Cadmium-induced nephropathy in the development of high blood pressure.
In recognition of a central role of the kidney in long-term blood pressure control, we undertook an in-depth analysis of the relationship between blood pressure and kidney damage caused by environmental exposure to the common pollutants cadmium and lead. The subjects were 200 healthy Thais, 16 and 60 years of age (100 female non-smokers, 53 male non-smokers, and 47 male smokers). None of these subjects had been exposed to Cd or Pb in the workplace and their urinary Cd concentrations ranged from 0.4 to 37 nM, whereas their urinary Pb concentrations ranged from 0.1 to 30 nM. The prevalence of high blood pressure was 2%, 8% and 19%, respectively in subjects with low, average and high Cd-burden (linear trend chi2=6.4, P=0.01). Multiple regression analysis revealed a significant positive association between Cd-burden and blood pressure in male non-smokers (adjusted beta=0.31, P=0.02) and an inverse association between blood pressure and urinary Pb excretion rate in male smokers (adjusted beta=-0.38, P=0.005). Associations between Cd-burden and nephropathies were evidenced by increases in urinary excretion of beta2-microglobulin (P=0.02) and N-acetyl-beta-d-glucosaminidase (P=0.005) in subjects with high Cd-burden, compared with the subjects with average Cd-burden. In addition, an association between Cd-related nephropathy and high blood pressure was evidenced by a 20% increase in the prevalence of high blood pressure in people with NAG-uria (linear trend chi2=4.3, P=0.04). Our present study provides first evidence for a possible link between renal tubular damage and dysfunction caused by environmental Cd exposure and increased risk of high blood pressure.[1]References
- Cadmium-induced nephropathy in the development of high blood pressure. Satarug, S., Nishijo, M., Ujjin, P., Vanavanitkun, Y., Moore, M.R. Toxicol. Lett. (2005) [Pubmed]
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