Sex-specific differences in early renal impairment associated with arsenic, lead, and cadmium exposure among young adults in Taiwan

Liao, Kai-Wei; Chien, Ling-Chu; Chen, Yang Ching; Kao, Ho-Ching

doi:10.1007/s11356-022-19521-3

Cited by 5 publications

(2 citation statements)

References 64 publications

(68 reference statements)

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“…In men, eGFR did not show a significant association with Cd exposure (β = −0.077), but hypertension (β =−0.203). In a Taiwanese study, an association of urinary Cd and a marker of tubular damage, Nacetyl-β-D-glucosaminidase (NAG), was observed in women only [42].…”

Section: Discussionmentioning

confidence: 99%

Environmental Cadmium Exposure Induces an Increase in Systolic Blood Pressure Partly by Its Effect on GFR

Satarug,

Vesey,

Yimthiang

et al. 2024

Preprint

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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.

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Section: Discussionmentioning

confidence: 99%

Environmental Cadmium Exposure Induces an Increase in Systolic Blood Pressure Partly by Its Effect on GFR

Satarug,

Vesey,

Yimthiang

et al. 2024

Preprint

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show abstract

“…However, when the kidney tubules become damaged or diseased, the urine β2-MG concentration increases. Therefore, elevated β2-MG in the urine signifies reduced tubular reabsorption and possible injury in kidney tubules [ 27 ]. In addition, under normal physiological conditions, trace levels of ALB pass through the glomerular basement membrane.…”

Section: Discussionmentioning

confidence: 99%

C/EBPβ–TFAM-Mediated NLRP3 Inflammasome Activation Contributes to Arsenic-Induced Rat Kidney Injury

Wang

Zhu

et al. 2023

Toxics

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Compelling evidence has demonstrated that arsenic (As) exposure is associated with kidney injuries. Given that inflammatory responses and immune imbalances are the root causes of several kidney diseases, this study investigated the potential mechanisms underlying NLRP3 inflammasome activation in As-induced kidney injury. A rat model of sub-chronic As exposure was established via oral administration of NaAsO2. The results revealed that urinary β-2-microglobulin (β2-MG), N-acetyl-β-D-glucosidase (NAG) and albumin (ALB) were increased in the As-exposed group, reflecting kidney impairment. Moreover, significant glomerular vacuole-like changes, tubular dilatation and inflammatory cell infiltration were observed. Meanwhile, the expression levels of neutrophil gelatinase-associated lipocalin (NGAL), IL-1β and IL-18 were enhanced in the kidney tissues of As-treated rats. Further, increased expression of NLRP3, ASC and caspase-1, which are NLRP3 inflammasome-associated proteins, were observed in the kidney tissues of rats in the As-treated groups. The expression levels of the NLRP3 upstream regulators C/EBPβ and TFAM were also elevated. These findings suggest that sub-chronic As exposure triggers inflammatory responses in rat kidney tissue and impairs kidney function. The underlying mechanisms may be related to the C/EBPβ–TFAM pathway and activation of the NLRP3 inflammasome pathway.

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Monitoring and evaluating the dietary risk of trace elements content in bottled and hand-shaken tea in Taiwan

Chin

Chien

Kao

et al. 2023

Environ Sci Pollut Res

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Sex-specific differences in early renal impairment associated with arsenic, lead, and cadmium exposure among young adults in Taiwan

Cited by 5 publications

References 64 publications

Environmental Cadmium Exposure Induces an Increase in Systolic Blood Pressure Partly by Its Effect on GFR

Environmental Cadmium Exposure Induces an Increase in Systolic Blood Pressure Partly by Its Effect on GFR

C/EBPβ–TFAM-Mediated NLRP3 Inflammasome Activation Contributes to Arsenic-Induced Rat Kidney Injury

Monitoring and evaluating the dietary risk of trace elements content in bottled and hand-shaken tea in Taiwan

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