding. Use, however, of such medication contradicts efforts to exclude aluminum from such patients, with all the dire consequences arising from aluminum absorption on one hand and the detrimental repercussions from a protracted hyperphosphatemia on the other. This dilemma has propelled research into developing secure aluminum-containing phosphate binders. The most widely used aluminum drugs in this case are antacids, containing Al(OH)3. Normo-phosphatemia can be promoted by using Al(OH)3 alone or by administering in combination with other drugs. Characteristic in this sense is the case of chronic renal insufficiency patients to whom antibiotics (e.g. ofloxacin) are administered in conjunction with the Al(OH)3 phosphate-binder therapy.34
Studies35,36 aimed at understanding the nature and reactivity of aluminum species, which promote reduction of hyperphosphatemia through the use of aluminum-containing antacids,37 delve into issues relating to the availability of Al(III) ions and the concomitant phosphate-binding forms that Al(III) generates under the pH-specific conditions prevalent in the alimentary tract. The studies suggest that aluminum-containing antacids (of variable composition and formulations like Alucap®, Aludrox® and others) provide the necessary pool of Al(III) ions when dissociated in the acidic environment of the stomach following oral ingestion. Some of the Al(III) will be absorbed there, with the majority of the metal ion being absorbed through the gut. There, the pH of the lumen is high, ~6, and remains between 6 and 8.5 in the distal intestines. In this fairly high pH range, Al(III) is freshly precipitated yielding colloidal amorphous Al(OH)3. In the presence of a large surface of such a preformed Al(OH)3 precipitate, phosphate is adsorbed38 (through chemistry involving the OH~ groups of Al(OH)339 and species like the predominantly present HPO42~ ions) and will pass intact through the intestine without any decomposition because of the high pH. Any aluminum phosphate complex that might form under acidic pH conditions is also driven through due to insolubility under such conditions.40 Finally, the phosphate-aluminum product will be excreted through the feces. Therefore, as far as phosphate binding is concerned, it is important from the pharmacological point of view to deliver Al(OH)3 in its most amorphous form into the proximal intestine, concurrently trying to avoid its release in the gastric fluids at low pH. Low pH would clearly generate soluble forms41,42 of Al(III) capable of promoting long-term toxic effects.43 Due to risks of aluminum toxicity, calcium-based lanthanum carbonate and other agents have also been introduced in phosphate-binding therapy.
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