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)

The immune status of the individual is an additional variable which has to be taken into account in any consideration of factors which influence the metabolism and toxicity of metals. The commonly occurring phenomena are described resulting from increased cellular reactivity to platinum, mercury, gold, nickel, chromium, and beryllium, and an attempt has attempt has been made to classify these into the four types of immune response. The clinical effects can be very varied, giving rise to conjunctivitis, rhinitis, asthma, urticaria, contact dermatitis, proteinuria, nephrotic syndrome or blood dyscrasia. Of these effects, cutaneous hypersensitivity is the most common, affecting both industrial and general population groups. Metal compounds used in therapeutics and metals used in prostheses have also been responsible for hypersensitive reactions.
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PMID:The role of hypersensitivity and the immune response in influencing susceptibility to metal toxicity. 72 Feb 96

The kidney is considered the critical organ following long term occupational or environmental exposure to cadmium. Tubular dysfunction in the form of low molecular weight proteinuria is the earliest manifestation of cadmium nephrotoxicity. The current acceptable critical concentration of cadmium in the urine is 10 ug Cd/g creatinine. The aim of this paper is to identify the presence of tubular dysfunction among workers with less than 10 ug Cd/g creatinine. The exposed group of 92 workers were from a nickel-cadmium battery factory. The control group of 122 workers were factory and sedentary office workers with no known history of exposure to nephrotoxic agents. The urinary excretion of N-acetyl-D-glucosaminidase (NAG), beta-2-microglobulin (beta 2m) and alpha-1-microglobulins (alpha 1m) were measured from morning spot urine samples. The age, sex and race adjusted NAG and alpha 1m showed increasing trend with rising urinary cadmium levels. Levels were significantly raised when the urinary cadmium was above 5 ug Cd/g creatinine. A similar trend was seen with increasing length of exposure. Renal tubular dysfunction is present among cadmium exposed workers with levels below the current critical concentration.
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PMID:Renal tubular function of cadmium exposed workers. 128 95

We report a patient with documented IgA nephropathy in whom microscopic hematuria, proteinuria, and hypertension first occurred after placement of nickel alloy base dental crowns. Progressive proteinuria culminating in nephrotic-range proteinuria occurred parallel to increased nickel placement and dramatically resolved following nickel alloy removal. That immunologic alterations occur as a result of nickel exposure has already been suggested by the common occurrence of nickel contact dermatitis, often exacerbated by intraoral nickel placement, increased carcinogenesis in nickel refinery workers, and animal models of nickel-associated carcinogenesis. Our patient may represent an example of nickel-induced sensitization and associated IgA glomerulopathy. Further study of patients with immune-mediated glomerulopathy with attention to dental nickel exposure appears indicated.
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PMID:IgA nephropathy associated with dental nickel alloy sensitization. 406 6

The effect of nickel on cadmium nephro-toxicity and hepato-toxicity in rats was investigated. The administration of nickel (6 mg per kg, i.p., three days) or cadmium (6 mg per kg, i.m., once) significantly enhanced the urinary excretion of alkaline phosphatase (ALP), lactate dehydrogenase (LDH), glutamate oxaloacetate transaminase (GOT), amino acids, and proteins. In addition, it increased the activity of serum ALP, GOT, and glutamate pyruvate transaminase (GPT). These biochemical alterations in urine and serum were used as a measure of kidney and liver damage. Cadmium-induced enzymuria, proteinuria, amino aciduria and increase in the activity of serum enzymes were significantly less marked in animals pretreated with nickel than in controls. However, the accumulation of cadmium in kidneys and liver and its urinary excretion were unaffected by nickel pretreatment. The results suggest protection by nickel against cadmium nephro- and hepato-toxicity.
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PMID:Preventive effects of nickel on cadmium hepatotoxicity and nephrotoxicity. 647 83

