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 this study, we examined the immune response and proteinuria caused by dietary polyunsaturated fatty acids in normal NZW/N and autoimmune NZB/NZW mice. Mice were maintained more than one year on five dietary groups: normal (5% corn oil), calorie-restricted, high fat (20% corn oil), high fat (20% fish oil), and Purina laboratory rodent chow. Normal mice fed with the fish oil diet had a more reduced anti-sheep red blood cells (SRBC) plaque-forming cell (PFC) response and less interleukin-2 (IL-2) enhancement of PFC than did the group with the restricted diet and the young control group. The corn oil (5 and 20%) diet animals also showed reduced PFC response and IL-2 utilization. NZB/NZW mice fed with the fish oil diet showed similar reduced PFC response but had a significantly lower response to IL-2 than did those on the corn oil diets and the restricted diet. The IL-2 production by macrophages from NZW/N mice was reduced in both the fish oil and corn oil diet groups. However, mice fed with the fish oil diet had less proteinuria and good survival rates, similar to the group with the restricted diet. These results suggest that the beneficial effect of the fish oil diet in these animals may be attributed in part to the immunosuppression mechanism.
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PMID:Effect of fish oil diet on immune response and proteinuria in mice. 194 15

The therapeutic effect of 15-deoxyspergualin (DSP) in old New Zealand Black/White F1 mice (B/W mice) with clinical nephropathy was studied and compared with cyclophosphamide (CY). The mice were treated with 0.05 ml phosphate-buffered saline, subcutaneously, four times/week, with DSP, 6 mg/kg body weight, s.c., four times/week, or with CY, 15 mg/kg, i.p., once a week, starting at the 28th week of age. They were serially semiquantitated for proteinuria, and serum IgG anti-dsDNA antibody was measured by ELISA. Spleen cell surface markers such as L3T4, Lyt2 and IgG were flow-cytometrically analyzed, and interleukin-2 (IL-2) activity in vitro was measured using CTLL cells. Kidney specimens were studied with light and immunofluorescence microscopy. The mice treated with either CY or DSP survived significantly longer than the control mice. L3T4+ cells in the DSP-treated mice at 40 weeks of age were significantly less than those in the 28-week-old control mice (p less than 0.05). In contrast, IL-2 generation in the three groups of mice showed no significant variations at 32-40 weeks of age. Serum anti-DNA antibody levels in both of the CY and DSP groups remained low and comparable with that in the 28-week-old mice, and the incidence of significant proteinuria decreased. Likewise, glomerular histology in the treated groups was improved compared with the 28-week-old control mice, and the deposition of IgG and C3 in the treated groups remained unchanged or further decreased. Accordingly, the renal (immuno)histological findings in the DSP group were quite comparable with or even better than those in the CY-treated mice. DSP may have suppressed the abnormal antibody production by modulating the T cell function(s), which is in contrast to the direct action against B cells due to CY.
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PMID:Reversal of established nephropathy in New Zealand B/W F1 mice by 15-deoxyspergualin. 204 19

To consider the mechanism of reduction of proteinuria by cyclosporine A (CYA) in the patient with intractable nephrotic syndrome, the effect of CYA on proteinuria and anionic sites (AS) of the glomerular basement membrane (GBM) was studied in puromycin aminonucleoside (PA) nephrotic rats. In addition the rats exogenously given human recombinant interleukin-2 (hrIL-2) every day repeated the same proteinuria were used. The PA nephrotic rats were made by single injection of PA 150 mg/kg excrete of urinary protein as compared 10 mg/day of urinary protein in the controls. The increase of urinary protein in the PA rats was inhibited by CYA10-20 mg/kg administrated orally from the day of PA injection for 15 days. To evaluate AS, the kidney were treated with a polyethyleneimine (PEI) staining method and the deposits in the lamina rara externa (LRE) of the GBM were counted on the electron micrographs. On the 15th day, in the PA rats, AS decreased greatly but were normal in the CYA-treated rats. On one hand, rats injected of hr IL-2 2.5 X 10(5)U/rat intraperitoneally for 14 days showed slight proteinuria on the 14th day, and the proteinuria was also inhibited by oral administration of CYA 25 mg/kg. As reduced in the rats treated with hrIL-2 as well as PA. The findings indicate that the proteinuria in the PA nephrotic rats and rats treated with hrIL-2 might result from reduction of AS and that the improvement of proteinuria in these rats by CYA might be due to the recovery of AS in the GBM.
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PMID:[Mechanism of reduction in proteinuria by cyclosporine A: effects on the glomerular anionic sites]. 222 90

