Roels H A, Lauwerys R R, Bernard A M, Buchet J P, Vos A, Oversteyns M
Industrial Toxicology and Occupational Medicine Unit, School of Medicine, Catholic University of Louvain, Brussels, Belgium.
Br J Ind Med. 1991 Jun;48(6):365-74. doi: 10.1136/oem.48.6.365.
It has been assessed whether an internal dose of cadmium (Cd), as reflected by a Cd concentration in urine not yet sufficient to induce a significantly increased urinary excretion of various plasma proteins (microproteinuria defined as beta 2-microglobulin in urine greater than 300 micrograms/g creatinine, or retinol-binding protein in urine greater than 300 micrograms/g creatinine, or albumin in urine greater than 15 mg/g creatinine, or a combination of these), may affect the filtration reserve capacity of the kidney. The last was determined by measuring the difference between the baseline creatinine clearance and the maximal creatinine clearance after an acute oral load of protein (400 g of cooked red meat). In total 215 men were examined of whom eventually 87 Cd exposed workers (concentration of Cd in urine greater than 2 micrograms/g creatinine) from zinc/cadmium smelters and 92 control workers (concentration of Cd in urine less than 2 micrograms/g creatinine, absence of microproteinuria, normal fasting serum creatinine) were retained for data analysis performed separately for workers aged less or more than 50 years. Microproteinuria was present in 20 Cd workers, all older than 50. This study confirmed the previous observation that the age related decline of the baseline glomerular filtration rate (GFR) is accelerated in male workers with Cd induced microproteinuria; the same observation was made for the maximal GFR. It was found, however, that a renal Cd burden that had not yet caused microproteinuria did not impair the filtration reserve capacity of the kidney. This study therefore validates the previous estimate of the threshold effect concentration of Cd in urine (10 micrograms/g creatinine) that is intended to prevent the occurrence of microproteinuria in male Cd workers. It should be kept in mind, however, that because of the likely interference of the healthy worker effect, this conclusion may not be directly extrapolated to the general population.
研究评估了镉（Cd）的体内剂量（以尿镉浓度反映，此时该浓度尚不足以引起多种血浆蛋白尿排泄量显著增加，微蛋白尿定义为尿β2-微球蛋白大于300微克/克肌酐，或尿视黄醇结合蛋白大于300微克/克肌酐，或尿白蛋白大于15毫克/克肌酐，或这些指标的组合）是否会影响肾脏的滤过储备能力。肾脏滤过储备能力通过测量急性口服蛋白质负荷（400克熟红肉）后基线肌酐清除率与最大肌酐清除率之间的差值来确定。总共检查了215名男性，最终保留了87名来自锌/镉冶炼厂的镉暴露工人（尿镉浓度大于2微克/克肌酐）和92名对照工人（尿镉浓度小于2微克/克肌酐，无微蛋白尿，空腹血清肌酐正常），分别对年龄小于或大于50岁的工人进行数据分析。20名镉暴露工人存在微蛋白尿，均大于50岁。本研究证实了先前的观察结果，即镉诱导微蛋白尿的男性工人中，与年龄相关的基线肾小球滤过率（GFR）下降加速；最大GFR也有同样的观察结果。然而，研究发现尚未导致微蛋白尿的肾脏镉负荷并未损害肾脏的滤过储备能力。因此，本研究验证了先前对尿镉阈值效应浓度（10微克/克肌酐）的估计，该浓度旨在预防男性镉暴露工人发生微蛋白尿。然而，应记住，由于可能存在健康工人效应的干扰，该结论可能无法直接外推至一般人群。
