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)

5(18.5%) of a group 27 coppersmiths exposed to cadmium fume had stone disease. When compared with a control group of assembly workers in the same factory they had evidence of renal impairment as shown by blood biochemistry and proteinuria. A greater tendency to liver damage was found in the coppersmiths. There was evidence that restrictive airways disease was more common in the coppersmiths than in the control group. Blood-cadmium concentrations were significantly higher in the coppersmiths and in the assembly workers than in a reference population.
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PMID:Clinical and biochemical abnormalities in coppersmiths exposed to cadmium. 7 55

For the range of exposure to heavy metals sustained by the different groups of workers, a significant increase in the urinary excretion of low and/or high molecular weight proteins was found in the workers exposed to cadmium or to lead + cadmium, but no in those exposed to lead only and those exposed to mercury. Our observations suggest that the classical "tubular" proteinuria induced by cadmium has two not necessarily concomitant components : a "tubular type" component with increased excretion of low molecular weight proteins and a "glomerular type" component with increased excretion of high molecular weight proteins.
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PMID:Urinary excretion of beta2-microglobulin and other proteins in workers exposed to cadmium, lead or mercury. 8 75

A study on the general population from both cadmium-polluted and control areas and on cadmium alloy workers indicates that beta 2-MG in urine is very closely correlated with aging, but it indicates an association with cadmium exposure. However, the age factor is stronger than cadmium exposre in both polluted and control areas among persons without clinical proteinuria. On the other hand, cadmium exposure is most likely correlated with beta 2-MG even in nonpolluted areas. Thus it seems that there is no noneffect level of cadmium dose in affecting the elevation of beta 2-MG in urine. beta 2-MG in serum indicated a very close correlation with cadmium in blood among cadmium alloy workers. This may suggest that an increase of beta 2-MG in both blood and urine in an early stage of cadmium exposure is caused by the increased level of beta 2-MG in blood, which may be a result of stimulation due to cadmium, but not necessarily by the clinical dysfunction of reabsorption of beta 2-MG in the renal.
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PMID:Increased urinary beta 2-microglobulin in cadmium exposure: dose-effect relationship and biological significance of beta 2-microglobulin. 9 Jun 11

The proteinuria rate and the relative clearances of beta 2-microglobulin, orosomucoid, albumin, transferrin and IgG were measured in forty-two workers exposed to cadmium and in seventy-seven control workers. A tubular type proteinuria with an increased excretion of beta 2-microglobulin and often also a glomerular type proteinuria with an increased excretion of orosomucoid, albumin, transferrin and IgG were observed mainly in workers exposed to cadmium for more than 25 years and whose cadmium concentration in blood exceeded 1 microgram Cd/100 ml and that in urine 10 microgram Cd/g creatinine. The glomerular dysfunction was also suggested by an increased plasma level of beta 2-microglobulin and creatinine. Both tubular and glomerular impairments occurred with the same prevalence and were not necessarily associated. The increased release of beta-galactosidase by the kidney suggested that cadmium can damage some epithelial cells.
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PMID:Renal excretion of proteins and enzymes in workers exposed to cadmium. 11 May 96

Ten male rhesus monkeys, each weighing 3.5 kg, were divided into four groups of 3, 3, 2, and 2, and were fed daily with 100 g pelleted food containing 300, 30, 3, and 0 ppm cadmium, respectively. Urine samples were collected every 2 weeks and blood samples every 4 weeks. One monkey each of the 300 and 30 ppm groups was autopsied for pathological examination and tissue cadmium determination at the week 24 of the experiment; the remaining 8 animals were killed after 55 weeks. The lowest exposed group (3 ppm) did not show any specific biological response to cadmium over a period of 55 weeks. In the 30 ppm group, no significant changes were observed for up to 24 weeks, although cadmium concentration in the renal cortex and urine at 24 weeks were 300 mug/g wet weight and 18 mug/l., respectively. Plasma urea nitrogen and urine protein (quantitative determination) increased after 30 and 36 weeks. At 55 weeks of the experiment, qualitative tests were negative for low molecular weight proteinuria and glycosuria, and the results remained normal for renal and liver function tests and blood analysis, although cadmium concentrations in the renal cortex of two monkeys were 460 and 730 mug/g wet weight and those in the liver were 110 and 160 mug/g wet weight, respectively. In the highest exposure group (300 ppm), urine cadmium increased to 250 mug/l. by 11 weeks, and urine retinol-binding protein, plasma GOT, GPT, and LDH increased after 12 weeks. Proteinuria (quantitative determination), glycosuria, aminoaciduria (panaminoaciduria), and erythrocytopenia were observed after 16 weeks, when urine cadmium was 500-900 mug/l. Hypohemoglobinopathy and proteinuria (qualitative determination) were observed after 20 and 24 weeks, while cadmium concentrations in the renal cortex and the liver were 760 and 430 mug/g wet weight at 24 weeks, respectively. Slightly depressed tubular reabsorption of phosphate, increased urine beta(2)-microglobulin, increased plasma urea nitrogen, and increased plasma alpha(2)-globulin fraction (electrophoresis) were observed between 28 and 30 weeks of the experiment. Creatinine clearance and plasma cholinesterase decreased after 47 and 54 weeks, respectively. Cadmium concentrations in the renal cortex and the liver of two monkeys at 55 weeks were 350 and 580 mug/g wet weight and 410 and 630 mug/g wet weight, respectively. Pathological examinations revealed denaturation, destruction, and regeneration of the epithelial cells in renal proximal tubules, but no pathological changes in osseous tissues. Critical cadmium concentration in the renal cortex was estimated to be 380 mug/g wet weight for low molecular weight proteinuria and 470 mug/g wet weight for proteinuria, glycosuria, and aminoaciduria. Critical concentration in the liver was also estimated to be 210 mug/g wet weight. The apparent biological half-time of cadmium in monkeys at autopsied stage was calculated to be 0.66, 6.4, 5.2, and 22.4 years for the 300, 30, 3, and 0 ppm groups, respectively.
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PMID:Effects of dietary cadmium on rhesus monkeys. 11 86

