Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0409974 (lupus)
22,386 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Platelet-activating factor (PAF) has been suggested recently to play an important role in immune glomerulonephritis, favoring the formation of immune deposits in glomeruli and contributing to the local inflammatory reaction. Here we sought to investigate whether urinary PAF excretion was modified in New Zealand Black x New Zealand White mice a model of genetically determined immune complex disease which mimics systemic lupus in humans and whether changes in PAF urinary excretion values correlated with the extent of proteinuria. To clarify the possible "in vivo" relevance of these findings we evaluated whether PAF receptor antagonist has any influence on the evolution of renal disease and survival of these mice. Our results showed that: 1) in lupus mice urinary PAF excretion increased progressively with age in New Zealand Black x White; 2) the increase in PAF excretion correlated with the severity of proteinuria; and 3) the chronic administration of a PAF receptor antagonist [L-659,989 [(+/- )-trans-2-(3-methoxy-5-methylsulfonyl-4-propoxyphenyl)-5- (3,4,5-trimethoxyphenyl)tetrahydrofuran]] starting from 26 weeks of age significantly delayed the onset of proteinuria and prolonged survival.
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PMID:Platelet-activating factor receptor blocking reduces proteinuria and improves survival in lupus autoimmune mice. 165 Aug 36

MRL/MpJ-lpr/lpr mice spontaneously develop a lupus-like autoimmune disorder characterized by massive proliferation of T cells and rapidly fatal immune complex glomerulonephritis. We evaluated the therapeutic effect of 5-azacytidine (5AC), a cytidine analogue known as an inhibitor of DNA methylation, in MRL/MpJ-lpr/lpr mice. Intraperitoneal injection of 5AC (50 micrograms, twice a week) starting from 6 weeks of age retarded the development of lymphadenopathy and autoimmune syndrome. Its beneficial effects included: (a) increased life-span, (b) diminution of lymphadenopathy and splenomegaly, (c) reduction in circulating levels of autoantibodies such as anti-DNA and rheumatoid factors, and (d) suppression of lupus glomerulonephritis. However, similar treatment in BALB/c mice did not affect the development of IgG anti-human IgG antibody responses. These results suggest that the protective effect of 5AC is related to the inhibition of the lpr gene-induced T cell proliferation, thereby suppressing the autoimmunity-accelerating effect mediated by the lpr gene.
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PMID:5-Azacytidine inhibits the lpr gene-induced lymphadenopathy and acceleration of lupus-like syndrome in MRL/MpJ-lpr/lpr mice. 169 37

As newer treatment modalities become available for patients with severe lupus nephritis, it becomes increasingly important to identify patients at risk for renal failure. In this study, the records of 90 children presenting with systemic lupus erythematosus over a 13-year period were reviewed. Nineteen were lost to follow-up prior to completion of the study. Of the 71 remaining children, 16 (22%) progressed to chronic renal failure. Persistent hypertension lasting greater than 4 months, anemia, abnormalities of the urinalysis, and elevated serum creatinine level were significantly associated with progression to renal failure. Sex, race, age, abnormalities of creatinine clearance, and 24-hour urine protein collection were not associated with progression to renal failure. Renal biopsies were obtained in 45 children. Biopsies were initially classified according to World Health Organization criteria. Diffuse proliferative glomerulonephritis was significantly associated with progression to renal failure. The 45 biopsies available were reviewed by one of the authors and categorized by activity and chronicity indices. Both the active lesions of fibrinoid necrosis, synechiae, tubular casts, and vasculitic lesions and the chronic lesion of glomerular sclerosis correlated with progression to renal failure. Of the 16 children who progressed to renal failure, 2 had cadaver kidney transplants and are well 5 years posttransplant; 4 had fulminant lupus and died within 1 month of commencing dialysis; 10 began chronic dialysis. Five of the 10 children on chronic dialysis died from sepsis. These data suggest that children with systemic lupus erythematosus who undergo dialysis do poorly.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Lupus nephritis: prognostic factors in children. 140 32

The authors analyze the course and outcomes of 33 pregnancies in 26 women suffering from systemic lupus erythematosus (SLE). In patients with active SLE the incidence of gestoses and abnormalities of the newborns is significantly higher than in those with inactive SLE, whose gestational and neonatal complication rate is almost the same as in healthy women. Pregnancy course and outcomes are particularly unfavorable in cases with lupus glomerulonephritis.
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PMID:[Systemic lupus erythematosus and pregnancy: specific features of gestation and course of the disease]. 174 89

To suppress the activity of glomerulonephritis, lupus and primary chronic mixed one, 13 children received plasmapheresis synchronously with pulse therapy with cyclophosphamide or prednisolone. Plasmapheresis was carried out daily for 3 days. Six hours after the last session and on days 4 and 5 of the treatment pulse therapy was provided, followed by conventional intake of prednisolone per os in combination with azathioprine or cyclophosphamide. Beneficial therapeutic results were obtained in 10 patients within 3 to 6 weeks. The effect turned out insufficient in a patient with associated systemic lupus erythematosus, and rapid-progressing nephritis and in a child with primary chronic glomerulonephritis of the mesangiocapillary type with fibroplastic transformation and persistent nephrotic syndrome. No therapeutic effect was attained in a patient with focal segmental glomerulosclerosis running its course with long persistent nephrotic syndrome.
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PMID:[Synchronization of plasmapheresis and pulse therapy in the complex treatment of children with highly active glomerulonephritis]. 175 31

