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)

Samples of renal tissue from 373 patients were examined for the presence of immunoglobulin E (IgE) by immunofluorescent techniques. Only trace to ++ amounts ( on a scale of ++++) were found in 20 patients: 4/9 with post-streptococcal acute glomerulonephritis (GN), 5/30 with GN associated with systemic lupus erythematosus, 3/20 with membranous GN, 1/4 with Goodpasture's syndrome, 2/18 with recurrent microhematuria and focal GN, 1/5 with hemolytic anemia and uremia, 3/73 with renal homografts, and 1/5 with dermatomyositis. No IgE was found in 18 patients with lipoid nephrosis, 8 of whom were being treated with prednisone, nor in 5 patients with focal glomerular sclerosis and the nephrotic syndrome. Serum IgE was measured in 9 of the 20 patients with glomerular deposits of this globulin. With one exception, levels of IgE were within the range generally considered to be normal. However, they were greater than the mean of this range in all but two and near the highest limits of normal in most. Neither the amounts of serum IgE nor the degree of proteinuria could be related to the intensity of stain for IgE in the glomeruli of these patients.
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PMID:Immunoglobulin E in renal disease. 5 86

Analysis is carried out of the clinical, pathomorphological and immunological characteristic of lupus nephropathy in 62 patients, 56 females and 6 males. A series of new investigation methods were used for that purpose. An early tendency towards kidney involvement in the course of LED is established and in 22 of the patients (36%) the renal symptoms have been the first clinical manifestations of the basic illness. Lupus nephropathy progresses most often with a nephrosis syndrome (in 66.1% of the patients), rarely pure and not combined with hypertension and/or with renal insufficiency. The pathomorphological changes are rather multiform but in the majority of the cases almost all structural elements of glomerules and the rest of the renal tissue are affected. The clinical picture severity, histopathological changes and nephropathy evolution course were established to be distinctly dependent on the course acuteness of the basic morbid process. The importance of the detailed study of the clinico-morphological and immune characteristic of lupus nephropathy upon the timely diagnosis. Proper treatment and the prognosis assessment of the illness is stressed upon.
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PMID:[Clinical morphological and immunological characteristics of lupus nephropathy]. 7 Aug 87

Human TNF alpha locus locates between HLA-B and DR region on the short arm of chromosome 6. The 5.5 kb and 10.5 kb of TNF alpha restriction fragment length polymorphic (RFLP) bands were identified by Southern hybridization using a restriction enzyme, NcoI. The frequencies of those bands were not different among patients with systemic lupus erythematosus (SLE), those with rheumatoid arthritis and normal controls. In the lupus patients, proteinuria was more frequent in the patients with the 5.5 kb RFLP band (19/39: 48.7%) than those without 5.5 kb band (7/35: 20%) (p less than 0.05). Furthermore, this band was strongly associated with the haplotype HLA B44-DRw13-DQw1. In order to investigate the association between this gene polymorphism and the production of TNF alpha, peripheral blood mononuclear cells from patients with SLE and normal controls were cultured for 24 hours with lipopolysaccharide and concanavalin A and the amount of TNF alpha in the supernatant was measured by enzyme linked immunosorbent assay. The TNF alpha production of lupus patients was not statistically different from that of normal controls. The production of TNF alpha was not related to 5.5 kb RFLP band, but in the patients with SLE, the mean value of TNF alpha in patients with the 5.5 kb RFLP band tended to be higher than those without the band. Lupus patients were divided into two groups by the production of TNF alpha i.e. low TNF alpha inducibility group and high TNF alpha inducibility group. Patients with proteinuria were more frequent in patients of the high TNF alpha inducibility group than those of low TNF alpha inducibility group (p less than 0.05). There were four patients with HLA B44-DRw13-DQw1 who had the 5.5 kb RFLP band and three of them belonged to the high TNF alpha inducibility group with nephrosis. These data suggest that TNF alpha and HLA are possibly associated with the severity of lupus nephritis.
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PMID:[Tumor necrosis factor alpha in systemic lupus erythematosus: evaluation by restriction fragment length polymorphism and production by peripheral blood mononuclear cells]. 135 65

