Environmental Cadmium Exposure Induces an Increase in Systolic Blood Pressure by Its Effect on GFR
Issued Date
2024-09-01
Resource Type
eISSN
26737140
Scopus ID
2-s2.0-85205037687
Journal Title
Stresses
Volume
4
Issue
3
Start Page
436
End Page
451
Rights Holder(s)
SCOPUS
Bibliographic Citation
Stresses Vol.4 No.3 (2024) , 436-451
Suggested Citation
Satarug S., Vesey D.A., Yimthiang S., Khamphaya T., Pouyfung P., Đorđević A.B. Environmental Cadmium Exposure Induces an Increase in Systolic Blood Pressure by Its Effect on GFR. Stresses Vol.4 No.3 (2024) , 436-451. 451. doi:10.3390/stresses4030029 Retrieved from: https://repository.li.mahidol.ac.th/handle/20.500.14594/101471
Title
Environmental Cadmium Exposure Induces an Increase in Systolic Blood Pressure by Its Effect on GFR
Corresponding Author(s)
Other Contributor(s)
Abstract
Chronic exposure to the nephrotoxic metal pollutant, cadmium (Cd), has been associated with hypertension, but the mechanism by which it raises blood pressure is not understood. We hypothesize that exposure to Cd reduces the glomerular filtration rate (GFR), which in turn causes a rise in blood pressure. Data were collected from 447 Thai subjects with a mean age of 51.1 years, of which 48.8% had hypertension, 15.4% had diabetes, and 6.9% had an estimated GFR (eGFR) below 60 mL/min/1.73 m2 (low eGFR). More than half (58.8%) and 23.9% had moderate and severe tubular proteinuria, respectively. The mean blood and urinary Cd concentrations were 2.75 and 4.23 µg/L, respectively. Doubling of body burden of Cd increased the prevalence odds ratios (POR) for low eGFR and severe tubular proteinuria 41% and 48%, respectively. The POR for hypertension rose twofold in those with blood Cd levels of 0.61–1.69 µg/L or urinary Cd excretion levels ≥ 0.98 µg/g creatinine. In the hypertensive group, the eGFR was inversely associated with age (β = −0.517), the Cd excretion rate (β = −0.177), and diabetes (β = −0.175). By mediation analysis, an increase in SBP was attributable totally to the effect of Cd on GFR. Thus, blood pressure appeared to rise as GFR fell. This finding is consistent with the well-known role of the kidney in long-term blood pressure regulation, and explains a universally high prevalence of hypertension among patients with low eGFR.