Version 1
: Received: 13 May 2024 / Approved: 14 May 2024 / Online: 14 May 2024 (08:34:57 CEST)
How to cite:
Satarug, S.; Vesey, D. A.; Yimthiang, S.; Khamphaya, T.; Pouyfung, P.; Buha Đorđević, A. Environmental Cadmium Exposure Induces an Increase in Systolic Blood Pressure Partly by Its Effect on GFR. Preprints2024, 2024050937. https://doi.org/10.20944/preprints202405.0937.v1
Satarug, S.; Vesey, D. A.; Yimthiang, S.; Khamphaya, T.; Pouyfung, P.; Buha Đorđević, A. Environmental Cadmium Exposure Induces an Increase in Systolic Blood Pressure Partly by Its Effect on GFR. Preprints 2024, 2024050937. https://doi.org/10.20944/preprints202405.0937.v1
Satarug, S.; Vesey, D. A.; Yimthiang, S.; Khamphaya, T.; Pouyfung, P.; Buha Đorđević, A. Environmental Cadmium Exposure Induces an Increase in Systolic Blood Pressure Partly by Its Effect on GFR. Preprints2024, 2024050937. https://doi.org/10.20944/preprints202405.0937.v1
APA Style
Satarug, S., Vesey, D. A., Yimthiang, S., Khamphaya, T., Pouyfung, P., & Buha Đorđević, A. (2024). Environmental Cadmium Exposure Induces an Increase in Systolic Blood Pressure Partly by Its Effect on GFR. Preprints. https://doi.org/10.20944/preprints202405.0937.v1
Chicago/Turabian Style
Satarug, S., Phisit Pouyfung and Aleksandra Buha Đorđević. 2024 "Environmental Cadmium Exposure Induces an Increase in Systolic Blood Pressure Partly by Its Effect on GFR" Preprints. https://doi.org/10.20944/preprints202405.0937.v1
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). The mean blood and urinary Cd concentrations were 2.75 and 4.23 µg/L, respectively. The prevalence odds ratio (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). Mean eGFR in the normotensive group was 7.5 mL/min/1.73 m2 higher than the hypertensive with a similar Cd body burden. Mean systolic blood pressure (SBP) in those with low or medium eGFR plus heavy Cd body burden was 9.5 mmHg higher than those with the same Cd body burden and a normal eGFR. By mediation analysis, a 22.7% increase in SBP and a 5% increase in diastolic blood pressure (DBP) were attributable to the effect of Cd on GFR. Thus, a rise of blood pressure appears to be a consequence of GFR loss due to Cd-induced kidney damage. This finding is consistent with a well-known role of the kidney in long-term blood pressure regulation.
Copyright:
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.
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