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)

In an attempt to examine the role of reactive oxygen species on bivalent hapten immune complex glomerulonephritis, superoxide dismutase (SOD) concentration in renal tissue was studied by Electron Spin Resonance (ESR) and the protective effect of radical scavengers were evaluated. Injection of immune complex (IC) induced severe glomerulonephritis, characterized by neutrophil and/or monocyte infiltration in glomeruli in an association with proteinuria. SOD concentration in renal tissue decreased when neutrophil and/or monocytes infiltration and proteinuria developed, indicating a possible role of reactive oxygen species on renal injury. SOD, superoxide scavenger, and catalase (CAT), which destroy hydrogen peroxide, apparently reduced proteinuria on 14th day (18.5 +/- 3.17 mg/day, 20.7 +/- 7.35 mg/day, respectively, in comparison with control group, 29.5 +/- 4.21 mg/day), but there was no statistical significance. On the other hand, hydroxy radical scavenger, dimethylthiourea (DMTU) significantly reduced proteinuria (15.3 +/- 4.21 mg/day) and remarkable improvement in renal histology was observed. It is concluded that reactive oxygen species, especially hydroxy radical, play a significant role on renal injury in bivalent hapten immune complex glomerulonephritis.
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PMID:[Role of reactive oxygen species (Ros) in model immune complex nephritis]. 214 98

1. The hypothesis was tested that the renal xanthine oxidase system provides a source of oxygen free radicals in puromycin aminonucleoside and adriamycin experimental nephrosis by generating uric acid from hypoxanthine and xanthine. 2. The concentrations in renal tissue of the putative intermediary products of puromycin aminonucleoside metabolism, hypoxanthine and xanthine, and of their precursors, adenosine and inosine, were lower in rats treated with puromycin aminonucleoside than in normal controls, whereas concentrations of the metabolites were normal after adriamycin intoxication. Their daily urinary excretion was lower in the 24 h after puromycin aminonucleoside administration compared with the baseline values and returned to near normal levels within 5 days. After adriamycin the 24 h urinary excretion of xanthine and uric acid was double the baseline levels (P less than 0.001). 3. When equimolar amounts of hypoxanthine were injected instead of puromycin aminonucleoside, the concentration of all bases increased slightly in renal tissue and their urinary efflux was double the baseline level: allantoin, uric acid, the unmodified nucleotide and xanthine were the most represented compounds in urine. 4. The enzymatic activities relative to xanthine oxidase (EC 1.1.3.22) and xanthine dehydrogenase (EC 1.1.1.204) in renal tissues were unchanged 1 day after puromycin aminonucleoside or hypoxanthine intoxication and only moderately increased in both groups at 13 days (the time of appearance of heavy proteinuria in the puromycin aminonucleoside-treated group). In contrast, xanthine oxidase and xanthine dehydrogenase activities were higher in adriamycin-treated rats at 1 and 15 days after the treatment (P less than 0.001). 5. Feeding rats with normoprotein diets containing tungsten induced a marked and constant decrease of renal xanthine oxidase and xanthine dehydrogenase activities to 20% of the baseline values in both puromycin aminonucleoside- and adriamycin-treated rats. Inhibition of renal xanthine oxidase and xanthine dehydrogenase activities by tungsten was associated with a marked reduction (P less than 0.001) of proteinuria in adriamycin-treated rats and the same occurred with allopurinol, a specific inhibitor of xanthine oxidase activity. In contrast, tungsten treatment did not reduce the proteinuria associated with puromycin aminonucleoside, which reached a maximum 13 days after puromycin aminonucleoside intoxication. Hypoxanthine-treated rats were normoproteinuric after 2 months of observation. 6. These data demonstrate an activation of renal xanthine oxidase and xanthine dehydrogenase after adriamycin intoxication which is relevant to the induction of proteinuria. They also argue against the involvement of the renal xanthine oxidase system as a source of free radicals in puromycin aminonucleoside nephrosis and suggest that the nucleotide cycle is not a normal route for puromycin aminonucleoside degradation.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Renal purine efflux and xanthine oxidase activity during experimental nephrosis in rats: difference between puromycin aminonucleoside and adriamycin nephrosis. 215 48

