changes not discernible with light microscopy may reflect continued retention of even small concentrations of uranium during postexposure followup.
The renal uranium concentrations sometimes found after acute exposure suggest that minimal transient effects (such as proteinuria and albuminuria) may occur after exposure at concentrations as low as 1 μg/g (Kathren and Moore 1986; Fisher et al. 1990). Renal effects have also been reported at renal concentrations around 1 μg/g in workers with chronic occupational exposure to uranium (Thun et al. 1985) and in Gulf War veterans with embedded DU fragments (Squibb et al. 2005). The Royal Society (2002) report also noted that transient renal effects occurred in humans at renal concentrations of 1 μg/g and that the trend for chronic exposures is toward greater renal effects with lower renal concentrations—possibly as low as 0.1 μg/g. The duration of exposure may be an important factor. Groups with longer exposure appear to have the greatest effects. How those findings compare with the renal uranium concentration thresholds chosen for the Capstone health risk assessments is presented in Chapter 8.
The primary target of uranium in the kidney is the proximal tubule, but glomerular effects also may occur.
Biomarkers of tubular effects include enzymuria and increased excretion of low-molecular-weight proteins, amino acids, and glucose.
Biomarkers of glomerular effects include urinary excretion of high-molecular-weight proteins (albuminuria) and increased blood creatinine or NPN.
Glucosuria is the most persistent tubular biomarker during recovery from acute uranium exposure in animals and humans.
Transient biomarkers of renal effects (such as proteinuria and albuminuria) have been observed at peak renal uranium concentrations as low as 1 μg/g.