Samples of protein from the urine of 23 patients with lupus nephropathy and 15 patients with proteinuria who did not have systemic lupus erythematosus (SLE) were studied for the presence of cytokines, soluble interleukin 2 receptors (sIL-2R), and free light chain immunoglobulins. The patients with lupus nephropathy were divided into two groups with active (nephritis) and inactive inflammation (nephrosis) based on the results of the analysis of urine samples and renal histology. The crude urine proteins (5 mg/ml) after precipitation by 80% ammonium sulphate from 14 patients with lupus nephritis contained higher concentrations of sIL-2R (4.88 (SEM 1.27 ng/ml) than those from nine patients with nephrosis (1.11 (0.52) ng/ml) or 15 patients without SLE (1.31 (0.87) ng/ml). The concentration of sIL-2R in protein from urine samples was not correlated with the concentration in plasma and was inversely correlated with the excretion of protein in urine over 24 hours in patients with SLE. It is suggested that, in addition to leakage from the circulation, the local production of sIL-2R by inflamed kidneys is possible. The crude proteins in urine were further fractionated by gel filtration on Sephacryl S-200. Arbitrarily, four fractions could be obtained from urine from patients with SLE but only three fractions were found in the urine of patients without SLE. Fraction IV derived from patients with nephritis or nephrosis augmented the pokeweed mitogen induced [3H]thymidine uptake of mononuclear cells. In addition, the positive rates of free kappa (kappa) (35.7%) and lambda (lambda) (42.9%) chains in proteins in urine from nephritic patients were higher than those in the other two groups. These results suggest that the severity of inflammation in the kidneys of patients with lupus can be reflected by the increased excretion of sIL-2R, free light chain immunoglobulins, and cytokine-like molecules in urine.
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PMID:Increased excretion of soluble interleukin 2 receptors and free light chain immunoglobulins in the urine of patients with active lupus nephritis. 155 Mar 98

Penicillamine is the drug of choice for the treatment of Wilson's disease, whatever the stage of the illness. Toxic manifestations may preclude the use of this life-saving drug in some patients and discontinuation of penicillamine therapy usually leads to death. We report our experience with Trientine in seven patients, aged 13 to 33 years, with Wilson's disease who developed toxic manifestations with penicillamine that required discontinuation of therapy. These include two with nephrosis, one with neutropenia, two with thrombocytopenia, and one each with a SLE-like and a Henoch-Schonlein-like syndrome. The patients were treated for periods from 6 weeks to 16 years with a dose of 0.5 to 2 g/day. Trientine proved to be an effective alternative copper chelating agent in the treatment of Wilson's disease in patients with penicillamine-induced neutropenia, thrombocytopenia, SLE, and nephrosis. No serious untoward side effects were noted.
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PMID:Treatment of Wilson's disease with triethylene tetramine hydrochloride (Trientine). 232 83

MHC class I and II molecules serve as restriction elements for the presentation of antigen-specific T cell reactions and may be implicated in the process of cellular transformation. We have analysed the expression of MHC class I and II antigens including the associated invariant gamma-chain in 100 consecutive renal biopsies by a sensitive immunoperoxidase method using monoclonal antibodies against HLA-ABC, HLA-DR, HLA-DQ, HLA-DP and the invariant gamma-chain (Ii). HLA-ABC was expressed by almost all parenchymal cells except for podocytes. Staining for HLA-DR was found consistently in glomerular and interstitial capillary endothelial cells, in "dendritic" (LCA positive) and most infiltrating interstitial cells but not in mesangial and most extracapillary cells. Similar but weaker positivity was observed for HLA-DQ and -DP. HLA-DR positive infiltrating mononuclear cells in glomeruli were noted in acute glomerulonephritis (GN) and Lupus GN associated with enhanced staining of endothelial cells. In addition, HLA-DR was uniformly or focally expressed by predominantly proximal tubules in 80% of biopsies, especially IgA-GN, focal glomerulosclerosis, acute GN but also in 54% of cases with minimal change nephrosis. HLA-DP and -DQ were only positive in a limited number of HLA-DR positive tubules. The expression of the invariant gamma-chain was comparable with the reactivity for HLA-DR. In addition, all HLA-DR-positive tubules expressed the invariant gamma-chain. Subtyping of T cells in biopsies with DR-positive tubules and interstitial infiltrates (n = 20) showed a predominance of CD 4 positive cells in the majority of cases.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Expression of class I and class II histocompatibility antigens in inflammatory kidney diseases]. 248 95

