Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0033687 (proteinuria)
24,015 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Studies suggest that cadmium is associated with several clinical complications, primarily renal dysfunction and bone disease, but also some cancers. Cadmium toxicity has been associated with clinical manifestations at exposure levels that are well below the limits set by the World Health Organization. Here I review the OSCAR study, which demonstrates an association between environmental and occupational cadmium exposure and renal tubular damage, as well as the Cadmibel study, a cross-sectional population study demonstrating an association of cadmium exposure with renal dysfunction. The paper also reviews the association of end-stage renal disease prevalence with occupational and environmental exposure to cadmium in the Swedish population of Kalmar County. Renal tubular damage was shown to develop at levels of exposure much lower than previously thought. Cadmium-induced tubular proteinuria is irreversible, and continued exposure may lead to glomerular damage with decreased glomerular filtration rate. Itai-itai disease in the Jinzu river basin is discussed, as are the implications of low-level cadmium exposure in the PheeCad project. Cadmium accumulates in bone and is associated with osteomalacia and osteoporosis. Other bone-seeking trace elements, such as chromium, lanthanum, strontium and zinc, are of concern because of low level environmental, occupational or clinical exposure. As techniques are perfected for detecting smaller amounts of trace elements in various tissues in the body, investigators are finding that the threshold for toxicity from trace elements is much lower than expected. Further research on cadmium is necessary to reveal the mechanisms of toxicity and true environmental and occupational exposure limits.
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PMID:Cadmium overload and toxicity. 1190 57

It is well known that high cadmium exposure causes renal damage, osteoporosis and osteomalacia, whereas the dose-response relationships at low-level exposure are less well established. WHO estimated (1992) that a urinary excretion of 10 nmol/mmol creatinine would constitute a 'critical limit' below which kidney damage would not occur. Later, Belgian and Swedish studies have shown signs of cadmium induced kidney dysfunction in the general population already at urinary cadmium levels around 2-3 nmol/mmol creatinine. The Swedish OSCAR (OSteoporosis-CAdmium as a Risk factor) study comprised 1021 individuals, exposed to cadmium in the environment. Blood and urinary cadmium were used as dose estimates. Protein HC (alpha-1-microglobulin) was used as an indicator of renal tubular damage. Forearm bone mineral density (BMD) was assessed with DXA (dual energy x-ray absorptiometry) technique. The study showed that tubular proteinuria occurred at much lower levels of cadmium dose than previously known. A negative dose-effect relationship was found between cadmium dose and BMD for people at the age of 60 or older. In this age group, there was also a dose-response relationship, showing a three-fold increased risk of low BMD in the group with urinary cadmium over 3 nmol/mol creatinine, as compared to the lowest dose group. There was also evidence of an increased risk of forearm fractures with increasing cadmium levels in the population 50 years of age or older. The potential public health consequences of low level cadmium exposure should be recognized, and measures taken to reduce cadmium exposure to an absolute minimum.
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PMID:Low level cadmium exposure, renal and bone effects--the OSCAR study. 1568 54