Blumberg A, Esslen E, Bürgi W
Nephron. 1978;21(4):186-91. doi: 10.1159/000181392.
In 28 patients predialysis plasma myoinositol was significantly elevated to 10.8 +/- 2.5 versus 0.75 +/- 0.15 mg/100 ml in normals (mean +/- 1 SD), and was weakly correlated with plasma creatinine concentrations (r = 0.42, p less than 0.05). Dialysis decreased plasma myoinositol concentrations to 3.5 +/- 1.1 mg/100 ml. In 16 patients studied more extensively plasma myoinositol was similarly elevated to 10.6 +/- 3.4 mg/100 ml, and spinal fluid myoinositol was increased to 9.4 +/- 2.3 mg/100 ml (versus 2.7 +/- 0.7 in normals, p less than 0.001). Nerve conduction velocities were reduced in 15 and EEG tracings were abnormal in 12 of the 16 patients. However, neither spinal fluid nor plasma myoinositol showed any correlation with nerve conduction velocities or EEG changes (r = 0.05-0.20, NS) Myoinositol is one of the substances retained in renal insufficiency but no indication was found that it is a toxin causing uremic neurological disturbances.
28例患者透析前血浆肌醇显著升高至10.8±2.5mg/100ml，而正常人血浆肌醇为0.75±0.15mg/100ml（均值±1标准差），且与血浆肌酐浓度呈弱相关（r = 0.42，p<0.05）。透析后血浆肌醇浓度降至3.5±1.1mg/100ml。在16例接受更广泛研究的患者中，血浆肌醇同样升高至10.6±3.4mg/100ml，脑脊液肌醇升高至9.4±2.3mg/100ml（正常人2.7±0.7mg/100ml，p<0.001）。16例患者中有15例神经传导速度降低，12例脑电图描记异常。然而，脑脊液和血浆肌醇均与神经传导速度或脑电图变化无相关性（r = 0.05 - 0.20，无显著性差异）。肌醇是肾功能不全时潴留的物质之一，但未发现其是导致尿毒症神经功能障碍的毒素。
