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 effects of a new aldose reductase inhibitor, 7-fluoro-2-(N-methyl-N-carboxymethyl)sulfamoyl xanthone (BAL-ARI8, CAS 124066-40-6), on the diabetic complications of streptozotocin-induced diabetic rats were studied. The daily administration of BAL-ARI8 throughout the 8-week course of the experiment sharply decreased the sorbitol accumulation in the lens of the diabetic rats. The incidence of cataract formation was also reduced, being detected in only 45% of BAL-ARI8 treated animals, against the 100% of diabetic controls showing cataract after 8 weeks from diabetes onset. On the other hand, the serum glucose levels remained unchanged. In diabetic controls, there was about a 2.5-fold increase of the total protein urinary excretion during the 24 h. Treatment with BAL-ARI8 prevented up to 70% of this increase. Individual protein components were examined by polyacrylamide gel electrophoresis and quantitated by laser densitometric analysis. Diabetic-induced proteinuria primarily resulted from excretion of newly detected proteins with molecular weight in the range 30,000-60,000 D, together with an increase of albumin (25% of the total excretion) and the presence of new higher molecular weight proteins (greater than 66,000 D). BAL-ARI8 administration resulted in a shift of the protein profile back toward normality i.e. 73% of proteins with molecular weight below 30,000 D, 7.5% albumin and no proteins above 66,000 D. These results suggest that BAL-ARI8 may represent a therapeutic approach for the management of diabetic complications.
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PMID:Effects of a new aldose reductase inhibitor on diabetic complications in rats. 181 Feb 61

At the instance of a case of severe Hg-induced proteinuria the efficiency of a complex former therapy with sulfactin (BAL) is demonstrated, which led to the complete elimination of the protein excretion in the urine. For this other possibilities of a complex-forming therapy for hydrargyrism are discussed and consequences for the occupational-medical and clinical treatment are shown.
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PMID:[Treatment of mercury-induced organ damage]. 233 69

A patient with serum monoclonal gammopathy, Bence-Jones proteinuria, and bone marrow plasmacytosis underwent fiberoptic bronchoscopic study for evaluation of interstitial lung disease. Bronchoalveolar lavage fluid contained 47 percent plasma cells, which were monoclonal by immunoperoxidase staining. This is the first time BAL plasmacytosis has been demonstrated in a patient with a plasma cell dyscrasia.
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PMID:Bronchoalveolar lavage plasmacytosis in a patient with a plasma cell dyscrasia. 290 39

One hundred thirty children aged 1 to 8 years with blood lead levels greater than 50 micrograms/100 ml of whole blood (WB) and free erythrocyte protoporphyrin (FEP) concentration greater than 250 micrograms/100 ml of WB received 207 chelation treatments for plumbism. All chelation treatments consisted of CaNa2 ethylenediaminetetraacetic acid (EDTA) 25 mg/kg per dose every 12 hours and 2,3-dimercapto-1-propanol (BAL) 3 mg/kg per dose every four hours for five days. Seventeen children demonstrated transient doubling of pre-chelation treatment serum creatinine (less than or equal to 2.0 mg/100 ml) during or following chelation treatment; 5/17 also had mild proteinuria. Four children developed severe oliguric (greater than 250 ml/sq m/day) acute renal failure. Serum creatinine levels were elevated six to seven days after chelation treatment was started and reached maximal values of 3.9 to 8.4 mg/100 ml, three to six days later. Renal function returned to pre-chelation treatment values during the subsequent six to 18 days. In the 21 nephrotoxic patients and the 109 nontoxic patients there were no significant differences in age (3.8 +/- 0.6 vs 3.2 +/- 0.2 years), sex (61% vs 53% males), percent who received multiple chelation treatments (38% vs 30%), blood lead levels (85 +/- 5 vs 79 +/- 1 microgram/100 ml of WB), FEP (380 +/- 30 vs 382 +/- 18 micrograms/100 ml of WB), hemoglobin (11.5 +/- 0.4 vs 11.1 +/- 0.2 gm/100 ml, and pre-chelation treatment serum creatinine (0.46 +/- 0.06 vs 0.58 +/- 0.03 mg/100 ml). It was concluded that 13% of children with plumbism who received chelation treatments developed mild transient biochemical evidence of nephrotoxicity and another 3% developed acute renal failure characterized by oliguria four to eight days after chelation treatment was discontinued.
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PMID:Reversible nephrotoxic reactions to a combined 2,3-dimercapto-1-propanol and calcium disodium ethylenediaminetetraacetic acid regimen in asymptomatic children with elevated blood lead levels. 709 93