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 hydroxyl radical scavengers dimethylthiourea (DMTU), sodium benzoate, and dimethylsulfoxide (DMSO) were administered to rats before doxorubicin hydrochloride (ADR) (5 mg/kg, IV) to probe the role of free radicals in mediating proteinuria in doxorubicin hydrochloride nephrosis (AN). Because ADR stimulates free radical production, the role of renal glutathione was also evaluated; glutathione metabolism is involved in tissue detoxification processes. DMTU administration to rats with AN caused a significant (p less than 0.01) reduction in their proteinuria after 7 days (52.84 +/- 13.21 mg/24 hours) when they were compared with ADR controls (155.81 +/- 20.16 mg/24 hours). In similar fashion, their urine albumin excretion was also significantly reduced when compared with that of ADR controls (11.13 +/- 2.75 mg/24 hours vs 32.08 +/- 4.14 mg/24 hours; p less than 0.01). DMTU-treated rats also had significantly (p less than 0.001) reduced urinary protein and albumin excretion at 14 days when compared with rats that received ADR alone. The urinary excretion of lysozyme and N-acetyl-glucosaminidase, markers of renal tubular injury, were significantly increased after 7 or 14 days in rats with AN, despite DMTU treatment. Creatinine clearance was significantly reduced (p less than 0.05) in rats receiving ADR alone (0.223 +/- 0.011 ml/min/100 gm) when compared with that in normal controls (0.331 +/- 0.027 ml/min/100 gm) or DMTU-treated rats (0.289 +/- 0.035 ml/min/100 gm). Unlike DMTU, neither sodium benzoate nor DMSO reduced proteinuria in rats with AN.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Amelioration of glomerular injury in doxorubicin hydrochloride nephrosis by dimethylthiourea. 165 68

The mechanism of cellular processes responsible for proteinuria induced by adriamycin (ADR) remains unclear. In this study, we examined whether oxygen radicals contribute to the development of proteinuria in ADR-induced nephrosis. The peak concentration of malondialdehyde (MDA) of kidney was found on 8th day after ADR treatment in rats. ADR-treated rats received either superoxide dismutase (SOD, scavenger of O2-, catalase (CAT, scavenger of . H2O2) or dimethyl sulfoxide (DMSO, scavenger of OH). The SOD, CAT or DMSO treated groups had a significant suppression of urinary protein excretion, serum and renal MDA compared to ADR control group. There were also less severe renal morphologic changes in the former three groups vs the ADR controls. These data provide indirect evidence that oxygen radicals generated by ADR are important mediators of ADR-induced proteinuria.
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PMID:Role of oxygen radicals in adriamycin-induced nephrosis. 211 39

We examined the effect of the administration of different oxygen radical scavengers on the development of glomerulonephritis induced by cationic bovine gamma-globulin (cBGG). Treatment with the H2O2 scavenger catalase or the superoxide anion (O2-) scavenger superoxide dismutase (SOD) did not significantly reduce proteinuria. In contrast, treatment with the hydroxyl radical (OH.) scavengers dimethyl sulfoxide (DMSO) or dimethylthiourea resulted in significant decrements in proteinuria, from 156 +/- 20 mg/24 hours in saline solution--treated control rats to 70 +/- 17 mg/24 hours (p less than 0.05) and 37 +/- 10 mg/24 hours (p less than 0.01) in DMSO- and dimethylthiourea-treated rats, respectively. Therapy with DMSO for 5 days after induction of glomerular disease also resulted in amelioration of proteinuria, 10.0 +/- 5.0 mg/24 hours versus saline solution-treated rats, 67.6 +/- 16.2 mg/24 hours (p less than 0.005). OH. scavenger therapy did not influence glomerular morphology, glomerular immunoglobulin G (IgG), or complement deposition, or creatinine clearances of rats with glomerulonephritis. Furthermore, there were no significant differences in serum levels of C3 and C5 or anti-BGG antibody production between DMSO-treated rats and control rats. None of the radical scavengers administered altered the enhanced glomerular thromboxane synthesis characteristic of this model. Our results suggest that OH. generation mediates in part glomerular injury in cBGG-induced glomerulonephritis.
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PMID:Hydroxyl radical scavengers ameliorate proteinuria in rat immune complex glomerulonephritis. 246 May 71

