Cases reported "Cadmium Poisoning"

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1/3. Chronic overexposure to cadmium fumes associated with IgA mesangial glomerulonephritis.

    BACKGROUND: Cadmium is a metal used in the zinc, copper and steel industries, and in the manufacture of electric batteries and solar cells. Acute cadmium poisoning is characterized by irritation of the respiratory tract, while in chronic poisoning the main target organ is the renal tubule. AIMS: We report a patient with chronic work overexposure to cadmium, who presented a IgA mesangial glomerulonephritis with no respiratory or renal tubule involvement. Case report A 39-year-old patient was referred to our hospital for evaluation of a glomerular nephropathy. For the past 12 years he had worked as a welder, using cadmium electrodes. The patient had no respiratory symptoms and the chest X-ray was normal. Tests showed a proteinuria of 2 g in 24 h with microhaematuria [150 red blood cells/high power field (rbc/hpf)], with preservation of the renal function (creatinine clearance of 137 ml/min). The concentrations of cadmium in blood and urine were 45 micro g/l and 25 micro g/g creatinine, and an environmental study showed that levels of cadmium in the workplace were 52 micro g/m(3). A renal biopsy showed an IgA mesangial glomerulonephritis. The patient ceased to work with cadmium, and 1 year later cadmium levels had decreased and renal function was found to be stable. CONCLUSIONS: IgA mesangial glomerulonephritis is a disease of unknown aetiology which has been associated with other diseases. Chronic overexposure to cadmium may contribute to the development of this nephrophathy.
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2/3. Cadmium-induced osteopathy: clinical and autopsy findings of four patients.

    Clinical and autopsy findings of 4 patients with chronic cadmium toxication by peroral uptake of cadmium are reported. Cadmium toxication was liable to occur in multiparous postmenopausal women, and it began with proteinuria, glycosuria, lumbago and bone pain. Then, renal function gradually decreased being accompanied with renal tubulopathy. autopsy disclosed renal tubulopathy, which consisted of the flattening of the epithelium of proximal convoluted tubules at the peripheral portion and the mild thickening of the tubular basement membrane. There was no primary change in the glomerulus and renal interstitium. osteomalacia was observed in the vertebrae and several other bones. The degree of osteomalacia was in good agreement with chronic renal tubular dysfunction. A decrease of the estrogen content, in addition to renal tubulopathy due to biological saturation of cadmium, seems to play an important role in the pathogenesis of cadmium-induced osteomalacia.
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3/3. Cadmium-induced osteomalacia.

    The detailed study of a battery plate maker, who had worked with cadmium for 36 years, showed that proteinuria, typical of renal tubular dysfunction, had been observed for 25 years and during the last 12 years of his life the patient had suffered increasing disability from gross bone disease. Several bone biopsies and detailed metabolic studies showed typical severe osteomalacia, which responded well initially to calcium and vitamin D treatment. Examination of the liver both in life and after death showed a gross excess of cadmium. This was also found in the kidneys after death. Previously unreported changes were present in the bones, especially the lumbar vertebrae which were probably more the result of gross bone deformity than cadmium deposition. The mechanism of development of the severe acquired fanconi syndrome was thought to be a combination of dietary calcium and vitamin d deficiency and impaired calcium absorption from abnormal vitamin D synthesis, related to the cadmium deposition in the renal tubules, which also caused the defect in renal tubular reabsorption.
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