Roels H A, Van Assche F J, Oversteyns M, De Groof M, Lauwerys R R, Lison D
Industrial Toxicology and Occupational Medicine Unit, School of Medicine, Catholic University of Louvain, Brussels, Belgium.
Am J Ind Med. 1997 May;31(5):645-52. doi: 10.1002/(sici)1097-0274(199705)31:5<645::aid-ajim21>3.0.co;2-y.
The study aimed at assessing the evolution of cadmium (Cd)-induced renal tubular dysfunction in Cd workers according to the severity of the microproteinuria observed at the time the exposure was substantially decreased. Male workers employed in the Cd production industry for whom formerly high exposure had markedly decreased by 1984 and for whom standardized medical data were available during two observation periods (1980-1984 and 1990-1992) were eligible for the study. A total of 32 Cd workers fulfilling this profile were divided into two groups on the basis of historical records of urinary Cd concentration (Cd-U) covering the period until 1984. The workers with Cd-U values of > 10 micrograms Cd/g creatinine were subdivided further on the basis of the urinary concentration of beta 2-microglobulin (beta 2 MG-U) measured during the first observation period (1980-1984). In each group, the tubular microproteinuria as reflected by beta 2 MG-U and the concentration of retinol-binding protein in urine as well as the internal Cd dose as reflected by the concentration of Cd in blood and urine were compared between the first and second (1990-1992) observation periods. Increased microproteinuria was often diagnosed in cases with Cd-U values of > 10 micrograms Cd/g creatinine. The evolution of tubular renal function has been found to depend on the extent of the body burden of Cd (as reflected by Cd-U) and the severity of the initial microproteinuria at the time high Cd exposure was reduced or ceased. When reduction of Cd exposure took place while beta 2 MG-U did not exceed the upper reference limit of 300 micrograms/g creatinine, the risk of developing tubular dysfunction at a later stage was likely to be low, even in cases with historical Cd-U values occasionally > 10 but always < 20 micrograms Cd/g creatinine. When the microproteinuria was mild (beta 2 MG-U > 300 and < or = 1,500 micrograms/g creatinine) at the time exposure was reduced, and the historical Cd-U values had never exceeded 20 micrograms Cd/g creatinine, there was indication of a reversible tubulotoxic effect of Cd. When severe microproteinuria (beta 2 MG-U > 1,500 micrograms/g creatinine) was diagnosed in combination with historical Cd-U values exceeding 20 micrograms Cd/g creatinine, Cd-induced tubular dysfunction was progressive in spite of reduction or cessation of Cd exposure.
该研究旨在根据在接触镉大幅减少时观察到的微量蛋白尿严重程度，评估镉作业工人镉诱导的肾小管功能障碍的演变情况。1984年以前高接触镉水平已显著下降且在两个观察期（1980 - 1984年和1990 - 1992年）有标准化医学数据的镉生产行业男性工人符合该研究条件。共有32名符合此特征的镉作业工人根据截至1984年的尿镉浓度（Cd-U）历史记录分为两组。Cd-U值>10微克镉/克肌酐的工人再根据第一个观察期（1980 - 1984年）测量的β2-微球蛋白尿浓度（β2 MG-U）进一步细分。在每组中，比较第一个观察期和第二个（1990 - 1992年）观察期之间由β2 MG-U反映的肾小管微量蛋白尿、尿中视黄醇结合蛋白浓度以及由血镉和尿镉浓度反映的体内镉剂量。在Cd-U值>10微克镉/克肌酐的病例中经常诊断出微量蛋白尿增加。已发现肾小管功能的演变取决于镉的体内负荷程度（由Cd-U反映）以及高镉接触减少或停止时初始微量蛋白尿的严重程度。当镉接触减少而β²MG-U未超过300微克/克肌酐的参考上限时，即使历史Cd-U值偶尔>10但始终<20微克镉/克肌酐，后期发生肾小管功能障碍的风险可能较低。当接触减少时微量蛋白尿为轻度（β2 MG-U>300且≤1500微克/克肌酐）且历史Cd-U值从未超过20微克镉/克肌酐时，有迹象表明镉具有可逆的肾小管毒性作用。当结合历史Cd-U值超过20微克镉/克肌酐诊断出严重微量蛋白尿（β2 MG-U>1500微克/克肌酐）时，尽管镉接触减少或停止，镉诱导的肾小管功能障碍仍会进展。