The effect of treatment with indomethacin on the ability of dimethyl sulfoxide (DMSO) to reduce proteinuria in rats with passive Heymann's nephritis (PHN) was studied. PHN rats treated with DMSO alone excreted significantly less protein by day 14 than PHN rats treated with buffer or with indomethacin alone. Rats treated with DMSO excreted 19 +/- 6.0 mg protein/24 hr, and those treated with DMSO and indomethacin excreted 161 +/- 27.4 mg protein/24 hr (P less than 0.001). Rats treated with DMSO alone had significantly higher serum albumin and significantly lower serum cholesterol and triglyceride concentrations than those given the two drugs together. Glomerular deposits of C3 were reduced in DMSO-treated rats, but serum C3 concentrations and rat antirabbit serum antibody titers were similar in the two groups. When a higher dose of indomethacin (5 mg/kg) plus DMSO was used, protein excretion was significantly reduced. Rats treated with DMSO and acetylsalicylic acid (ASA) (37 mg/kg/day) or DMSO and meclofenamate (5 mg/kg/day) did not have a significant reduction in protein excretion compared with untreated controls. High-dosage indomethacin alone did not reduce proteinuria. Low doses of nonsteroidal anti-inflammatory agents therefore appear to block the effect of DMSO on proteinuria. This was in marked contrast to the finding of reduction of proteinuria induced by larger doses of indomethacin (5 mg/kg) plus DMSO. DMSO did not reduce proteinuria in rats with nephrosis induced by puromycin of aminonucleoside.
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PMID:Interactions of dimethyl sulfoxide and nonsteroidal anti-inflammatory agents in passive Heymann's nephritis. 293 60

Dimethylsulfoxide was given to NZB/W F1 female mice from age 10 weeks to see if proteinuria and glomerular injury could be reduced. Twenty mice were randomly assigned to saline or DMSO treatment groups and the following studies were done: urine protein determination, serum concentrations of creatinine, IgG, C3, and albumin; and ANA titers. Kidney tissue were studied by light, immunofluorescent and electron microscopy. DMSO-treated mice had significant reductions in protein excretion at 5 and 6.5 months of age; in urine protein/creatinine ratio at 6.5, 7, and; 7.5 months; in serum C3 at 7.5 months; and in serum creatinine concentration. There were no significant differences among serum IgG, nor among the ANA titers. Histopathologic studies revealed nearly normal kidneys in 5/6 DMSO-treated mice whereas 4/8 controls had severe mixed membranous and membranoproliferative glomerulonephritis. Ultrastructural studies revealed mesangial, subendothelial, and subepithelial deposits and membranous transformation of the glomerular capillary wall. DMSO therefore appears capable of ameliorating glomerular injury in NZB/W F1 mice.
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PMID:Amelioration of murine lupus nephritis by dimethylsulfoxide. 349 77

Colchicine was given to rats in the heterologous phase of passive Heymann nephritis to see whether this drug could reduce proteinuria. Treatment with 0.06 mg/day for 14 days caused significant reductions in proteinuria and albuminuria. Administration of dimethyl sulfoxide (DMSO) alone or in combination with colchicine also reduced protein and albumin excretion. In a long-term experiment, rats treated with colchicine had significantly less proteinuria. After stopping therapy, urine protein excretion was similar to controls. No differences in glomerular C3 and IgG deposition were found between treated and control rats 24 h, 3,7 and 14 days after immunization. Depressed serum C3 levels were measured at 24 h in colchicine-treated rats. No difference in serum-circulating immune complexes was detected between the two groups. Concurrent administration of indomethacin and colchicine to rats with passive Heymann nephritis (PHN) partially reversed the reduction in proteinuria and albuminuria seen in rats treated with colchicine alone. The G.F.R, however, was significantly reduced in colchicine-treated rats as well as in rats treated with colchicine and indomethacin. Serum cholesterol and triglyceride levels were significantly lower in colchicine-treated rats than in controls. Serum cholesterol concentrations in rats given both colchicine and indomethacin were similar to control values. These findings suggest that colchicine reduces urine protein and albumin excretion, and hyperlipidemia in PHN. The finding that indomethacin partially blocks the effects of colchicine suggests that renal prostaglandin stimulation by colchicine may have been involved in the reduction in proteinuria.
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PMID:Colchicine reduces proteinuria in passive Heymann nephritis. 360 Sep 7

