Adler A J, Berlyne G M
Nephron. 1986;44(1):36-9. doi: 10.1159/000183909.
In 36 patients suffering from chronic renal failure (mean creatinine clearance 26 ml/min), serum silicon levels were significantly increased (mean 0.52 microgram/ml compared with 0.265 microgram/ml in normals; p less than 0.005). Urinary silicon excretion per 24 h was significantly decreased (15.71 mg/24 h compared with 21.4 mg/24 h in normals; p less than 0.001). Fractional excretion of silicon (FESi) was significantly increased in chronic renal failure (p less than 0.001), with overall tubular secretion of silicon in 33% of patients. Urinary excretion of silicon was significantly related to urinary calcium excretion (p less than 0.0001) urinary magnesium excretion (p less than 0.0001) creatinine clearance (p less than 0.05) and sodium excretion (p less than 0.05). It is suggested that urinary silicon is in the form of orthosilicate, principally bound to calcium and magnesium; and that in chronic renal failure the increase in FESi, and the decrease in absorbed Si from the gastrointestinal tract, moderate the increase in plasma silicon levels and prevent excessive entry of silicon into the tissues.
在36例慢性肾衰竭患者(平均肌酐清除率为26 ml/min)中,血清硅水平显著升高(平均为0.52微克/毫升,而正常人则为0.265微克/毫升;p<0.005)。每24小时尿硅排泄量显著降低(15.71毫克/24小时,而正常人则为21.4毫克/24小时;p<0.001)。慢性肾衰竭患者的硅排泄分数(FESi)显著升高(p<0.001),33%的患者存在硅的整体肾小管分泌。尿硅排泄与尿钙排泄(p<0.0001)、尿镁排泄(p<0.0001)、肌酐清除率(p<0.05)和钠排泄(p<0.05)显著相关。提示尿硅以原硅酸形式存在,主要与钙和镁结合;并且在慢性肾衰竭中,FESi的升高以及胃肠道吸收硅的减少,可减轻血浆硅水平的升高,并防止硅过度进入组织。