Dahl hypertension-resistant (R) and hypertension-sensitive (S) rats were used to determine whether cadmium-induced hypertension is dependent on genetic predisposition. In experiment I, 16 wk-old R and S rats of both sexes were injected with two doses of cadmium (1 and 2 mg/kg body wt, ip), whereas the controls received the same volumes of saline. Hypertension and renal vascular changes were observed in cadmium-injected S rats but not in R rats. The S females appeared more sensitive than S males to the hypertensinogenic effect of cadmium. In experiment II, groups of weanling female R and S rats were given 0, 1, 2.5, 5, or 10 mg cadmium/liter drinking water and fed either a low-salt (0.4% NaCl) or a high-salt (4% NaCl) diet for 28 wk. Cadmium produced cardiac hypertrophy (1 mg cadmium/liter) and hypertension associated with renal vascular changes (1--5 mg cadmium/ liter), and it enhanced proteinuria (1-10 mg cadmium/liter) in S rats on a low-salt diet. Also, the development of salt-induced hypertension was accelerated in cadmium-fed (1 and 2.5 mg/liter) S rats. These adverse effects of cadmium were not detected in R rats on either salt diet. In experiments I and II, cadmium concentrations in the kidneys and liver of S rats were higher (P less than 0.001) than in those of R rats. These data indicate that genetic differences influence the pathogenesis of cadmium-induced hypertension.
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PMID:Genetic influence on cadmium-induced hypertension. 15 9

Health examinations were performed in 147 people living in a cadmium-polluted area, Kosaka Town, Japan. 33 of 147 residents had some indications of proximal tubular dysfunction, such as renal glucosuria, tubular proteinuria, and aminoaciduria, and 10 of them were diagnosed as having multiple proximal tubular dysfunctions. Detailed examinations revealed that none of the cases had any causal diseases other than chronic cadmium poisoning. Residents' mean cadmium intake and mean urinary cadmium concentration were over 3 times as high as those in control areas. From these findings, renal lesions identified in these residents were concluded as chronic cadmium poisoning induced by environmental cadmium pollution.
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PMID:Cadmium-induced proximal tubular dysfunction in a cadmium-polluted area. 19 20

Female wistar rats, 170--190 g, were exposed for 90 days to cadmium oxide aerosols containing 25 and 50 microgram Cd/m3 and for 63 days to 100 microgram Cd/m3. Simultaneously female wistar rats, 170--190 g, were fed 25, 50, and 100 ppm cadmium in drinking water for 90 days. After inhalation and ingestion of the metal, there were comparable kidney cadmium levels, but higher liver and blood levels after oral uptake. Coincident with the higher blood cadmium concentrations, proteinuria was observed only after oral administration. Likewise, there was a significant decrease of serum iron after ingestion and no lowering of the serum iron after inhalation of the metal. The inhalation led to a marked dose dependent weight increase of the lungs, which was followed by an impairment of gas exchange. Obviously, after inhalative cadmium uptake of 90 days pulmonary changes precede renal damage.
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PMID:Early signs of oral and inhalative cadmium uptake in rats. 20 65

Recently we have reported that the proteinuria developed by workers exposed to cadmium was characterized by an increased excretion of high and low molecular weight proteins. These observations were confirmed experimentally. Female rats which were injected intraperitoneally with CdCl2 (1 mg Cd2+/kg) 5 times a week developed after 2 months of treatment a proteinuria qualitatively similar to that observed in workers exposed to cadmium. The analysis of this proteinuria by electrophoresis and gel filtration revealed an increased excretion of low and high molecular weight proteins. This animal study, which confirms previous observations on man, strengthens our hypothesis that the cadmium-induced proteinuria, classically considered as a tubular type proteinuria, is in fact a mixed type proteinuria, involving not only the tubule but also the glomerulus.
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PMID:Experimental confirmation in rats of the mixed type proteinuria observed in workers exposed to cadmium. 21 79

Cadmium is an inessential trace metal which accumulates in human tissues from contamination of food, water or air. The kidney is the critical organ following long-term, low-level absorption either by inhalation or ingestion; accumulation occurring in tubular epithelium in the form of a cadmium-metallothionein complex, giving rise to tubular dysfunction. In a group of 12 cadmium workers some of whom were followed for up to 16 years, tubular proteinuria, renal glycosuria, aminoaciduria, hypercalciuria and defects of concentration and acidification have been observed. Two men became recurrent renal stone formers and 1 man, who had nephrocalcinosis when first seen, later developed vitamin D-resistant osteomalacia. Renal tubular dysfunction following cadmium exposure may continue symptom-free for long intervals, but in a proportion of cases serious clinical effects may eventually develop.
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PMID:Cadmium nephropathy. 22 11


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