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)

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

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

Renal tubular dysfunction was induced in Hartley guinea pigs by injection of sodium aurothiomalate (gold) as manifested by excretion of tubular basement membrane (TBM) antigen and renal tubular epithelial (RTE) antigen in urine and tubular proteinuria. Following the tubular dysfunction, autoimmune tubulointerstitial nephritis (TIN) and/or immune complex nephropathy (ICN) developed in a large proportion of animals. TIN was associated with anti-TBM antibodies, and the histological features were characterized by tubular lesions with interstitial mononuclear cell infiltration, destruction of tubules, and interstitial fibrosis. In ICN, the glomerular lesions consisted of partial thickening of capillary walls and mesangial cellularity, and granular immune deposits were seen in the mesangial area and on capillary walls. Furthermore, electron-dense deposits were demonstrated in the mesangial area and in the glomerular basement membrane (GBM) by electron microscopy. Anti-RTE antibodies were detected in the sera and eluates from the kidney of animals with ICN. RTE antigens were also detected in the glomerular deposits by indirect immunofluorescence using anti-guinea pig RTE antibody. These results suggest that TBM and RTE antigens released from renal tubules damaged by a direct toxic action of gold may lead to antibody formation against these antigens and induce TIN and/or ICN.
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PMID:Experimental gold nephropathy in guinea pigs: detection of autoantibodies to renal tubular antigens. 308 39

The health effects of human exposure to cadmium are discussed with emphases on intake, absorption, body burden, and excretion; osteomalacia in Japan; hypertension; and proteinuria, emphysema, osteomalacia, and cancer in workers. Elevated blood pressure has not been observed as a result of excessive exposures to cadmium in Japan or the workplace. Renal tubular dysfunction and consequent proteinuria is generally accepted as the main effect following long-term, low-level exposure to cadmium. Studies of workers show that proteinuria may develop after the first year of exposure or many years after the last exposure. Proteinuria and deterioration of renal function may continue even after cessation of exposure. The immediate health significance of low-level proteinuria is still under debate. However, there is evidence that long-term renal tubular dysfunction may lead to abnormalities of calcium metabolism and osteomalacia. The few autopsy and cross-sectional studies of workers do not permit conclusions to be drawn regarding the relationship between cadmium exposure and emphysema. Retrospective and historical-prospective studies are needed to settle this important question. No conclusive evidence has been published regarding cadmium-induced cancer in humans. However, there is sufficient evidence to regard cadmium as a suspect renal and prostate carcinogen. Because of equivocal results and the absence of dose-response relationships, the studies reviewed should be used with caution in making regulatory decisions and low-dose risk assessments.
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PMID:Human health effects of exposure to cadmium. 352 15

The cadmium body burden, blood and urine cadmium concentrations, and renal function were studied in a group of 53 cadmium solderers. The results showed raised blood and urine cadmium concentrations and raised cadmium body burden in all workers (31) with more than five years exposure, with 27 having urine cadmium concentrations in excess of the proposed biological threshold of 10 nmol/mmol creatinine. Renal tubular dysfunction was found in 17 of the subjects with more than five years exposure and in one this was associated with glomerular dysfunction. These data indicate that cadmium body burden and frequency of tubular dysfunction in end users of cadmium may be as high as those found in smelters or production workers. Subjects with tubular dysfunction did not show greatly increased urine cadmium concentrations compared with those without dysfunction, supporting a previous suggestion that tubular dysfunction occurs before the wash out of cadmium from the kidney. At the time of our study, cadmium exposure stopped as cadmium free soldering rods were introduced. Repeat urine samples from 19 subjects, one to two years after exposure ended indicated that there was no further increase in the level of excretion of low molecular weight proteins, perhaps indicating that the tubular proteinuria does not increase or more severe renal dysfunction develop without continuous exposure.
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PMID:Occupational cadmium exposure in jig solderers. 377 36

The health effects of human exposure to cadmium are discussed with emphasis on intake, absorption, body burden, and excretion; osteomalacia in Japan; hypertension; and proteinuria, emphysema, osteomalacia, and cancer in workers. Elevated blood pressure has not been observed as a result of excessive exposures to cadmium in Japan or the workplace. Renal tubular dysfunction and consequent proteinuria is generally accepted as the main effect following long-term, low-level exposure to cadmium. Studies of workers show that proteinuria may develop after the first year of exposure or many years after the last exposure. Proteinuria and deterioration of renal function may continue even after cessation of exposure. The immediate health significance of low-level proteinuria is still under debate. However, there is evidence that long-term renal tubular dysfunction may lead to abnormalities of calcium metabolism and osteomalacia. The few autopsy and cross-sectional studies of workers do not permit conclusions to be drawn regarding the relationship between cadmium exposure and emphysema. Retrospective and historical-prospective studies are needed to settle this important question. No conclusive evidence has been published regarding cadmium-induced cancer in humans. However, there is sufficient evidence to regard cadmium as a suspect renal and prostate carcinogen. Because of equivocal results and the absence of dose-response relationships, the studies reviewed should be used with caution in making regulatory decisions and low-dose risk assessments.
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PMID:Human health effects of exposure to cadmium. 636 79

X-linked recessive nephrolithiasis (XRN) is a rare hereditary form of progressive renal failure characterized by (1) proximal tubular dysfunction and low molecular weight proteinuria; (2) hypercalciuria with nephrocalcinosis and nephrolithiasis. Because the clinical features are non-specific and variable, affected families in different parts of the world were initially thought to have several distinct syndromes. However, positional cloning of the relevant gene (CLCN5) demonstrated that these families have, in common, mutations affecting a chloride channel expressed throughout the renal tubule. To expand the description of early clinical and pathological manifestations of XRN, we describe three patients diagnosed in the 1st decade of life. Renal tubular dysfunction may be evident even in the neonatal period, hypophosphatemic rickets may develop in the first years of life, and nephrocalcinosis (but not nephrolithiasis) with glomerulosclerosis are consistent features in childhood. One of our patients is indistinguishable from the others on clinical grounds, yet no mutations of the coding regions of the CLCN5 gene were found, raising the possibility of genetic heterogeneity in the XRN syndrome.
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PMID:Clinical features of X-linked nephrolithiasis in childhood. 981 83