Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0024141 (systemic lupus erythematosus)
 44,322 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Since immunological events were found to be pathogenetically involved in various forms of glomerulonephritis, corticosteroids and immunosuppressive drugs were introduced in the treatment of nephritis. However, as opposed to the findings in the paediatric nephrotic syndrome, controlled and multicentric trials with immunosuppressive therapy revealed disappointing results in the management of renal disease in adults. Significantly better results under immunosuppressive therapy, were seen only in the nephrotic syndrome based on the so-called "no changes" or "minimal changes" nephritis. In chronic membranous and proliferative glomerulonephritis the clinical course in the treated group was not statistically different from that of the untreated group. In some disorders of connective tissues, such as systemic lupus erythematosus, polyarteritis nodosa and Wegener's granulomatosis, corticosteroids and immunosuppressive agents seem to exert a favourable effect on the course of renal disease. Encouraging results concerning the combined use of immunosuppressive drugs, anticoagulants and platelet aggregation inhibitors in mesangiocapillary (membrano-proliferative) glomerulonephritis and rapidly progressive nephritis have also been presented. Several factors such as incomplete immunosuppression, druginduced antigen tolerance and increased immune complex formation as a consequence of inhibited antibody production may contribute to the fact that many patients with different forms of nephritis do not benefit from long-term immunosuppressive therapy.
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PMID:[Immunosuppressive therapy in renal disease (author's transl)]. 0 14

In a comparative study the hemolytic activity of C3, C5, C6, C7, C8, C9 and the C3 proactivator (C3PA) were measured in sera of 22 patients with chronic membrano-proliferative glomerulonephritis (CMPGN), 15 patients with idiopathic nephrotic syndrome, 10 patients with systemic lupus erythematosus, 7 patients with anaphylactoid purpura and 10 patients with acute poststreptococcal nephritis. In CMPGN, C3, C5, C6, C7 and C8 were low in the majority of the patients, whereas C9 and C3PA were depressed only in 21% and 11% of the patients, respectively. By contrast, C3PA and C8 showed striking depressions in the idiopathic nephrotic syndrome. In lupus erythematosus, all the C factors, including C3PA were found to be low with the exception of C9, which was normal in 80% of the patients studied. C3, C5, C6 and C7 were found to be depressed in acute glomerulonephritis; C8 and C9 titers were normal. In all patients studied with anaphylactoid purpura, CH50 and C3 titers were elevated markedly.
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PMID:A study of complement components C3, C5, C6, C7, C8 and C9 in chronic membranoproliferative glomerulonephritis, systemic lupus erythematosus, poststreptococcal nephritis, idiopathic nephrotic syndrome and anaphylactoid purpura. 4 34

A 125I-DNA preparation for the detection of human anti-DNA antibodies (ADA) was evaluated as a diagnostic test for systemic lupus erythematosus (SLE). A normal range of 0-25 U/ml was established. Serum ADA level greater than 110 U/ml were diagnostic in clinically active SLE and levels greater than 45 U/ml were found in 75% of patients with inactive disease. This value was significantly greater than that found in rheumatoid arthritis, renal disease caused by non-immune mechanisms, post-streptococcal glomerulonephritis and a miscellaneous group of disorders comprising connective tissue diseases, auto-immune disorders and chronic active hepatitis. Anti-nuclear factor (ANF) titres greater than 1/160 and LE cells were found in 85% of these patients. In inactive disease the ADA levels ranged between 25 and 98 U/ml, ANF titres varied from 1/40 to 1/640, and LE cells were detected in only 20% of the cases. In 3 patients investigated during the course of the disease, the ADA levels correlated best with clinical improvement. Two patients with apparent active lupus nephritis showed intermediate ADA levels, which were probably caused by antigen-antibody formation and immune complex deposition in the kidneys.
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PMID:Evaluation of 125I-DNA for detecting anti-DNA antibodies in the diagnosis of systemic lupus erythematosus. 6 46