The role of the synthetic immunomodulator AS101 on the production of interleukin-2 (IL-2) by spleen cells of mice with SLE was investigated. BALB/c female mice, in which SLE was induced by immunization with the pathogenic idiotype of anti-DNA antibody 16/6 Id were treated with AS101 for 7 weeks 2 and 4 months after induction of the disease. The ability of the splenocytes of the mice with SLE to produce IL-2 was restored after administration of AS101. This effect was particularly impressive when the 7-week AS101 treatment was initiated 4 months after immunization. Despite its beneficial effect on IL-2 production, AS101 exerted no influence on the titres of autoantibodies in the sera of the mice. It also had no effect on clinical parameters of SLE, such as the increased sedimentation rate, proteinuria and low white blood cell counts. Our data indicate that defective IL-2 production in SLE is probably secondary to other disease processes and is not necessarily associated with the production of autoantibodies in this disorder.
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PMID:The effect of the immunomodulator agent AS101 on interleukin-2 production in systemic lupus erythematosus (SLE) induced in mice by a pathogenic anti-DNA antibody. 231 48

The effect of ciclosporin on the cellular immunoregulation was examined in 19 patients with IgA nephropathy. The patients were randomly divided into two groups: 9 patients receiving oral ciclosporin (5 mg/kg/day) for 12 weeks and 10 patients receiving placebo and acting as controls. T lymphocyte subpopulations were determined using OKT monoclonal antibodies. The functional capability of lymphocytes was assessed by in vitro immunoglobulin synthesis of cultured peripheral mononuclear cells, thymidine uptake by cultured lymphocytes, and t lymphocyte activation with expression of interleukin-2 receptors. A fall of in vitro IgA production by cultured lymphocytes (p less than 0.05), a reduction of thymidine uptake by Staphylococcus aureus Cowan-stimulated cultured lymphocytes (p less than 0.05), and a reduction of activated lymphocytes expressing interleukin-2 receptor (p less than 0.05) were observed in patients after 12 weeks of ciclosporin therapy. The percentages of OKT4 and OKT8 lymphocytes and OKT4/8 ratios were not altered with therapy. A simultaneous reduction of proteinuria and a transient impairment of renal function were observed. Similar changes in cellular immune parameters and clinical response were not observed in the controls. Our study suggests ciclosporin could modulate the cellular immunity in IgA nephropathy.
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PMID:Effect of ciclosporin on lymphocyte subpopulations and immunoglobulin production in IgA nephropathy. 277 Sep 45

We treated 20, steroid resistant or steroid dependent and cyclophosphamide or chlorambucil treated, relapsing nephrotic patients with oral cyclosporine A for eight weeks. Cyclosporine A was started at 7 mg/kg/day and titrated to maintain HPLC level of 100 to 200 ng/ml. Of 20 patients, 14 had a complete remission and the remaining 6 had a reduction in their proteinuria. The mean serum albumin of the 14 responders rose from 2.1 g/dl to 4.1 g/dl (P less than 0.00001) after cyclosporine A therapy. The mean serum cholesterol of the 14 responders decreased from 394 mg/dl to 184 mg/dl (P less than 0.0001) after cyclosporine A therapy. The mean creatinine clearance of the 20 patients (104 ml/min/1.73 m2) was unchanged (107 ml/min/1.73 m2) after eight weeks of cyclosporine A. By life table analysis, 40% of the responders show a sustained remission of up to a year. Cyclosporine A responders had a higher T3 cell count prior to therapy compared to nonresponders (69 +/- 5.54% vs. 61 +/- 6.4%, P less than 0.02). Pre-therapy interleukin-2 levels measured in 10 patients were normal or supranormal in 8, 6 of whom were treatment responders. Two patients with low interleukin-2 levels were nonresponders. Cyclosporine A can be used to induce a remission in relapsing nephrotic patients, and short-term cyclosporine A therapy does not produce nephrotoxicity.
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PMID:Cyclosporine A induced remission of relapsing nephrotic syndrome in children. 296 73