We examined the immunoregulating effect of 22-oxa-1 alpha,25-dihydroxyvitamin D3 (22-oxa-1 alpha,25(OH)2D3), a synthetic analogue of vitamin D3 with an oxygen atom at C22 in the side chain skeleton, on spontaneously developing autoimmune disorders in MRL/Mp-lpr/lpr (MRL/l) mice. The oral administration of the compound significantly prolonged the average life span of the mice and showed a significant reduction in proteinuria. Histopathological investigations also revealed that pathological conditions such as renal arteritis, granuloma or arthritis of the knee joints were much lighter in the treated group than in the untreated group. Furthermore, the lymphocyte phenotypes in thymus, lymphnode, and spleen were partially normalized and became similar to those found in young control animals by the treatment with 22-oxa-1 alpha,25(OH)2D3. These results suggest that this compound inhibits the development of lupus nephritis in MRL/l mice and may be therapeutically effective on the mice.
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PMID:Prevention of immunological disorders in MRL/l mice by a new synthetic analogue of vitamin D3: 22-oxa-1 alpha,25-dihydroxyvitamin D3. 216 40

1. The function of the kidney glomerulus, and the formation of reactive oxygen species in the glomerulus, is reviewed. 2. Experimental models of glomerular injury, resulting from immunological and non-immune reactions, are known to give rise to morphological and functional changes of the glomerulus, resulting in proteinuria. 3. From the use of oxygen radical scavengers and inhibitors, glomerular injuries have been shown to be associated with the production of hydrogen peroxide, hydroxyl radical, and superoxide anion radical.
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PMID:Reactive oxygen and glomerular dysfunction. 223 11

The aetiology of pregnancy-induced hypertension (PIH) is at present unknown. Epidemiological data lead us to assume, that two main mechanisms could be responsible for the development of PIH. They are not well understood in their complexity, but result in the same pattern of signs and symptoms: Oedema, proteinuria and hypertension. 1. "Goldblatt-Phenomenon" in the uterus, as a result of a disturbed maternal immune response to the cytotrophoblast, followed by the reduction of uterine blood flow and the liberation of vasoactive substances from the placenta. 2. Renal factors, especially in elderly women, result in a manifestation of nephrotic diseases during pregnancy. No screening methods are at the present time available to diagnose PIH in advance. It is therefore necessary, to look at typical clinical manifestations, i.e. the development of hypertension. It is also important to estimate the weight gain and the occurrence of oedema before rising blood pressure demonstrates a general vasoconstriction in the maternal vascular system. The basic therapeutical concept is to reduce the peripheral vascular resistance, to prevent maternal complications and to reduce the uterine vascular resistance to improve foetal oxygenation. In many cases an improvement of the oxygen supply to the foetus is not possible, since irreversible alterations of the uterine arterial vascular bed have already taken place. For the treatment of PIH, different drugs are available which act on different targets. In cases of special medical history, the early application of magnesium and acetyl salicylic acid (ASA) should be included in the therapeutical concept of prophylaxis.
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PMID:["Goldblatt phenomenon of the uterus" and latent kidney disease as the cause of pregnancy-induced hypertension--epidemiology and therapeutic consequences]. 193 79

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 isolated kidney perfused with modified Krebs-Henseleit buffer with amino acids yields heavy proteinuria associated with reduced ATP levels characteristic of partial ischemia. These conditions are associated with a similar perfusion time dependent release of degraded vascular [35S]heparan sulfate proteoglycan into the perfusate solution which included a 60% loss of [35S]macromolecular material from the glomerulus after 2h of perfusion. Small amounts of [35S]macromolecular material were found in the urine and lymph. These results demonstrate that partial ischemia promotes a specific response in the overall renal vasculature, probably involving oxygen reactive metabolites, that results in the preferential release of heparan sulphate from the basement membrane and endothelial cells on the luminal side of the capillary wall.
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PMID:Partial ischemia and proteinuria during isolated kidney perfusion is accompanied by the release of vascular [35S]heparan sulfate. 253 69

