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)

It is suggested that Tamm-Horsfall protein, a specific renal glycoprotein, may be involved in the pathogenesis of some renal diseases. In cadmium nephropathy and Fanconi syndrome (primary tubular diseases of the kidney) an increased excretion rate of Tamm-Horsfall protein has been observed. Balkan endemic nephropathy is a chronic tubulointerstitial disease of unknown etiology, most probably a primary disease of the kidney tubules with secondary reaction of the interstitial tissue. Investigation of Tamm-Horsfall proteinuria in Balkan endemic nephropathy has shown that subjects living in the area where this condition is prevalent have a significantly higher Tamm-Horsfall protein /creatinine ratio than those living in the control area where the condition has not been observed. Differences in this ratio among diseased, suspect and subjects "at risk" were not observed, despite differences in their glomerular filtration rates. But excretion of Tamm-Horsfall protein per litre of glomerular filtrate was significantly different among diseased, suspect and subjects "at risk" and significantly higher compared to control subjects. a relatively significant correlation was obtained between Tamm-Horsfall protein excretion rate and glomerular filtration rate as measured by creatinine clearance in both control and subjects living in the area of Balkan endemic nephropathy. Determination of Tamm-Horsfall protein in urine together with determination of proteinuria by electrophoresis on cellulose acetate membranes as a screening procedure, and by SDS -electrophoresis in polyacrylamide gell may be useful laboratory tests in detecting this nephropathy.
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PMID:Tamm-Horsfall protein in Balkan endemic nephropathy. 400 27

Urinary beta 2 microglobulin (beta 2m) estimation has been added to an existing pre-employment and periodic medical surveillance programme for cadmium workers. Pre-employment values were measured in 203 men not occupationally exposed to cadmium. The overall geometric mean was 76 microgram/l (adjusted to specific gravity 1016): a significantly higher level of 96 microgram/l was found in the specimens stored continually at -20 degrees C after voiding, compared with 73 microgram/l in specimens that thawed during transport. Sodium azide had been added to all specimen bottles. Employees exposed to cadmium pigments at various stages of their manufacture had no evidence of raised urinary beta 2m despite exposures above 50 microgram/m3 for up to 11 years. This is believed to be due to the insolubility of the compounds. Five known cases of cadmium induced proteinuria whose exposure ceased up to 15 years ago had raised urinary beta 2m concentrations. Moderately raised concentrations were found in seven others with a history of cadmium oxide exposure and in whom proteinuria has never been detected. The place of urinary beta 2m in the health care of cadmium workers is discussed and the question of correct management of a cadmium worker with a high beta 2m is raised.
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PMID:Urinary beta 2 microglobulin in the biological monitoring of cadmium workers. 616 78

Retinol-binding protein (RBP) in the Rhesus monkey had the same electrophoretic mobility, molecular weight, and common antigens as human RBP; beta 2-microglobulin protein (MG) had similar electrophoretic mobility and partial common antigens to human MG. After a prolonged oral administration of cadmium chloride to 10 monkeys over a period of 55 weeks, one monkey of the 30 mg Cd/day group indicated RBPuria and MGuria with the use of anti-human RBP and MG sera when proteinuria appeared. The immunological assay of low-molecular-weight proteins in urine was not applicable for the early detection of cadmium health effects in monkeys.
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PMID:Retinol-binding protein and beta 2-microglobulin in urine of cadmium-fed rhesus monkeys. 616 10