Main components of kinin system, the arginine-esterase activity and proteinase inhibitors were estimated in blood serum of patients with nephrotic syndrome of various etiology (glomerulonephritis, amyloidosis, systemic lupus erythematous) and also in patients with latent nephritis and in healthy donors. Content of all the kinin system components (kallikreinogen, kininogen and kininase 1) proved to be increased in all the forms of nephropathy studied. Free kallikrein was found in blood serum of patients with nephrotic syndrome as distinct from healthy persons and patients with latent nephritis. The arginine-esterase activity, which shows the level of trypsin-like proteinases, was altered dissimilarly, depending on the nephrotic syndrome etiology: it was maximally increased in nephrotic syndrome of amyloid genesis and decreased in patient with systemic lupus erythematosus. High content of kallikrein and kininase I with simultaneous decrease in kininogen was typical for patients with severe form of nephrotic syndrome. Impairment of kidney in nephrotic syndrome was also characterized by an increase in alpha1-antitrypsin and in the total antitryptic activity, which reached the maximal value in nephrotic syndrome of the I degree and decreased at the II degree of the disease. In nephrotic syndrome content of alpha2-macroglobulin was maximally increased at the II degree of nephrotic syndrome and decreased in severe form of the disease. The primary alteration in content of proteinase inhibitors and high level of kinin system components were assumed to determine the conditions for activation of kinin system in blood serum and to impair the nephrotic syndrome pathogenesis, which was complicated by systemic manifestations. High content of kinin system components was apparently determined by the increased synthesis in liver tissue in response to inflammation and massive proteinuria; kininase I and alpha2-macrolgobulin, as proteins with high molecular weight, were likely to be selectively retained in blood circulation when the capillary penetration was increased.
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PMID:[State of the kinin system and level of serum proteinase inhibitors in latent nephritis and the nephrotic syndrome of different etiology]. 7 Jan 11

The specific binding of antigens by antibodies leads to the development of antigen-antibody-complexes. Apart from the connected with this and desirable immunological protection immune complexes, however, may also have an pathogenic effect on certain conditions (e. g. transmission of the capacity of phagocytosis), depositing themselves in the vascular regions concerned, activating complement and after binding to cell membranes causing the release of unspecific mediators. Finally these lead through increased vascular permeability, local ischaemia and hyperaemia, respectively, and the release of proteolytic enzymes to a lesion of the tissues. In a series of in most cases chronic inflammatory diseases depositions of immune complexes may be proved in the tissues concerned. However, it is difficult to establish exactly in the individual case, whether they considerably participated in the development of the clinical picture. By analogies to experimentally produced immune complex diseases at least some entities of diseases (e. g. lupus erythematodes disseminatus) or defined local alterations of the tissues (e. g. glomerulonephritis of immune complex type) may be defined pathogenetically.
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PMID:[Immune complexes and their pathogenetic significance]. 7 38

163 patients with diffuse lupus glomerulonephritis, proven by renal biopsy, were divided into four therapeutic trial groups: 67 were put on corticosteroids alone, 11 on corticosteroids and azathioprine, 32 on corticosteroids and cyclophosphamide, and 53 on corticosteroids and chlorambucil and were followed up for several years. The addition of azathioprine to corticosteroids did not increase the survival rate, improve the renal function or alter the grim prognosis of the patients. Cyclophosphamide appeared to influence favourably the pathological lesion and the renal function when added to corticosteroids, and the disease progressed at a slower rate. The fatal side effects nearly balanced the therapeutic value of cyclophosphamide. Patients on corticosteroids and chlorambucil had an excellent course. This therapeutic regimen resulted in resolution or regression of the renal pathology, marked improvement of the renal function and marked improvement of the survival rate. The authors believe that this therapeutic regimen holds the best chance of becoming the standard treatment for lupus nephritis, particularly since the side effects of chlorambucil were minimal.
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PMID:Comparison of chlorambucil, azathioprine or cyclophosphamide combined with corticosteroids in the treatment of lupus nephritis. 8 55

