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Toxics 2018, 6(2), 26; https://doi.org/10.3390/toxics6020026

Urinary Cadmium Threshold to Prevent Kidney Disease Development

1
National Research Centre for Environmental Toxicology, the University of Queensland, Brisbane 4108, Australia
2
UQ Diamantina Institute and Centre for Health Services Research, Centre for Kidney Disease Research and Translational Research Institute, Woolloongabba, Brisbane 4102, Australia
3
Division of Toxicology, Department of Forensic Medicine, Chiang Mai University, Chiang Mai 50200, Thailand
4
Department of Public Health, Kanazawa Medical University, Uchinada, Ishikawa 920-0293, Japan
5
Computational Toxicology and Methods Development Laboratory, Division of Toxicology and Human Health Sciences, Agency for Toxic Substances and Disease Registry, Centers for Disease Control and Prevention, Atlanta, GA 30333, USA
*
Author to whom correspondence should be addressed.
Received: 9 March 2018 / Revised: 12 April 2018 / Accepted: 23 April 2018 / Published: 1 May 2018
(This article belongs to the Special Issue Cadmium Sources and Toxicity)
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Abstract

The frequently observed association between kidney toxicity and long-term cadmium (Cd) exposure has long been dismissed and deemed not to be of clinical relevance. However, Cd exposure has now been associated with increased risk of developing chronic kidney disease (CKD). We investigated the link that may exist between kidney Cd toxicity markers and clinical kidney function measure such as estimated glomerular filtration rates (eGFR). We analyzed data from 193 men to 202 women, aged 16−87 years [mean age 48.8 years], who lived in a low- and high-Cd exposure areas in Thailand. The mean (range) urinary Cd level was 5.93 (0.05–57) μg/g creatinine. The mean (range) for estimated GFR was 86.9 (19.6−137.8) mL/min/1.73 m2. Kidney pathology reflected by urinary β2-microglobulin (β2-MG) levels ≥ 300 μg/g creatinine showed an association with 5.32-fold increase in prevalence odds of CKD (p = 0.001), while urinary Cd levels showed an association with a 2.98-fold greater odds of CKD prevalence (p = 0.037). In non-smoking women, Cd in the highest urinary Cd quartile was associated with 18.3 mL/min/1.73 m2 lower eGFR value, compared to the lowest quartile (p < 0.001). Evidence for Cd-induced kidney pathology could thus be linked to GFR reduction, and CKD development in Cd-exposed people. These findings may help prioritize efforts to reassess Cd exposure and its impact on population health, given the rising prevalence of CKD globally. View Full-Text
Keywords: β2-microglobulin; cadmium; chronic kidney disease; clinical kidney function measure; estimated glomerular filtration rate; N-acetyl-β-d-glucosaminidase; population health; tubular dysfunction; toxicity threshold limit; urine protein β2-microglobulin; cadmium; chronic kidney disease; clinical kidney function measure; estimated glomerular filtration rate; N-acetyl-β-d-glucosaminidase; population health; tubular dysfunction; toxicity threshold limit; urine protein
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This is an open access article distributed under the Creative Commons Attribution License which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. (CC BY 4.0).
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Satarug, S.; Ruangyuttikarn, W.; Nishijo, M.; Ruiz, P. Urinary Cadmium Threshold to Prevent Kidney Disease Development. Toxics 2018, 6, 26.

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