Pretreatment with nickel has earlier been shown to protect against cadmium intoxication. The effect of cadmium pretreatment on the nephro- and hepatotoxicity of nickel has been investigated. The administration of cadmium (6 mg/kg, i.m., once) to rats significantly enhanced urinary excretion of ALP, LDH, GOT, amino acids and proteins and increased the activity of serum ALP, GOT, and GPT, while the administration of nickel (6 mg/kg, i.p., 3 days) altered these parameters less significantly. These changes in urine and serum were used as a measure of renal and hepatic damage. The administration of nickel for three days, one week after cadmium treatment, caused significantly more marked enzymuria, aminoaciduria, proteinuria and an increase in the activity of serum enzymes than induced by either of them individually. However, cadmium pretreatment had no influence on urinary excretion or hepatic uptake of nickel, but increased renal uptake of nickel on the fourth day. The results suggest that cadmium enhances the nephro- and hepatotoxicity of nickel.
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PMID:Effect of cadmium pretreatment on nickel toxicity. 653 85

The extent of cadmium exposure was studied in a cadmium-nickel battery factory and 8 PVC factories using cadmium stabilisers in the compounding of PVC. A total of 101 cadmium-exposed workers and 21 control subjects matched by sex, age, ethnic group and smoking history was investigated. Blood and urine cadmium levels were considerably elevated in the battery workers but were not raised in the PVC workers. These findings were consistent with the results of cadmium-in-air assessments. Among the female battery workers, urine cadmium excretion increased significantly with employment time. There was good correlation between blood and urine cadmium levels among the female subjects. A significant association between blood cadmium levels and prevalence of chest pain was also noted among the females. No low molecular weight proteinuria was detected, but two female battery workers had slight albuminuria and one male PVC worker had glucosuria but had abnormal GTT results.
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PMID:Study on workers exposed to cadmium in alkaline storage battery manufacturing and PVC compounding. 707 22

A redundant nickel/cadmium battery worker was investigated for non-specific fatigue after completing five years in the industry. Sensitive techniques for in-vivo organ cadmium measurement showed a moderate accumulation in the liver but a very large concentration in the kidneys. Despite this, overall glomerular and tubular function were not impaired. It was concluded that the mechanism of proteinuria observed in some cadmium workers is obscure and not clearly related to the degree of kidney saturation with cadmium.
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PMID:Renal cadmium overload without nephrotoxicity. 723 44

The elution profile of urine from rats given 63Ni i.p. using a Sephadex G-25 column was studied to investigate the chemical form and pattern of nickel (Ni) excretion. Ni was excreted probably as a mixture of complexes with chemical constituents of urine (molecular weight 200-250) within 24 h after 63Ni injection. 63Ni increased significantly the excretion of proteins, absorbing at 280 nm, which were not associated with Ni. The administration of N-acetyl-DL-penicillamine 24 h after 63Ni injection increased significantly the urinary excretion of the metal and restored proteinuria during the next 24 h. It could not be ascertained whether N-acetyl-DL-penicillamine enhanced urinary excretion of 63Ni by forming an excretable complex or by modifying the excretory pathway.
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PMID:Pattern of urinary 63Ni excretion in rats. 746 50

A 44-year-old patient died from amyotrophic lateral sclerosis (ALS) after nine years of heavy exposure to cadmium (Cd) in a nickel cadmium (Ni-Cd) battery factory. Two years after starting work he and co-workers had experienced pruritus, loss of smell, nasal congestion, nosebleeds, cough, shortness of breath, severe headaches, bone pain, and proteinuria. Upper back pain and muscle weakness progressed to flaccid paralysis. EMG findings were consistent with motor neuron disease. Cd impairs the blood-brain barrier, reduces levels of brain copper-zinc (Cu-Zn) superoxide dismutase (SOD), and enhances excitoxicity of glutamate via up-regulation of glutamate dehydrogenase and down-regulation of glutamate uptake in glial cells. High levels of methallothionein, a sign of exposure to heavy metals, have been found in brain tissue of deceased ALS patients. The effects of Cd on enzyme systems that mediate neurotoxicity and motor neuron disease suggest a cause effect relationship between Cd and ALS in this worker.
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PMID:Amyotrophic lateral sclerosis in a battery-factory worker exposed to cadmium. 1137 40

Young male albino mice of Swiss strain were exposed to nickel by oral route of 20 mg nickel sulfate/kg body weight for 5 d/wk for 6 mo. A decrease in normal (testosterone-dependent) proteinuria was shown, and morphological examination of the seminal vesicles revealed a lower weight and smaller size as well as a histological indication of lower secretory activity of the epithelium compared to controls. The findings are consistent with a theory implying a decreased testosterone activity in nickel-treated animals.
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PMID:Seminal toxicity of nickel sulfate in mice. 1169 69


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