The solid-phase C1q binding assay for circulating immune complexes has been evaluated. The assay provides a rapid, sensitive (detecting as little as 1 microgram of aggregated IgG) and reproducible procedure for the detection of immune complexes in biological fluids. Using artificially prepared immune complexes, the assay detects complexes at four-times antigen-excess. Gel filtration over Sepharose 6B showed that these complexes were distributed over a range of molecular weights from greater than 4 x 10(6) to 300,000 daltons. Using radiolabelled anti-BSA, antigen (BSA) could be detected in these complexes. Screening of gel-filtered SLE showed that the assay detects complexes of both high and low molecular weight, but does not detect all complexes in the SLE sera. Clinical studies showed that immune complexes are frequently found in the sera of patients with SLE and measurement of the concentrations of complexes provides a more sensitive index of disease activity than either serum C3 or C4 concentrations or DNA binding capacity. In patients with RA concentrations of immune complexes were generally higher in synovial fluid than serum, although a patient with systemic rheumatoid disease with hypocomplementaemia had an extremely high level of circulating immune complexes. The assay only infrequently detects circulating immune complexes in glomerulonephritis and in renal transplant recipients. It is concluded that the assay provides a useful clinical tool, but detects only a limited species of immune complexes. It can be used in the detection of antigens in complexes.
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PMID:Evaluation of the C1q solid-phase binding assay for immune complexes. A clinical and laboratory study. 9 1

A 61-year-old man developed clinical lupus syndrome with positive antinuclear antibody, positive lupus erythematosus (LE) cell preparation, and diffuse proliferative glomerulonephritis following 26 months of procainamide therapy. He was treated sequentially with prednisone and azathioprine (2 weeks), decreasing doses of prednisone alone (21 months), and no immunosuppressive drugs (10 months). Coincidental with this treatment, the immunopathology of the glomerulonephritis improved dramatically, dramatically, renal function returned almost to normal, and both antinuclear antibody and LE cell preparation became negative. The course of this patient's renal disease contrasts sharply with diffuse proliferative glomerulonephritis of idiopathic systemic lupus, and suggests that this rare complication of procainamide therapy may have a favorable course.
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PMID:Glomerulonephritis in procainamide induced lupus erythematosus: report of a case and review of the literature. 9 11

A polyclonal IgM-RF-binding assay (pRF-BA) for the detection of circulating immune complexes (IC) is described. The method is based on the competitive binding of heat-treated iodinated IgG (deltaIgG) and naturally occurring IC to solid phase IgM-RF. The sensitivity limit of the assay was 300--400 ng deltaIgG/ml dilute serum. The coefficient of variation for the assay varied from 6 to 12% of the total binding when deltaIgG concentrations up to 1 microgram/ml were measured. One hundred and six patient sera were examined for IC occurrence and significant differences (p less than 0.01) were observed between 30 normal control sera and sera from SLE, sarcoidosis and glomerulonephritis patients. About 40% of patients suffering from acute myocardial infarction (AMI) gave IC-positive reactions with samples taken 5 to 10 days after the infarction. The kinetics of IC appearance was studied in AMI patients by the pRF-BA and three complement-dependent assays. IC appearance was registered in the RF assay 5 to 12 days after the rise in ASAT enzyme values and the IC reactivity corresponded to complexes ranging from 2 to 5 x 10(6) in molecular weight.
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PMID:A solid-phase, polyclonal IgM-RF binding assay for circulating immune complexes. 10 21

304 cases of glomerulonephritis were biopsied in Tunisia and studied morphologically. The incidence of glomerulonephritis with marked proliferation of endocapillary cells was 60%, a figure considerably higher than in other large series. Using a Clq binding assay, statistically significant levels of immune complexes were found in cases of acute proliferative glomerulonephritis. Amongst other types of glomerulonephritis, circulating immune complexes were frequently found in systemic lupus erythematosus but only in a low percentage of primary glomerulonephritis with or without immunoglobulin deposits.
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PMID:A clinical and immunopathological study of 304 cases of glomerulonephritis in Tunisia. 11 Jun 4


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