Dimethyl sulphoxide (DMSO), 3 g/kg body weight, administered daily by the intraperitoneal route, potentiated the proteinuria and formation of tubular casts in aminonucleoside of puromycin (PA) induced nephrosis in Sprague-Dawley rats. The effect was evident at 4 as well as 8-9 days following PA administration. In the absence of PA, DMSO did not induce proteinuria or cast formation. The mechanism by which DMSO enhanced proteinuria and cast formation is not known.
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PMID:DMSO potentiates aminonucleoside of puromycin nephrosis in rats. 369 23

Passive Heymann nephritis, a model of immune complex nephritis, was produced in rats by injection of rabbit antibrush border membrane vesicle antibodies to examine the effect of treatment of epimembranous glomerulonephritis with dimethyl sulfoxide. Administration of DMSO twice a day, 5 days a week for 4 weeks significantly reduced protein excretion in the autologous phase of the model. This beneficial effect occurred in animals in which treatment was started a day after administration of the antibody and persisted for 4 weeks after treatment was discontinued. Serum triglyceride concentrations were significantly decreased, whereas, BUN, serum cholesterol, and globulin levels were significantly, but not reproducibly, reduced. That DMSO did not reduce proteinuria to normal values in rats treated after proteinuria was well established, but was able to reduce proteinuria significantly. Treatment of normal rats and those with nephrotoxic serum nephritis did not reduce protein excretion. Glomeruli of rats with passive Heymann nephritis treated with DMSO studied by immunofluorescent microscopy appeared to have less fluorescence for IgG than control rats, but these differences were not significant. However, C3 deposits were significantly decreased in treated rats, but only during the first week of the disease and in vitro C3 fixation was also significantly reduced in glomeruli of rats that had been treated with DMSO. There was very little effect on serum complement activity: CH50 was reduced only on day 1 of treatment, whereas the alternate pathway activity and serum C3 concentration were unaffected. DMSO may therefore reduce protein excretion, in part, by inhibiting C3-dependent proteinuria. These studies indicate that DMSO is capable of significantly reducing protein excretion in rats with passive Heymann nephritis and that its action may involve reduction of complement deposition within the glomeruli during the heterologous phase. Toxic effects included a 2.5% mortality and decreased weight gain while being treated with larger doses of DMSO. Treatment with a much smaller dose succeeded in reducing proteinuria significantly without affecting weight gain. There was no evidence of drug-induced liver or renal damage.
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PMID:Reduction of protein excretion by dimethyl sulfoxide in rats with passive Heymann nephritis. 647 64

There is no specific therapy for primary amyloidosis, and acquired generalised amyloidosis can be treated only if the underlying disease is eliminated. In this study we have investigated the role of colchicine therapy in primary amyloidosis, and dimethylsulphoxide (DMSO) in leprosy associated secondary amyloidosis. No effect on creatinine clearance or 24 h proteinuria could be observed in the patients with primary amyloidosis. In the DMSO group renal function was considerably improved in 3 patients with moderate renal failure but not in those with severe renal impairment (creatinine clearance less than 10 ml/min). Serum SAA determinations were not particularly informative. These findings point to a beneficial effect of DMSO in human secondary amyloidosis when given at an early stage of renal involvement.
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PMID:DMSO and colchicine therapy in amyloid disease. 674 5

Familial Mediterranean fever was diagnosed in a 34-year-old Turkish patient with severe nephrotic oedema. Immunohistochemical classification of a biopsy specimen showed amyloidosis of the AA-type. There was a definite increase of serum amyloid-A-protein (SAA). The typical recurrent fever, attacks of abdominal pain with symptoms of subileus and joint swelling could be treated successfully with colchicine, the oedema with diuretics. The progression of renal failure and proteinuria as indicator of the degree of amyloid-induced renal damage remained unaffected by this treatment. With dimethyl-sulfoxide (DMSO) a marked improvement in renal function and a lowering of the SAA level could be achieved. Thus this treatment inhibits the progression of amyloidosis of the AA-type in Mediterranean fever and may be considered for other forms of AA-type amyloidoses. It is possible that the lowering of the SAA-serum concentration and the improvement of renal function is due to an antiphlogistic effect of DMSO, the mechanism of action of which is so far unknown.
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PMID:[Familial Mediterranean fever with amyloidosis. Recent pathogenetic and therapeutic aspects]. 682 96


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