Urinary calcium as a biomarker of renal dysfunction in a general population exposed to cadmium

Urinary beta2-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 inve stigate the feasibility of using urinary calcium as a biomarker of renal dy sfunction induced by cadmium, two areas were selected in this study, namely , a polluted area with a 3.71 mg/kg cadmium concentration in tire and a con trol area with a 0.07 mg/kg cadmium concentration. The total number of part icipants was 499, made up of 252 in the control group and 247 from the cadm ium-polluted area. Urinary cadmium, urinary calcium, and zinc concentration s were measured by atomic absorption spectrometry, and beta2-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 s ignificantly higher (P < 0.05) than those in the control area for both men and women, but there was no significant difference regarding urinary zinc b etween the two areas. A significant dose response relationship between the prevalence of hypercalciuria and the excretion of urinary cadmium was obser ved, and a significantly increased prevalence of calciuria was found when e xcretion of urinary cadmium exceeded 2 mug/g creatinine. The findings were similar to those for excess urinary secretion of beta2-microglobulin and N- acetyl-beta -D-glucosaminidase. Because cadmium can affect Ca2+ uptake by t ubular cells, with decreased renal Ca2+ reabsorption, calciuria may reflect tubular cell damage caused by cadmium. It was concluded that cadmium expos ure can result in increased excretion of urinary calcium in a general popul ation and that there is a significant dose-response relationship. Urinary c alcium can therefore be used as a biomarker of renal dysfunction induced by cadmium.