In experimental membranous nephropathy, antibody binding to glomerular epithelial cell membrane antigens results in complement activation and formation of complement C5b-9 membrane attack complexes in glomeruli. During active disease, the C5b-9 complexes are shed into the urine. To test the hypothesis that a similar mechanism might be operative in human membranous nephropathy, we measured urinary excretion of C5b-9 and C5 in 146 proteinuric patients with biopsy-proven glomerular diseases or diabetes mellitus. Urinary excretion of C5b-9 relative to C5 excretion was higher in 40 patients with membranous nephropathy than in 106 patients with proteinuria due to non-membranous glomerulonephritis when analyzed by covariance analysis (P less than 0.0002). Urinary C5b-9 excretion was higher in membranous nephropathy than in membranoproliferative glomerulonephritis (N = 13, P less than 0.05), minimal change-focal sclerosis (N = 33, P less than 0.001), mesangial proliferative glomerulonephritis (N = 9, P less than 0.02) and IgA nephropathy (N = 7, P less than 0.025). Urinary C5b-9 excretion was also higher in patients with lupus nephritis (N = 18, P less than 0.02) compared to those with non-membranous glomerulonephritis. The lupus patients with the highest excretion had clinical or pathological features of membranous nephropathy. Nine patients with membranous nephropathy and elevated urinary C5b-9 excretion had a shorter duration of disease (P less than 0.05), lower serum creatinine levels (P less than 0.05) and more proteinuria (P less than 0.02) than the 31 membranous nephropathy patients with normal values.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Elevated urinary excretion of the C5b-9 complex in membranous nephropathy. 178 50

The authors report their experience, based on 21 cases, on lupus glomerulonephritis with clinic-morphological correlation and follow-up. They classified renal biopsies utilizing WHO classification and applying a numerical score system proposed by Austin. This system considers the morphological characters referable to duration (chronicity index: C.I.) and activity (activity index: A.I.) of renal disease. Histological data have been connected with clinical evolution of renal disease. Patients have been followed for periods varying from 8 months to 8 years. From data obtained we can see that there is not a constant relation between a high chronicity index or activity index and unfavorable evolution of disease. Besides the authors report a revision of literature considering the possibility of connection between morphological data and the prognosis of lupus glomerulonephritis. They refer contrasting judgements about this.
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PMID:[Lupus glomerulonephritis. Study of 21 cases: clinico-morphological correlations]. 179 5

As many as 96 patients with chronic glomerulonephritis (CGN) and 25 with lupus glomerulonephritis (LGN) were examined for chromosomal aberrations (CA) in peripheral blood lymphocytes in different clinical variants and morphological forms of CGN and LGN as well as for their dynamics under the influence of cytotoxic drugs. In patients with active CGN and LGN, chromosomal instability may develop. The treatment with cyclophosphamide in a dose of 2.0-2.5 mg/kg/day appreciably increases chromosomal instability the level of which rises progressively with the treatment period increase. The treatment with azathioprine in a dose of 1.5-2.0 mg/kg/day is not associated with a noticeable increment of the rate of CA. The studies of the level of CA can be used for estimating CGN and LGN activity. Chronic renal failure did not change the level of CA either in CGN or in LGN. In different morphological forms of glomerulonephritis, the rate of CA was determined by the clinical variant of the disease. In order to reduce potential complications provoked by the treatment with cytotoxic drugs, dynamic studies of the CA rate should be carried out in addition to the conventional tests.
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PMID:[Chromosome aberration levels and their dynamics during the treatment with cytotoxic preparations of patients with primary and lupus glomerulonephritis]. 179 27

A morphological and morphometrical study has been carried out on glomerular lesions in mink with spontaneous Aleutian disease, using the WHO classification for Systemic Lupus Erytematous Nefritis. 154 renal samples from sick animals and 10 samples from uninfected mink were processed by routine histopathological techniques and metacrylate inclusions. The samples were studied quantitatively with an automatic image analyzer. 5 forms of glomerulonephritis (GN) were identified: mesangial glomerulonephritis (n = 13), focal and segmental GN (n = 10), diffuse GN (n = 99), membranous GN (n = 12) and advanced sclerosing GN (n = 10) and were associated with the degree of interstitial plasmocytosis. Glomerule morphometry was shown to be an excellent method for identifying the type of lesion, while it quantified the participation of various glomerular elements in the lesion.
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PMID:Glomerular lesions in Aleutian disease of mink (Mustela vison): a morphological and differential morphometrical study. 180 15

In six patients with selected inflammatory rheumatic diseases the authors found increased numbers of LGL in the peripheral blood. Concurrently in these patients an increase of lymphocytes with the CD57 sign was found. In one patient with rheumatoid arthritis more detailed analysis revealed a reduced number of lymphocytes with sign CD16. In this patient in the peripheral blood cells with signs CD3+ and CD57 were found and the function of NK cells was markedly reduced. The clinical course of the disease in the patients was severe, in particular in SLE, where in three patients the disease was associated with the development of lupus glomerulonephritis. The patients were treated by immunosuppressive therapy. The authors reflect on the causes of the increase of LGL cells and do not rule out the possible presence of a serious immunoregulatory disorder between T and B lymphocytes.
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PMID:[Increased numbers of large granular lymphocytes in the peripheral blood in selected inflammatory rheumatic diseases]. 189 39


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