Urinary Calcium as a Biomarker of Renal Dysfunction in a General Population Exposed to Cadmium

Abstract

Urinary beta 2-microglobulin and N-acetyl-beta-D-glucosaminidase have been recommended as sensitive indicators of renal dysfunction induced by cadmium. However, an increase in urinary calcium in early renal damage induced by cadmium has been reported both in humans and in animal experiments. To investigate the feasibility of using urinary calcium as a biomarker of renal dysfunction induced by cadmium, two areas were selected in this study, namely, a polluted area with a 3.71 mg/kg cadmium concentration in rice and a control area with a 0.07 mg/kg cadmium concentration. The total number of participants was 499, made up of 252 in the control group and 247 from the cadmium-polluted area. Urinary cadmium, urinary calcium, and zinc concentrations were measured by atomic absorption spectrometry, and beta 2-microglobulin and N-acetyl-beta-D-glucosaminidase in urine were analyzed. The levels of urinary cadmium and urinary calcium in persons from the exposed area were significantly higher (P < 0.05) than those in the control area for both men and women, but there was no significant difference regarding urinary zinc between the two areas. A significant dose-response relationship between the prevalence of hypercalciuria and the excretion of urinary cadmium was observed, and a significantly increased prevalence of calciuria was found when excretion of urinary cadmium exceeded 2 micrograms/g creatinine. The findings were similar to those for excess urinary secretion of beta 2-microglobulin and N-acetyl-beta-D-glucosaminidase. Because cadmium can affect Ca2+ uptake by tubular cells, with decreased renal Ca2+ reabsorption, calciuria may reflect tubular cell damage caused by cadmium. It was concluded that cadmium exposure can result in increased excretion of urinary calcium in a general population and that there is a significant dose-response relationship. Urinary calcium can therefore be used as a biomarker of renal dysfunction induced by cadmium.

Kidney Dysfunction and Hypertension: Role for Cadmium, P450 and Heme Oxygenases?

“…These female-linked effects are consistent with the previously described studies linking Cd absorption with reduced Fe stores mentioned earlier. In a Chinese population including residents from low-and high-exposure areas based on Cd concentrations in rice, the prevalence of calciuria was increased by 10% in subjects whose urinary Cd excretion of greater than 2 μ g/g creatinine (Wu et al 2001).…”

Effect of Toxic Metals on Human Health

“…Increasing intakes of zinc can reduce the renal toxicity of cadmium. An exposure to cadmium increases calcium excretion thus causes skeletal demineralization, probably leading to increases in bone fragility and risk of fractures [49]. Cadmium and its compounds are currently classified by IARC as a Group 1 carcinogen for humans.…”

Early biomarkers of cadmium exposure and nephrotoxicity

“…One notable exception, however, is Ca 2? , which has been shown to be a reliable indicator of Cd-induced proximal dysfunction in exposed human subjects (Staessen et al 1996;Wu et al 2001). …”