Natural history of cadmium health effects was studied on monkeys and rabbits given cadmium chloride orally or subcutaneously for a long period: 6 male monkeys were given pelleted food containing 100 micrograms Cd/g over a period of 180 weeks, 15 male rabbits pelleted food containing 300 micrograms Cd/g over a period of 24 weeks, 13 male rabbits daily subcutaneous injections at a dose level of 0.5 mg Cd/kg over a period of 44 weeks, and 23 rabbits subcutaneous injections at a dose level of 0.5 mg Cd/kg 6 times a week over a period of 21 weeks, respectively. Sodium dodecyl polyacrylamide gel electrophoresis and silver staining (detection limit of protein: 80 micrograms/dl) revealed that urinary protein of molecular weight 12,000 (probably beta 2-microglobulin) increased slightly prior to the appearance of proteinuria, glycosuria or aminoaciduria. Remarkable increase in urinary protein of molecular weight 12,000 was observed by Amidoblack 10 B staining (detection limit: 4 mg/dl) around the time when renal dysfunctions appeared. The above result might suggest that the remarkable increase in urinary beta 2-microglobulin is associated with renal dysfunctions, while the slight increase is caused by other mechanisms than renal dysfunctions.
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PMID:[Mechanism of beta 2-microglobulinuria in experimental chronic cadmium intoxication]. 619 Oct 63

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

In workers chronically exposed to cadmium and without signs of renal insufficiency, plasma proteins with molecular weight ranging from 11,800 to 450,000 are excreted in greater amount in urine. Increased urinary excretion of low and high molecular weight proteins can occur independently. Because of its greater stability in urine and provided a sensitive immunological technique is used, the determination of retinol-binding protein is a more practical and reliable test of proximal tubular function than beta 2-microglobulin. The evaluation of renal function of workers removed from cadmium exposure indicates that cadmium-induced renal lesions, albeit of slow progression, are not reversible when exposures ceases. In workers chronically exposed to cadmium or removed from cadmium exposure, metallothionein in urine is directly correlated with cadmium in urine but not with cadmium in blood or years of cadmium exposure. The association between cadmium in urine and metallothionein in urine is independent of the status of renal function and the intensity of current exposure to cadmium. Whereas the repeated IP injection of high doses of cadmium to rat gives rise to a mixed or tubular type proteinuria, the prolonged oral administration of cadmium results mainly in the development of a glomerular type proteinuria. The former is usually reversible after cessation of treatment whereas the latter is not. Circulating antiglomerular basement membrane antibodies have been found in man and in rat chronically exposed to cadmium. The pathogenic significance of this finding deserves further investigation.
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PMID:Characterization of cadmium proteinuria in man and rat. 637 88

The relationship between abnormal urinary findings and renal function was investigated for 33 Itai-Itai patients, 17 suspected patients, 235 subjects exposed to Cd and 41 subjects not exposed to Cd pollution. High correlation coefficients were observed between urinary findings and renal function in advanced cases of chronic cadmium poisoning, and multiple correlation coefficients between them are as high as 0.73 to 0.86. beta 2-microglobulin in urine also correlated closely with renal function and age in slight to moderate cases of cadmium poisoning. It is concluded that urinary findings such as proteinuria, glucosuria and low molecular weight proteinuria are good indicators of renal dysfunction in moderate to severe cases of chronic cadmium poisoning. In slight to moderate cases beta 2-microglobulin in urine has a close relation with renal dysfunction.
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PMID:Biologic indicators of cadmium nephrotoxicity in persons with low-level cadmium exposure. 637 89

Four groups of cadmium-exposed persons, from different workplaces and with different types of exposure, have been followed for periods of 9-20 years. In one group the total observation time is over 30 years, since they were included in Friberg's original study. The studies include determination of inulin or creatinine clearance, protein excretion and specific indicators of renal tubular dysfunction. The results indicate that once tubular dysfunction is established, it is irreversible, even when it is minor. In some persons it was noted that the development of renal dysfunction seemed to be a multistage process. The initial stage is characterized by an increased excretion of low molecular weight proteins like beta 2-microglobulin and ribonuclease. After a period of several years with no or low exposure, there was a relatively sharp increase in excretion of total proteins and albumin and a decrease in glomerular filtration rate. This is interpreted as being the result of further increases in renal concentration of cadmium and in spread of cadmium along the tubules. Metallothionein absorption in the tubules, its catabolism and synthesis must play an important role for the development and progress of the tubular dysfunction. It was not possible to show that a decrease in glomerular filtration rate occurs before low molecular weight proteinuria.
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PMID:Long-term observations on tubular and glomerular function in cadmium-exposed persons. 637 91