Authors studied the dispersion of immunoreactive HSPG with monoclonal antibody specific to protein nucleus of HSPG in renal diseases associated with nephrosis syndrome. Their results showed that the dispersion of HSPG in GBM does not fully agree with dispersion of anion linkage places known in literature. In membrane and diffuse proliferative lupus glomerulonephritis immunoreactive HSPG cannot be demonstrated in the place of immune deposits, concurrent with dispersion of anion places, while it appears in GBM newly developed round the deposits. Inconsistent with this, in glomerulonephritis having minimal changes, the anion loss of GBM is not associated with absence of nuclear protein, the immunoreactive HSPG remains intact. These observations reflected in literature indicate that--similarly to proteinuria--presumably, deficiency of anion linkage places of GBM is caused by different pathomechanisms.
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PMID:[Heparan sulfate proteoglycan distribution in the glomerular basal membrane in human glomerulonephritis]. 253 43

Cathepsin D-like activity was measured in the sera of 62 patients with active systemic lupus erythematosus (SLE), 9 patients with progressive systemic sclerosis, 9 patients with chronic glomerulonephritis and 18 with glomerulonephritis with nephrosis syndrome. The in vitro and in vivo effect of corticosteroid treatment on enzyme activity was also investigated. Cathepsin D-like activity appeared measurably in the sera of all patient groups but not in controls. The highest values were found in SLE patients. The increase in serum activity correlated with renal involvement. In vivo corticosteroid treatment significantly decreased serum activity in all groups except in systemic sclerosis patients. In vitro prednisolone treatment decreased enzyme activity in a dose-dependent manner. Determination of serum cathepsin D-like activity seems to be useful in the establishment of diagnosis and prognosis of SLE. Cathepsin D may be of pathogenetic significance in autoimmune disease especially in SLE.
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PMID:Cathepsin D-like activity in serum of patients with systemic lupus erythematosus. 263 63

Careful ultrastructural studies of the rat model of nephrotic syndrome induced by puromycin aminonucleoside have demonstrated morphological features which are only seen in proteinuric glomeruli fixed without interruption of the blood pressure. These consist of balloon-like swellings bounded by attenuated epithelial cell cytoplasm, with an area of bare basement membrane at the base. A theory of the mechanism of proteinuria was proposed on the basis of these findings. To test the proposed wide validity of that theory, we improved the method of surface fixation and performed similar studies in sequential manner, using chronic serum sickness glomerulonephritis in the rat as a model of proteinuria. Glomeruli were studied by light microscopy, transmission and scanning electron microscopy. The findings were correlated with the level of proteinuria in the 24 h preceding death and with the duration of serum sickness. Epithelial cell 'balloons' are also demonstrated in this model, correlating with the presence of proteinuria, but with slightly different configurations from those seen in puromycin nephrosis. Surface fixation revealed similar balloons in two other models of proteinuria: a graft versus host induced model of systemic lupus erythematosus in the mouse, and chronic streptozotocin-induced diabetes in the rat. A lengthy search failed to find bare basement membranes in any of these models of proteinuria. We conclude, therefore, that the mechanism of proteinuria proposed in puromycin nephrosis does not apply in these models, and we suggest an alternative mechanism by which the 'balloons' may develop, as a further manifestation of the epithelial cell dysfunction which causes foot process effacement.
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PMID:A morphological study of experimental proteinuria using a novel form of surface fixation. 264 11

In December, 1986, a 29 year old woman developed nephrosis due to systemic lupus erythematosus after taking oral contraceptives (OC) for 6.5 years. Hospitalized for 3 months, she received steroid treatment, which lowered albumin in urine. At the time of hospitalization, the following symptoms were noted. Edema on all her limbs, 4.5 g/dl of urine albumin per day, white blood cell count of 2600/mm, 640 time positive anti-nuclear antibodies, pseudo-positive response to syphilis via bentonite flocculation on particle (BFP). OC she had taken since 1980 were 0.5 mg of norgestrel day and 0/05 mg of ethinyl estradiol day. She had been routinely checked on her kidney function biannually and everything had been normal till then. For 2 months starting in December, 1987, at the patient's request, progesterone along (dydrogesterone 10 mg/day) was administered for contraception. No urine albumin was detected. It appears that autoimmune-type thyroid gland abnormality preceded systemic lupus erythematosus (SLE) which was triggered by the oral contraceptive use. Estrogen metabolism of SLE patients is characterized by estrogen active 16 alpha hydroxyestrone.
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PMID:[A case of systemic lupus erythematosus after taking oral contraceptives]. 276 93


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