in a locale with uranium-contaminated drinking water varied from 1 to 33 years, and in the high-exposure group, it varied from 3 to 59 years. The indicators of kidney function included urinary excretion of glucose, creatinine, protein, and beta2-microglobulin (BMG). The markers for cell toxicity were alkaline phosphatase (ALP), gamma-glutamyltransferase (GGT), lactate dehydrogenase (LDH), and N-acetyl-beta-D-glucosaminidase (NAG). For males and females, the urinary glucose levels differed in the high- and low-exposure groups, and the amount increased with increasing uranium intake. Increases in ALP and BMG also correlated positively with increasing uranium intake. In contrast, there was no evidence for glomerular injury, as measured by normal serum creatinine concentration and no proteinuria. The authors suggest that intakes of uranium between 0.004 μg/kg and 9 mg/kg body weight are associated with altered kidney function but that the proximal tubule, rather than the glomerulus, is the site of this effect.

Fragments of depleted uranium. Uranium concentrations in the urine of Gulf War veterans have been found at higher levels in those with retained DU shrapnel than in those without when measured at 2, 4, and 7 years after first exposure (Hooper et al., 1999; McDiarmid et al., 2000). A recent study found that levels of urinary uranium ranged from 0.01 to 30.74 μg/g creatinine4 in veterans with retained shrapnel fragments (McDiarmid et al., 2000). The concentration of uranium in the urine of nonexposed veterans ranged from 0.01 to 0.047 μg/g creatinine. Despite much higher levels of urinary uranium in the veterans with retained fragments of DU, renal function parameters (serum creatinine, BMG, and retinol-binding and urine proteins) were the same in the two groups, strongly suggesting that years of exposure to uranium does not damage the kidneys (McDiarmid et al., 2000).

Conclusions on Nonmalignant Renal Disease

Although uranium is a heavy metal that causes transient renal dysfunction, the preponderance of evidence indicates little or no clinically important renal effects of exposure to uranium. A few studies have shown changes in renal function (Lu and Zhao, 1990; Zamora et al., 1998), but the number of cases has been quite small. Perhaps the strongest evidence is the absence of kidney damage in workers that had been exposed to high levels of soluble uranium compounds (Kathren and Moore, 1986) and in veterans exposed to DU from embedded shrapnel. Kidney function was normal in Gulf War veterans with embedded DU fragments, years after exposure, despite urinary uranium concentrations up to 30.74 μg/g creatinine (McDiarmid et al., 2000).


The unit of measurement for urinary uranium is expressed as micrograms per gram creatinine.

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