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)

Anticoagulation in experimental GN has not uniformly reduced inflammation and prevented functional impairment. The observation that platelet thrombi are occasionally present in nephritic kidneys prompted the suggestions that platelet aggregation may play a fundamental role and that inhibition of aggregation may be of therapeutic value. To test this hypothesis, the effect of selective platelet depletion on acute IC GN in the rabbit was evaluated. IC GN was induced with bovine albumin, and platelet depletion with APS. Platelet depletion preceded proteinuria by more than 36 hr and was sustained for 5 days. Platelet accumulation within the nephritic kidney was quantitated with chromium-labeled platelets. The hemodynamic effect of parenteral administration of APS on the evolution of IC GN was assessed by comparing IV with IP administration. Thrombocytopenia in the absence of hypotension had no inhibitory effect on IC GN, nor was there platelet accumulation within the nephritic kidneys of the platelet-depleted animals. These results indicate that platelet aggregation is not essential in the pathogenesis of IC GN and that inhibition of platelet aggregation may be of little value.
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PMID:The influence of selective thrombocytopenia on immune complex glomerulonephritis. 15 43

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

A 46-year-old male chromium plating worker visited our hospital due to rhinorrhea, sneezing and cough with blood-tinged sputum for more than 10 years. He also had skin ulceration and chronic dermatitis on both hands Medical therapy was inefficient. Physical examinations revealed nasal septum perforation, severe inflammation of the nasopharynx cavity, and eczema of both hands. Laboratory investigations showed significant tubule proteinuria, enzymuria, hypercalciuria, etc. It is evident that renal tube damage was present in this patient. The blood chromium level was 25 ng/mL, and the 24-hour urine chromium excretion level was 2.8 mg/day. A pulmonary function test showed reduced functional residual capacity (FRC), which may be due to either long-term smoking or chromate acid exposure. To our knowledge this is the first case of renal tubal damage induced by chronic chromate intoxication Taiwan. Further evaluation of the occupational safety and health of chromium plating workers is needed on this island.
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PMID:[Chronic chromate intoxication with renal tubular damage--report of a case]. 135 17

A comparison of the effects of intraperitoneal and subcutaneous routes of administration of sodium dichromate on nephrotoxicity in rats was studied. Dichromate when injected subcutaneously (SC group) produced a higher degree of nephrotoxicity than when administered intraperitoneally (IP group). It caused severe progressive proteinuria followed by polyuria and glucosuria, reaching maximum levels at 3 days after treatment in the SC group, whereas it produced mild proteinuria without glucosuria in the IP group. The dose-dependent increases in blood urea nitrogen (BUN) and creatinine concentrations, shown in the SC group, were not observed in the IP group. However, between the two groups, there were no great differences in either the urinary excretion rate of chromium or the electrophoretic patterns of urinary protein in the day 1 urine specimens. Pretreatment of phenobarbital (PB) had no remarkable effect on the dichromate-induced nephrotoxicity. In contrast, it potentiated dichromate-induced hepatotoxicity, the indices of which were the elevation in serum alanine aminotransferase (ALT) activity and hepatic lipid peroxide formation. These results suggest that the dependence of dichromate-induced nephrotoxicity on the route of administration is related to the chemical forms of chromium reaching the kidney, and the necrotizing property of dichromate results from its metabolic fate in vivo.
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PMID:Nephrotoxicity of sodium dichromate depending on the route of administration. 178 35

Kidney disease is often cited as one of the adverse effects of chromium, yet chronic renal disease due to occupational or environmental exposure to chromium has not yet been reported. Occasional cases of acute tubular necrosis (ATN) following massive absorption of chromate have been described. Chromate-induced ATN has been extensively studied in experimental animals following parenteral administration of large doses of potassium chromate (hexavalent) (15 mg/kg body weight). The chromate is selectively accumulated in the convoluted proximal tubule where necrosis occurs. An adverse long-term effect of low-dose chromium exposure on the kidneys is suggested by reports of low molecular weight (LMW) proteinuria in chromium workers. Excessive urinary excretion of beta 2-microglobulin, a specific proximal tubule brush border protein, and retinol-binding protein has been reported among chrome platers and welders. However, LMW proteinuria occurs after a variety of physiologic stresses, is usually reversible, and cannot by itself be considered evidence of chronic renal disease. Chromate-induced ATN and LMW proteinuria in chromium workers, nevertheless, raise the possibility that low-level, long-term exposure may produce persistent renal injury. The absence of evidence of chromate-induced exposure may produce persistent renal injury. The absence of evidence of chromate-induced chronic renal disease cannot be interpreted as evidence of the absence of such injury. Rather, it must be recognized that no prospective cohort or case-control study of the delayed renal effects of low-level, long-term exposure to chromium has been published.
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PMID:Chromium-induced kidney disease. 193 54

Fifteen cases were selected for study from 100 consecutive cases of membranous nephropathy diagnosed by renal biopsy and light, immunofluorescence, and electron microscopy. The cases were chosen because during a pretreatment observation period ranging from 8 to 66 months (median, 18 months), the patients' disease state had progressed. Data gathered during this period served as a baseline against which to evaluate the effects of treatment with prednisone; thus, the patients served sequentially as their own controls. All but one of the patients had nephrotic syndrome, and 11 had renal insufficiency. Treatment with prednisone administered on alternate days was accompanied by decreasing proteinuria and increasing serum levels of albumin in all the patients. Healing, defined as proteinuria of no greater than 0.2 grams per 24 hours for at least a year with maintenance of normal creatinine clearance, occurred in eight patients. Renal function, judged by rate of creatinine clearance or level of creatinine in serum, improved in all 11 patients with renal insufficiency; in eight of these, normal function was attained. Poor renal function could not be attributed to diminished blood volume measured by chromium 51 red-blood-cell tag.
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PMID:Membranous nephropathy: high-dose alternate-day therapy with prednisone. 725 74

