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)

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

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

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

Anti-basement membrane antibodies and tissue deposition of immune complexes appear to be responsible for most glomerulonephritides and for some tubulo-interstitium injury accompanying glomerulonephritis or occuring primarily. Anti-tubular basement membrane antibodies complicate immunologic and toxic renal injury, including transplantation, and widespread tubulo-intersitial immune complex deposits are present in most patients with systemic immune complex disease, such as lupus erythematosus. Radioimmunoassay is now available for detecting and monitoring circulating anti-glomerular basement membrane antibodies. The effect of aggressive therapy with immunosuppression and plasma exchange is being studied to determine is value in minimizing tissue damage produced by the usual transient production of anti-glomerular basement membrane antibodies. Techniques are being explored to detect circulating immune complexes. Vigorous efforts are under way to identify antigen-antibody systems involved in the production of nephritogenic immune complexes, which may lead to antigen irradiation or specific manipulation of the immune response or its products.
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PMID:Recent advances in the immunological aspects of renal disease. 14 79

The F1 hybrid of New Zealand black and New Zealand white mice--the NZB/NZW mouse--spontaneously develops a disease similar to human systemic lupus erythematous, characterized by impaired cell-mediated and enhanced humoral immune responses, development of antibodies to nuclear antigens, and immune complex glomerulonephritis. Because there is experimental evidence that prostaglandin E1 (PGE1) can enhance T-cell function and cell-mediated responses and suppress B-cell activity, NZB/NZW mice were treated with 200 microgram PGE1 subcutaneously once or twice daily from 6 weeks of age. PGE1 treatment of female and male mice prevents giomerular deposition of immunoglobulins and complement (monitored by immunofluorescence), and development of the proliferative glomerulonephritis (determined by light and electron microscopy) characteristic of untreated NZB/NZW mice. After 1 year of treatment, 18 of 19 female mice survived, whereas only 2 of 19 untreated control mice were alive. Male mice treated with 200 microgram PGE1 daily were also protected: 9 of 11 versus 2 of 9 untreated mice were alive at 65 weeks. PGE1 treatment did not prevent development of antibodies to nuclear material in any of the treated groups.
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PMID:Prostaglandin E1 treatment of NZB/NZW F1 hybrid mice. II. Prevention of glomerulonephritis. 14 6

The impact of aging on the severity of chronic immune-complex glomerulonephritis was studied in 144 patients from whom diagnostic renal biopsies were obtained over a 3-year period. Glomerulonephritis was related to an antecedent streptococcal infection in nine of these patients. In 58, glomerulonephritis occurred in association with a systemic disease; 27 of these had lupus erythematosus. At the time of the renal biopsy, serum creatinines were more frequently abnormal in men over 40 years of age. Similarly, histological evidence of irreversible glomerular injury was more evident in men over 40. Histological indices of renal glomerular injury correlated with the presence of intense fluorescent antibody reactions specific for C3 and C4 and IgG in the glomeruli. High serum Clq binding activities (Clq BA), an indication of the presence of circulating immune complexes, also were found significantly more often in males over 40. High serum Clq BA correlated with renal functional and biopsy evidence of severe glomerulonephritis. The renal biopsies in 89 cases were tested with fluorescein-conjugated heat-aggregated IgG (FAIgG) to determine how many contained focal immunoglobulin deposits with antiglobulin activity. Antiglobulins were detected in glomeruli of 24 patients and were found significantly more often in biopsies which revealed histological evidence of severe and irreversible histological injury. Binding of FAIgG was not selectively associated with any sex or age groups. Thus, detection of circulating immune complex-like materials in sera and the presence of glomerular deposits with antiglobulin activity were both features associated with severe glomerular injury. Both correlated with the quantity of complement deposited in the glomeruli. But only serum Clq binding activity was age and sex related. Similarly, in cancer patients, abnormal Clq BA were found more frequently in sera of older men with cancer but not in age- and sex-matched controls. Examination of selected sera by sucrose density gradient ultracentrifugation revealed that the complexes from cancer patients were relatively small (less than 19S greater than 7S) whereas those in most nephritis patients were heterogeneous in size. Sera with relatively high Clq binding activity from patients with chronic glomerulonephritis tended to contain relatively greater quantities of Clq binding materials sedimenting more rapidly than 19S.
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PMID:The effect of age on the character of immune complex disease: a comparison of the incidence and relative size of materials reactive with Clq in sera of patients with glomerulonephritis and cancer. 15 3

An antigen related to mammalian type-C RNA viral p30 proteins was shown by the use of anti-p30 sera and the indirect immunofluorescence method to be present in the kidneys and spleen in a fulminant fatal case of human systemic lupus erythematosus and to be located in the glomeruli, the site of active lupus diffuse glomerulonephritis.
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PMID:Antigen related to mammalian type-C RNA viral p30 proteins is located in renal glomeruli in human systemic lupus erythematosus. 17 99

Kidneys from patients with lupus nephropathy, non-lupus immune-complex glomerulonephritis and other renal diseases were examined by indirect immunofluorescence for antigens related to a C-type virus from human cells (HEL-12 virus). All 11 specimens of lupus nephropathy contained HEL-12 virus antigens deposited in the same pattern as the immune complexes. The intensity of immunofluorescence with anti-HEL-12 virus serum correlated with the extent of immune-complex deposition. In contrast, nine renal lesions other than lupus nephropathy and seven normal tissues did not react with anti-HEL-12 virus serum. Antibody eluted from one kidney with lupus nephropathy reacted by indirect immunofluorescence with human and dog cells infected with HEL-12 virus but not with uninfected control cells. These findings demonstrate a specific association of lupus nephropathy with a C-type viral antigen that is deposited as antigen-antiviral antibody complex.
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PMID:C-type virus expression in systemic lupus erythematosus. 18 76


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