Effects of aging on cadmium concentrations and renal dysfunction in inhabitants in cadmium‐polluted regions in Japan

Abstract

The absorption of cadmium (Cd) may lead to Cd-related diseases such as renal tubular dysfunction and bone disease, and it is known to take around 10-30 years to reduce Cd concentrations to half their original levels. Urinary β -microglobulin (β -MG), N-acetyl-β-D-glucosaminidase (NAG), protein, glucose and albumin were used as indicators of renal dysfunction caused by Cd exposure. Our previous study found that urinary Cd concentrations had increased recently and that age was more strongly associated with urinary β -MG concentration than recent Cd body burden. Therefore, the purpose of the present study was to investigate the effect of aging on Cd concentrations and renal dysfunction. The Cd, β -MG, NAG, protein, glucose and albumin concentrations in the urine of 40 Japanese subjects (20 females and 20 males) environmentally exposed to Cd were collected. They lived in the Kakehashi River basin and were divided into three age categories: 50-69, 70-79 and 80-99 years. Significant differences in urinary Cd and β -MG concentrations were found among age groups, with urinary Cd levels tending to increase with age in both sexes. No significant correlations were found between urinary Cd and any indicators of renal dysfunction. The correlation between age, Cd and indicators of renal dysfunction was observed more clearly in females than in males. Age is more strongly correlated with indicators of renal dysfunction than Cd body burden. Copyright © 2017 John Wiley & Sons, Ltd.

An assessment of sensitivity biomarkers for urinary cadmium burden

“…including urinary N-acetyl-β-Dglucosidase (UNAG), urinary β 2 -microglobulin (Uβ 2 -MG), and urinary retinol binding protein (URBP) [15][16][17]. These three are likely valid biomarkers due to their origin in the renal tubules or in glomeruli breakage under urinary (UCd) pressure [18][19][20]. However, it is not yet clear which is the most sensitive to UCd.…”

Factors Affecting the Environmentally Induced, Chronic Kidney Disease of Unknown Aetiology in Dry Zonal Regions in Tropical Countries—Novel Findings

“…Proposed causes of CKDmfo include agrochemicals; fungi, algae, and microbial toxins; viruses and spirochetes; heavy metals (HMs); high-fructose diets; heat stress and chronic dehydration (due to excessive sweating, reduced water intake because of unpalatable hard water, and daily ingestion of illicitly brewed alcohol); abuse of non-steroidal anti-inflammatory agents [35]. Exposure to high doses of some of the above have been shown to cause acute renal failure with associated renal damage that can lead to chronic renal failure [36,37]. Here we proposed that CKDmfo/CKDu is caused by a combination of naturally present elements in drinking water-hard water, Ca 2+ , PO 4 3− , fluoride, etc., when the susceptibility conditions are prevalent.…”

“…However, the amount of phosphate present is water, such as in reservoirs are insufficient to cause renal damage or noticeable harm to humans and animals [12]. Toxins such as snake venom and high doses of HMs [e.g., cadmium (Cd), lead (Pb), or metalloid arsenic] also cause direct renal damage [37,40], whereas fluoride and aristolochic acid cause tubular cell harm via destruction of intracellular functions and oxidative damage [41], via caspase-mediated DNA damage, inflammation, cell apoptosis, and subsequent renal tissue fibrosis [42,43].…”

Review of polyphenol‐rich products as potential protective and therapeutic factors against cadmium hepatotoxicity

“…Cd is characterized by strong cumulative properties and an extremely long half‐life (one to three decades) in the human body. It accumulates mainly in the liver and kidneys, which are the critical target organs for this heavy metal (Baba et al, ; Phuc et al, ; Satarug, Baker, Reilly, Moore, & Williams, , ; Yoo et al, ). However, data on Cd concentration and xenobiotic‐induced changes in the liver of humans are very limited, as they come from the autopsy materials of people who died because of Cd poisoning or other random cases (trauma, suffocation, traffic accidents, natural death, etc.).…”

“…Population‐based studies on the harmful effects of Cd have been focused mainly on its nephrotoxic action. It has been stipulated that the kidney is the major organ damaged during prolonged low‐level exposure to this metal, while the liver has been considered as the critical target for high, but short‐term exposure to Cd (Brzóska, Gałażyn‐Sidorczuk, et al, ; Dudley et al, ; Phuc et al, ; Wang et al, ; WHO, ). However, in recent years, due to the forecasts that exposure to this toxic metal will rise in future decades (WHO, ) and the increasing rate of liver diseases (Estes, Razavi, Loomba, Younossi, & Sanyal, ), a growing interest has been focused on the risk of liver injury under low‐level environmental exposure to this xenobiotic (Hyder et al, ; Kang et al, ).…”