The role of silicic acid in the renal excretion of aluminium.

The chemical affinity of silicic acid for aluminium (AI) has been shown to reduce the bioavailability of AI in studies of human gastrointestinal (GI) absorption. Investigations were carried out to ascertain whether or not similar interactions may also enhance the renal excretion of AI by assessing the urinary output of both elements. Healthy individuals given monosilicic acid as naturally found in beer, excreted the majority of the silicic acid content (mean 56 percent) within 8 hours, concomitant with a significant increase in AI excretion (P < 0.05). Ingestion of increasing doses of silicic acid resulted in dose related increases in excretion of Si. Excretion of AI reached a maximum and then declined, consistent with depletion of AI body stores. This was confirmed using the 26AI isotope. The low serum but high urine concentration of Si suggests that if AI and Si interact to form an excretable species they do so in the kidney lumen such that Si limits the reabsorption of AI. Silicic acid's effect on the depletion of aluminium stores and reduced GI absorption suggest its addition to municipal water supplies may be a low risk public health measure to reduce the AI burden in the general population.