Schentag J J, Sutfin T A, Plaut M E, Jusko W J
J Med. 1978;9(3):201-10.
We used a radioimmunoassay to evaluate the changes in the urinary excretion of beta2-microglobulin (beta2M) in 21 patients receiving aminoglycosides for treatment of infection. Excretion of this protein rose to a peak at least 5 times the baseline value in the urine, and declined rapidly to control values after drug administration ceased. In six patients who developed aminoglycoside nephrotoxicity, urinary beta2M excretion rose 5 days or more before serum creatinine rose, and 5 of 6 nephrotoxic patients excreted more than 50 mg/day (normal, less than 0.1 mg/day). Urinary beta2M is a non-specific indication of renal tubular damage, but heralds aminoglycoside-induced damage before standard tests of kidney function change.
我们采用放射免疫分析法评估了21例接受氨基糖苷类药物治疗感染患者尿中β2-微球蛋白（β2M）排泄量的变化。该蛋白的排泄量在尿中升至至少为基线值5倍的峰值，并在停药后迅速降至对照值。在6例发生氨基糖苷类肾毒性的患者中，尿β2M排泄量在血清肌酐升高前5天或更久就已升高，6例肾毒性患者中有5例排泄量超过50毫克/天（正常为低于0.1毫克/天）。尿β2M是肾小管损伤的非特异性指标，但在标准肾功能检测出现变化之前就能预示氨基糖苷类药物所致的损伤。