The effect of 'scavengers' of reactive oxygen products (ROPs) was studied in the heterologous phase of anti-glomerular basement (anti-GBM) nephritis induced in rats. Glomerulonephritis was induced by the intravenous administration of sheep anti-GBM antibody (5 mg/100 g) to rats on day 0. The intraperitoneal administration of superoxide dismutase (SOD) 30 mg/kg/day or 150 mg/kg/day leads to a significant reduction in proteinuria on day 1 and also on day 3 in animals given SOD 30 mg/kg/day. Proteinuria was not significantly reduced by the intraperitoneal administration of inactivated SOD (150 mg/kg/day). In rats given polyethylene glycol coupled catalase (PEG-catalase) intraperitoneally at a dose of 10,000 iu/kg/day and 100,000 iu/kg/day proteinuria was lower than in rats with unmodified anti-GBM nephritis. These differences were significant on day 1 (P less than 0.05) in rats given PEG-catalase 100,000 iu/kg/day and on days 3 and 5 in rats treated with either dose of PEG-catalase (P less than 0.01). These data suggest a role for superoxide anion and hydrogen peroxide, or a product of their interaction such as hydroxyl radical, in glomerular injury induced by anti-GBM antibody.
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PMID:Reactive oxygen products in heterologous anti-glomerular basement membrane nephritis in rats. 278 25

Neutrophils (PMNs) mediate injury in experimental glomerulonephritis (GN) in part via the release of reactive oxygen species, particularly hydrogen peroxide (H2O2). Recent kidney perfusion studies demonstrate that H2O2 can cause glomerular injury by reaction with halides in the presence of the PMN cationic enzyme myeloperoxidase (MPO) to form oxidants which can oxidize and halogenate tissue. We sought evidence for participation of the MPO system in a model of PMN-mediated immune complex (IC) GN. A PMN-dependent model of GN was developed in rats by perfusing the renal artery with concanavalin A followed by anticoncanavalin A antibody. PMN depletion abolished glomerular PMN infiltration and significantly reduced proteinuria (35 +/- 7 mg/day vs. 113 +/- 10, P less than 0.001). Rats that received Na125I (5.0 microCi) three and six hours following disease induction had more 125I incorporation in glomeruli and GBM at 48 hours than similarly treated rats that were PMN depleted (1200 cpm vs. 88 cpm, P less than 0.01). Glomerular iodination could not be demonstrated in a PMN-independent model of nephrotoxic nephritis induced with noncomplement fixing anti-GBM antibody. These data indicate that this model of PMN-mediated IC GN is associated with activation of the MPO-H2O2-halide system, which may participate in mediating glomerular injury.
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PMID:Participation of the myeloperoxidase-H2O2-halide system in immune complex nephritis. 282 92

Neutrophilic polymorphonuclear leukocytes can mediate glomerulonephritis by releasing reactive oxygen species such as H2O2. We have previously demonstrated that H2O2-mediated glomerular injury can be potentiated by reaction with polymorphonuclear leukocyte myeloperoxidase (MPO). When MPO was perfused into renal arteries of rats, it bound to the glomerular capillary wall due to its cationic charge. Subsequent perfusion with nontoxic concentrations of H2O2 and halides resulted in acute glomerular injury, halogenation of the glomerular basement membrane, and proteinuria. The studies reported here document the morphologic changes that accompany MPO-mediated glomerular injury. Acutely, there is severe injury to the endothelium with cell swelling and lysis. Within 10 minutes, a marked platelet influx occurs. Platelets frequently occlude capillary lumens and bind to areas of denuded glomerular basement membrane where platelet degranulation results. By 4 days, the platelet infiltration has ceased, and a reparative phase develops characterized by marked proliferation of resident endothelial cells and possibly mesangial cells. By 21 days postperfusion, the glomerular lesion had largely resolved. In contrast, control rats perfused with MPO alone, H2O2 alone, or buffered saline alone demonstrate minimal glomerular injury at all times studied. MPO-mediated glomerular disease results in endothelial and mesangial cell injury, activation of platelets, and a subsequent proliferative response. These morphologic changes resemble those seen in several forms of inflammatory and proliferative glomerulonephritis in man.
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PMID:Morphologic correlates of glomerular oxidant injury induced by the myeloperoxidase-hydrogen peroxide-halide system of the neutrophil. 283 32


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