Assessment of urinary protein 1 and transferrin as early markers of cadmium nephrotoxicity.

Abstract

Transferrin and protein 1, a sex linked a2-microprotein, were assayed in urine from 58 workers exposed to cadmium (Cd) in a nonferrous smelter and from 58 age matched referents. These two new markers of nephrotoxicity were compared with urinary f2-microglobulin (fi2-m), retinol Materials and methods STUDY POPULATIONSThe study was conducted on 58 male workers exposed to Cd in a non-ferrous smelter. The control group consisted of 58 age matched men recruited from a factory with no risk of exposure to Cd or other heavy metals. None of the exposed workers or referent subjects was occupationally exposed to lead or mercury as shown by the concentrations of these metals in blood (<35 jg/100 ml) and urine (< 5 pg/g creatinine). The characteristics of the two populations are summarised in table 1.

Determination of Clara cell protein urinary elimination as a marker of tubular dysfunction

“…Since the early 1990s the determination of urinary CC16 has sporadically been used as a marker of tubular renal proximal dysfunction [12]. In this study, we have determined the urinary elimination of CC16 in a group of pediatric patients and compared the results with those of two other known markers of tubular proximal function, Nacetyl-β-D-glucosaminidase (NAG) and β2-microglobulin.…”

The Late and Persistent Pathogenic Effects of Cadmium at Very Low Levels on the Kidney of Rats

“…The biological effects of Cd at high doses have been extensively investigated (Moulis and Thevenod 2010). Chronic exposure of animals to Cd at low levels has been studied by several groups (Bernard et al 1992;Bernard et al 1990;Jarup and Alfven 2004). However, most of those studies have focused on the effects during or at the end of Cd exposure.…”

“…Several population stud-ies have shown that not only occupationally Cd-exposed workers but also environmentally Cd-exposed populations can experience moderate to severe health problems (Bernard et al 1992;Bernard et al 1990;Jarup and Alfven 2004). Unfortunately, human contact with Cd is an inescapable consequence of human life, from both occupational and environmental sources.…”

Assessment of occupational exposure to cadmium in the Netherlands, 1980–1989

“…Braithwaite and Cowtan [ 19841 observed an increase of MG in occupationally exposed workers at CdU levels above 15 pg/g creatinine. Bernard et al [1990] concluded that MG is increased only in workers with CdU higher than 10 pg/g creatinine. In the present study, a significant increase of MG was found in urine samples with CdU > 10 pg/g creatinine.…”