Certain chromium compounds are known to be nephrotoxic, but renal damage from long-term environmental or occupational exposure to chromium has not been documented. To detect possible preclinical renal damage, we tested the urine of 55 lifelong residents of an area contaminated with chromium landfill. The levels of four proteins were determined in urine samples: (1) human intestinal alkaline phosphatase, (2) tissue nonspecific alkaline phosphatase, (3) N-acetyl-beta-D-glucosaminidase, and (4) microalbumin. No elevated levels of proteins were found, and there were no significant correlations between urine protein and urine chromium concentrations. We concluded that long-term environmental exposure to chromium dust did not lead to tubular proteinuria.
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PMID:Absence of tubular proteinuria following environmental exposure to chromium. 875 13

Of 17 patients with idiopathic membranous nephropathy (IMN) and nephrotic syndrome, 9 were allocated to treatment with simvastatin (an HMG CoA-reductase inhibitor) and low cholesterol diet, and 8 to diet alone. At entry, the treatment and control groups did not differ in mean serum creatinines, chromium-labelled EDTA clearances, urinary protein/creatinine ratios, serum albumins, and lipid profiles. The mean follow up period (+/- SEM) in the treated group was 19.3 (+/- 4.4) months compared with 16.6 (+/- 5.9) months in the control group. At the end of the trial the fall in chromium-labelled EDTA clearances was similar (-1.27 versus -1.28 mls/min/months/1.73 m2) in the treatment and control groups respectively. The mean (+/- SEM) total and LDL-cholesterol had gone from 10.5 (+/- 0.94) and 8.02 (+/- 1) mmol/l to 5.2 (+/- 0.49) and 3.47 (+/- 0.44) respectively in the treated patients. Additionally the mean (+/- SEM) albumin and urinary protein/creatinine ratio went from 25.6 (+/- 2.4) gm/l and 0.52 (+/- 0.09) gm/mmol to 45.5 (+/- 2.8) and 0.13 (+/- 0.04) respectively. There was little change in total and LDL-cholesterol; albumin and urinary protein/creatinine ratio in the control group. This study supports the observation that lowering serum cholesterol in the nephrotic syndrome reduces proteinuria and increases serum albumin levels. No difference in the rate of decline in renal function could be demonstrated.
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PMID:A prospective clinical trial comparing the treatment of idiopathic membranous nephropathy and nephrotic syndrome with simvastatin and diet, versus diet alone. 890 5

Because subclinical renal disease may be aggravated during pregnancy--as reflected in the occurrence of proteinuria, for example--we investigated whether a subclinical glomerulonephritis (SG) in the non-pregnant rat (passive Heymann nephritis), a condition without proteinuria, is aggravated when the animals become pregnant and, if so, whether this is associated with a glomerular inflammatory reaction. SG was induced in non-pregnant rats 8 days before pregnancy. On day -1, part of the group of rats became pregnant. Three experiments were performed. In experiment 1, 4-hour urine albumin excretions and blood pressure (tail cuff) were measured. In experiment 2, the glomerular filtration rate (GFR) was measured with the chromium 51-labeled ethylenediaminetetraacetic acid method, while in experiment 3, parameters characteristic of a glomerular inflammation were studied. Experiment 1 revealed that non-pregnant rats with SG did not exhibit proteinuria. However, after the rats became pregnant, a significant proteinuria occurred, without an increase in systolic blood pressure. Experiment 2 revealed that the GFR did not increase in pregnant rats with SG, while experiment 3 showed that only pregnant animals exhibited a significant glomerular inflammation; this glomerular inflammation was characterized by intraglomerular influx of polymorphonuclear cells and monocytes. The results suggest that an SG in the rat may flare up during pregnancy. This exacerbation is characterized by proteinuria and coincides with a glomerular inflammatory reaction. It is suggested that proteinuria and the glomerular inflammatory reaction are causally related and promoted by the pregnant condition.
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PMID:Pregnancy aggravates proteinuria in subclinical glomerulonephritis in the rat. 1048 12

Studies suggest that cadmium is associated with several clinical complications, primarily renal dysfunction and bone disease, but also some cancers. Cadmium toxicity has been associated with clinical manifestations at exposure levels that are well below the limits set by the World Health Organization. Here I review the OSCAR study, which demonstrates an association between environmental and occupational cadmium exposure and renal tubular damage, as well as the Cadmibel study, a cross-sectional population study demonstrating an association of cadmium exposure with renal dysfunction. The paper also reviews the association of end-stage renal disease prevalence with occupational and environmental exposure to cadmium in the Swedish population of Kalmar County. Renal tubular damage was shown to develop at levels of exposure much lower than previously thought. Cadmium-induced tubular proteinuria is irreversible, and continued exposure may lead to glomerular damage with decreased glomerular filtration rate. Itai-itai disease in the Jinzu river basin is discussed, as are the implications of low-level cadmium exposure in the PheeCad project. Cadmium accumulates in bone and is associated with osteomalacia and osteoporosis. Other bone-seeking trace elements, such as chromium, lanthanum, strontium and zinc, are of concern because of low level environmental, occupational or clinical exposure. As techniques are perfected for detecting smaller amounts of trace elements in various tissues in the body, investigators are finding that the threshold for toxicity from trace elements is much lower than expected. Further research on cadmium is necessary to reveal the mechanisms of toxicity and true environmental and occupational exposure limits.
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PMID:Cadmium overload and toxicity. 1190 57


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