Cadmium has been shown to manifest its toxicity in human and animals by mainly accumulating in almost all of the organs and kidney is the main target organ where it is concentrated mainly in cortex. Environmental exposure of cadmium occurs via food, occupational industries, terrestrial and aquatic ecosystem. At molecular level, cadmium interferes with the utilization of essential metals e.g. Ca, Zn, Se, Cr and Fe and deficiencies of these essential metals including protein and vitamins, exaggerate cadmium toxicity, due to its increased absorption through the gut and greater retention in different organs as metallothionein (Cd-Mt). Cadmium transport, across the intestinal and renal brush border membrane vesicles, is carrier mediated and it competes with zinc and calcium. It has been postulated that cadmium shares the same transport system. Cadmium inhibits protein synthesis, carbohydrate metabolism and drug metabolizing enzymes in liver of animals. Chronic environmental exposure of cadmium produces hypertension in experimental animals. Functional changes accompanying cadmium nephropathy include low molecular weight proteinuria which is of tubular origin associated with excess excretion of proteins such as beta 2 microglobulin, metallothionein and high molecular weight proteinuria of glomerular origin (excretion of proteins such as albumin IgG, transferrin etc.). Recent data has shown that metallothionein is more nephrotoxic to animals. Cadmium is also toxic to central nervous system. It causes an alterations of cellular functions in lungs. Cadmium affects both humoral and cell mediated immune response in animals. Cadmium induces metallothionein in liver and kidney but under certain nutritional deficiencies like protein-calorie malnutrition and calcium deficiency, enhanced induction and greater accumulation of cadmium metallothionein has been observed.
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PMID:Molecular basis of cadmium toxicity. 638 35

The gastrointestinal absorption, transport, tissue deposition and excretion of cadmium was studied in adult male mice given a single oral LD50 dose of 109Cd-labeled CdCl2 alone or in combination with nitrilotriacetic acid (NTA), sodium tripolyphosphate (STPP) or ethylenediaminetetraacetic acid (EDTA). Blood, intestinal mucosa, liver and kidneys were analyzed for 109Cd at different times after exposure and the influence of the chelating agents on Cd binding to metallothionein and other tissue ligands was also studied. Acute toxicity was noted. Complex formation between Cd and EDTA was studied in solutions containing Cd:EDTA at 1:04 and 1:4 molar ratios. Adult male mice were exposed orally or by direct infusion into the stomach to either of the two solutions (containing an LD50 dose of Cd). Body retention and tissue deposition of Cd was recorded after 4 (direct infusion) or 21 days (oral exposure), and the mortality in different exposure groups observed. Adult male were also exposed to a low oral dose of 109Cd-labeled cadmium (0.5 mg/kg), followed by 18 months continuous administration of NTA, (500 ppm) STPP (500 ppm) or EDTA (50 ppm) in the drinking water or the chelating agent in combination with Cd (50 ppm), Cd alone (50 ppm) or deionized water. Whole-body retention of 109Cd, tissue deposition of 109Cd and total Cd and development of proteinuria were observed. When cadmium was given with an excess of EDTA, all Cd ions were bound in a 1:1 Cd-EDTA complex. Decreased acute toxicity was observed which was related to increased body elimination of cadmium. The Cd passes though the body still bound to EDTA and is excreted via the kidneys in this form. Similar results were found in mice exposed to Cd + NTA, while gavage of CD + STPP led to an initially decreased systemic uptake of Cd and thereafter to a prolongation of the biological half-time and thus a comparatively higher body retention of the metal. Cd may form a 2:1 complex with EDTA in the presence of excess cadmium. An increased retention and toxicity of cadmium was seen after direct infusion of this solution, while gavage resulted in a decreased toxicity. The effect of different chelating agents on acute cadmium toxicity and metabolism seemed to be due to changes in the stability of the administered chelate complexes, due to variation in pH and to the availability of metal binding ligands such as metallothionein in vivo. NTA, STPP and EDTA had no effect on the metabolism or toxicity of cadmium after long-term low dose oral exposure.
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PMID:Effects of chelating agents on oral uptake and renal deposition and excretion of cadmium. 642 73


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