A study was conducted of the chemical effects on the human kidney induced by the chronic ingestion of uranium in drinking water. Subjects were divided into two groups: The low-exposure group, whose drinking water was obtained from a municipal water system and contained < 1 microgram uranium/L, and the high-exposure group, whose drinking water was obtained from private drilled wells and contained uranium levels that varied from 2 to 781 micrograms/L. Years of residence varied from 1 to 33 years in the low-exposure group and from 3 to 59 years in the high-exposure group. The indicators of kidney function measured in this study included glucose, creatinine, protein, and beta 2-microglobulin (BMG). The markers for cell toxicity studied were alkaline phosphatase (ALP), gamma-glutamyl transferase (GGT), lactate dehydrogenase (LDH), and N-acetyl-beta-D-glucosaminidase (NAG). Urinary glucose was found to be significantly different and positively correlated with uranium intake for males, females, and pooled data. Increases in ALP and BMG were also observed to be correlated with uranium intake for pooled data. In contrast, the indicators for glomerular injury, creatinine and protein, were not significantly different between the two groups nor was their urinary excretion correlated to uranium intake. These results suggest that at the intakes observed in this study (0.004 microgram/kg to 9 micrograms/kg body wt), the chronic ingestion of uranium in drinking water affects kidney function and that the proximal tubule, rather than the glomerulus, is the site for this interference.