A 5-year-old Chinese girl had had absence seizures and received sodium valproate (VPA) treatment which provided good control. Six months later, she developed interstitial nephritis with proteinuria and microhematuria. Renal biopsy revealed interstitial nephritis with granular deposition of immunoglobulin G (IgG) and C3 in the renal tubular basement membrane (TBM). Ultrastructurally, dilated smooth endoreticular cisternae with mitochondrial degeneration in the tubular cells and scattered electron-dense deposits within the TBM were also noted. Serum circulating immune complexes were detectable, ACH50 and properdin factor B increased. Mononuclear cells (MNC) from the patient after in vitro incubation with VPA (100 micrograms/ml) induced interleukin-2 (IL-2) production and lymphoproliferative response. However, there was no response in controls. The serum VPA level ranged from 84 to 92 micrograms/ml. After VPA was stopped, the microhematuria and proteinuria disappeared. These observations indicate that VPA-induced interstitial nephritis represents a sequence of interrelationships among multiple immunologic factors.
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PMID:Sodium-valproate-induced interstitial nephritis. 312 10

We studied levels of soluble interleukin-2 receptors (IL-2R), which are released by activated lymphocytes, in 139 serum samples from 12 patients with systemic lupus erythematosus (SLE). Concentrations of soluble IL-2R were significantly increased in SLE patients compared with controls (P less than 0.001), and they were significantly higher in patients during active SLE defined by low C3 levels (P less than 0.001), low C4 levels (P less than 0.001), or proteinuria (P less than 0.05) than during inactive SLE. Elevated levels of soluble IL-2R correlated with hypocomplementemia in longitudinal studies (P less than 0.001). Measurement of serum concentrations of soluble IL-2R may provide a sensitive and specific method for monitoring disease activity and immune activation in patients with SLE.
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PMID:Soluble interleukin-2 receptors in systemic lupus erythematosus. 313 27

Twelve patients with acquired immunodeficiency syndrome were treated with a natural product, highly purified human interleukin-2. Doses ranged from 250 to 250,000 units. No clinical responses were seen. Minimal toxicity was noted and consisted of mild prolongation of partial thromboplastin time and proteinuria. Immunologic changes during the study included a decrease in the number of circulating T8 lymphocytes, increased skin test reactivity, and a decline in serum immunoglobulin levels.
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PMID:Use of interleukin-2 in patients with acquired immunodeficiency syndrome. 633 38

DAB486IL-2 is a novel fusion toxin in which the ADP-ribosyltransferase and membrane-translocating domains of diphtheria toxin have been combined with the interleukin-2 (IL-2) gene, creating a recombinant protein capable of selectively intoxicating cells bearing the high-affinity IL-2 receptor. Clinical activity has been documented in Hodgkin disease and the non-Hodgkin lymphomas; toxicities have been minimal and include mild hepatic transaminitis, proteinuria, and hypersensitivity reactions. In this report, a patient with tumor-stage cutaneous T-cell lymphoma developed clinical adrenal failure with bilateral adrenal hemorrhage and necrosis 7 weeks after completing a 5-day course of treatment with DAB486IL-2. The relationship of fusion toxin therapy to the development of this unusual toxicity is discussed.
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PMID:Bilateral adrenal hemorrhage and adrenal insufficiency in a patient with lymphomatous adrenal infiltration following administration of a fusion toxin (DAB486 interleukin-2). 783 23


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