Silicon and aluminium interactions in haemodialysis patients.

BACKGROUND: Aluminium toxicity in dialysis patients is well described. Aluminium has a close chemical affinity with silicon. Silicon may have a role in protection against aluminium toxicity. METHODS: We measured serum aluminium and silicon levels from haemodialysis patients from four different centres. RESULTS: Though no relationship was seen across all centres combined, in one centre there was a reciprocal relationship in patients on home haemodialysis (who did not require reverse osmosis). Median (range) aluminium levels were higher, 2.2 (0.4-9.6) micromol/l when serum silicon was less than 150 micromol/l, and lower, 1.1 (0.2-2.8) micromol/l when serum silicon levels were greater than 150 micromol/l (P = 0.03). CONCLUSIONS: In patients treated by haemodialysis without reverse osmosis high serum silicon concentrations were associated with lower serum aluminium concentrations than those with low serum silicon. Further work needs to confirm a preventative role for silicon in the accumulation and subsequent toxicity of aluminium in dialysis patients.

Increased absorption of aluminium from a normal dietary intake in dementia.

Serum aluminium was significantly raised (p < 0.01) up to 2-3-fold, in patients with dementia including Alzheimers Disease (AD) 0.66 +/- 0.2 (mumol/l mean +/- 1 s.d.) and patients on regular aluminium hydroxide therapy 0.54 +/- 0.17, compared with healthy volunteers 0.21 +/- 0.13, although not as high as in patients with end stage renal failure on regular dialysis 0.88 +/- 0.42. The urine outputs (mumol/l mean +/- 1 s.d.) of aluminium and silicon, respectively, were also significantly increased up to 5-fold in dementia 2.89 +/- 1.78 (n = 23) and 1587 +/- 645 (n = 22) and patients on regular aluminium hydroxide therapy 5.03 +/- 2.08 (n = 8) and 998 +/- 364 (n = 21) compared with healthy volunteers 0.95 +/- 0.82 (n = 84) and 471 +/- 332 (n = 114). The increase in urine aluminium was thus associated with a similarly marked increase in the output of silicon. The increased absorption of aluminium in dementia patients is equivalent to the intestinal loading in Aludrox therapy. Also silicon appears to be important in the renal excretion of the absorbed aluminium. Whether this is a phenomenon related to the elderly or the process of dementia warrants further study.

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.

Silicon and aluminium and their inter-relationship in serum and urine after renal transplantation.

The present study was undertaken to establish the relationship between serum and urine silicon and improve renal function and examine whether the increased urinary excretion of aluminium observed after successful renal transplantation was associated with silicon. The changes in silicon and aluminium concentrations in serum and urine were measured in 15 patients for a period of up to 17 days following a first renal transplant. Serum silicon, unlike aluminium, progressively decreased with improving renal function and was significantly positively correlated with serum aluminium but not with the silicon excretion. The urine excretion of aluminium peaked between 4-8 days post-transplantation and was highly significantly positively correlated with urine silicon. The individual patient fractional excretion profiles of aluminium and silicon were variable but in general gave significant positive correlations suggesting that the elements may be cleared by the kidney through a common mechanism or as a chemical species, possibly an hydroxyaluminosilicate. If soluble silicon can chemically interact with aluminium in vivo it may, as in the biosphere, be important in the control of aluminium toxicity and eventual detoxification. Thus, elevated serum silicon concentrations may help to alleviate aluminium toxicity in end-stage renal disease and assist in the rapid clearance of aluminium seen after kidney transplantation.