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Abstract Background Urinary kidney injury molecule 1 is a recently discovered early biomarker for renal damage that has been proven to be correlated to urinary cadmium in rats. However, so far the association between urinary cadmium and kidney injury molecule 1 in humans after long-term, low-dose cadmium exposure has not been studied. Methods We collected urine and blood samples from 153 non-smoking men and women aged 60+, living in an area with moderate cadmium pollution from a non-ferrous metal plant for a significant period. Urinary cadmium and urinary kidney injury molecule 1 as well as other renal biomarkers (alpha1-microglobulin, beta2-microglobulin, blood urea nitrogen, urinary proteins and microalbumin) were assessed. Results Both before (r = 0.20; p = 0.01) and after (partial r = 0.32; p < 0.0001) adjustment for creatinine, age, sex, past smoking, socio-economic status and body mass index, urinary kidney injury molecule 1 correlated with urinary cadmium concentrations. No significant association was found between the other studied renal biomarkers and urinary cadmium. Conclusions We showed that urinary kidney injury molecule 1 levels are positively correlated with urinary cadmium concentration in an elderly population after long-term, low-dose exposure to cadmium, while other classical markers do not show an association. Therefore, urinary kidney injury molecule 1 might be considered as a biomarker for early-stage metal-induced kidney injury by cadmium.

Toxic metals such as cadmium (Cd) pose serious risks to human health. However, even though the importance of Cd as environmental health hazards is now widely appreciated, the specific mechanisms by which it produces its adverse effects have yet to be fully elucidated. Cd is known to enter cells, it binds and interacts with a multitude of molecules, it may indirectly induce oxidative stress and interfere with gene expression and repair of DNA. It also interacts with transport across cell membranes and epithelia and may therefore disturb the cell's homeostasis and function. Interaction with epithelial transport, especially in the kidney and the liver, may have serious consequences in general health. A lot of research still needs to be done to understand the exact way in which Cd interferes with these transport phenomena. It is not always clear whether Cd has primary or secondary effects on cell membrane transport. In the present review we try to summarize the work that has been done up to now and to critically discuss the relevance of the experimental work in vitro with respect to the in vivo situation. [ABSTRACT FROM AUTHOR]

Background: Urinary kidney injury molecule-1 (KIM-1) is a recently discovered biomarker for early renal damage. However, little is known about the collection and storage requirements prior to its measurement in human urine., Methods: Samples of healthy volunteers were collected and aliquoted. The effect of pre-freezing time, thawing, addition of protease inhibitors, centrifugation, storage time (up to 1.5 years) and temperature (4°C, -20°C and -80°C) was tested., Results: Addition of protease inhibitors and centrifugation prior to freezing did not affect the KIM-1 measurements. When samples were kept at room temperature for longer than 3 h before freezing or defrosted more than 1 h before measurement, mean KIM-1 values differed significantly compared to aliquots with minimal pre-freezing and thawing time. Samples frozen at -80°C were stable for up to 1.5 years; however an increasing number of freeze-thaw cycles adversely affected KIM-1 measurements. When stored at 4°C and -20°C, samples were less stable compared to those stored at -80°C., Conclusions: This study recommends that urine samples collected for KIM-1 measurements are frozen within 3 h after voiding and only be defrosted immediately prior to measurement. Addition of protease inhibitor and centrifugation prior to measurement is not necessary. Samples are preferably stored at -80°C and freeze-thaw cycles should be avoided.