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Reversibility of microproteinuria in cadmium workers with incipient tubular dysfunction after reduction of exposure
Author(s) -
Roels Harry A.,
Van Assche Frank J.,
Oversteyns Maurice,
De Groof Marc,
Lauwerys Robert R.,
Lison Dominique
Publication year - 1997
Publication title -
american journal of industrial medicine
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.7
H-Index - 104
eISSN - 1097-0274
pISSN - 0271-3586
DOI - 10.1002/(sici)1097-0274(199705)31:5<645::aid-ajim21>3.0.co;2-y
Subject(s) - medicine , reduction (mathematics) , cadmium , endocrinology , cardiology , physiology , materials science , geometry , mathematics , metallurgy
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 μg Cd/g creatinine were subdivided further on the basis of the urinary concentration of β 2 ‐microglobulin (β 2 MG‐U) measured during the first observation period (1980–1984). In each group, the tubular microproteinuria as reflected β 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 μg 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 time high Cd exposure was reduced or ceased. When reduction of Cd exposure took place while β 2 MG‐U did not exceed the upper reference limit of 300 μg/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 μg Cd/g creatinine. When the microproteinuria was mild (β 2 MG‐U > 300 and ≤1,500 μg/g creatinine) at the time exposure was reduced, and the historical Cd‐U values had never exceeded 20 μg Cd/g creatinine, there was indication of a reversible tubulotoxic effect of Cd. When severe microproteinuria (β 2 MG‐U > 1,500 μg/g creatinine) was diagnosed in combination with historical Cd‐U values exceeding 20 μg Cd/g creatinine, Cd‐induced tubular dysfunction was progressive in spite of reduction or cessation of Cd exposure. Am. J. Ind. Med. 31:645–652, 1997. © 1997 Wiley‐Liss, Inc.