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)

Acute glomerulopathy due to pneumococcal infection occurred in a patient with chronic discoid lupus. The onset of renal involvement in this context suggested that cutaneous lupus may have developed into systemic lupus erythematosus. Renal biopsy established the correct diagnosis. The physiopathology of glomerular involvement in lupus and infections is discussed. Attention is drawn to the significance of complement activation, either by the classical or the alternative pathways according to the etiology.
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PMID:[Proliferative glomerulopathy in pneumococcal septicemia in a patient with lupus (author's transl)]. 628 6

Neurological syndromes are prominent in systemic lupus erythematosus, but the neuropathological and mechanisms resulting in neurological dysfunction are unknown. We report a neuropathological study of the central nervous system in female NZB/W F1 mice, an animal model of systemic lupus erythematous. NZB/W mice were studied at 3, 5, 8, 12, and 14 months of age, and 36-month-old female C57B16N/NIA mice were studied as aged controls. A lymphoproliferative process was identified in the central nervous system of 39% of 8- to 12-month-old and all 14-month-old NZB/W mice. Infiltrates of lymphocytes and plasma cells were seen in subarachnoid, choroid plexus interstitial, and Virchow-Robin spaces. Lymphoid cells occasionally infiltrated brain parenchyma or accumulated as nodular masses. Concomitant visceral lymphoid infiltration was noted in 14-month-old mice. Dense deposits were seen ultrastructurally in the basal lamina of brain parenchymal capillaries of 14-month-old NZB/W mice. These dense deposits were similar in appearance to immune complexes described in glomerular basal lamina, and appeared concomitantly with an advanced lupus-like glomerulopathy. Similar deposits were not observed in choroid plexus. The possible relevance of these neuropathological changes to human central nervous system lupus is discussed.
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PMID:Neuropathological features of a lupus-like disorder in autoimmune mice. 631 72

Two sisters and a brother from one family are described whose sera were deficient in haemolytic complement function. This defect was restored by addition of purified C1q. In their sera, C1q like material was found, whereas C1r and C1s were normal or increased in concentration, as were the other complement components tested. All three had suffered from glomerulonephritis during childhood. A renal biopsy in the brother recently disclosed a membranous glomerulopathy stage 1; otherwise, he is apparently healthy. In both sisters, a systemic lupus erythematosus like disease became manifest at the age of 20 and 23, respectively, resulting in the death of one of them. In the serum of these three family members, the C1q like material was antigenically deficient compared with normal C1q and had, on sucrose gradient analysis, a molecular weight of approximately 65,000 daltons. It did not bind to C1r and C1s. Binding of the dysfunctional C1q to aggregated human gammaglobulin could be demonstrated. On double immunodiffusion analysis, the abnormal C1q was identical with reduced and alkylated C1q. The possible structure of the abnormal C1q molecule is discussed.
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PMID:SLE like syndrome and functional deficiency of C1q in members of a large family. 631 55

The following clinical and pathologic features were evaluated in 170 patients with electron microscopically documented membranous glomerulopathy: age, sex, race, American Rheumatism Association lupus criteria, serum ANA, serum complement, glomerular hypercellularity, stage of subepithelial dense deposits, endothelial tubuloreticular inclusions, tubular basement membrane deposits, tissue ANA, glomerular deposition of IgG, IgM, IgA, C3, C4, and Clq. At the time of biopsy 148 patients had no clinical evidence for lupus, and 22 had a clinical diagnosis of lupus. Six additional patients eventually developed overt lupus after an average of 12 months. Incidences of serologic and pathologic features in lupus as compared with nonlupus membranous glomerulopathy were determined. These data were used to calculate sensitivity, specificity, positive and negative predictive values, and overall efficiency of each parameter in differentiating between lupus and nonlupus membranous glomerulopathy. In general, serologic, morphologic and immunohistopathologic features are more accurate at ruling out lupus than making the diagnosis of lupus. However, a number of features are significantly more frequent in lupus membranous glomerulopathy. Therefore, identification of these features, especially more than one, warrants a high suspicion of lupus rather than nonlupus membranous glomerulopathy even in patients without clinically overt systemic lupus erythematosus. The positive/negative predictive values of some of the pathologic features studied are as follows: mesangial dense deposits 63/99, subendothelial dense deposits 77/93, tubuloreticular inclusions 61/96, intense C1q deposition 47/95, tubular basement membrane deposits 100/87, and glomerular hypercelularity 26/86.
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PMID:Pathologic differentiation between lupus and nonlupus membranous glomerulopathy. 635 33

Two patterns of immune aggregate localization were demonstrated by immunofluorescence and electron microscopy in the choroid plexus of four young women with fatal systemic lupus erythematosus. The two patients with granular immune aggregates localized to the basement membrane of the choroid epithelium (membranous choroidopathy) had subepithelial and intramembranous electron-dense deposits and membranous glomerulopathy in their kidneys. The two patients with immune aggregates in the walls of choroidal blood vessels (vascular choroidopathy) had subendothelial electron-dense deposits and proliferative glomerulonephritis. Vascular deposits in the choroid plexus were associated with capillary thrombi and extravasation of fibrinoid material, while isolated membranous choroidopathy had no histopathologic evidence of inflammation. The clinical presentation and serological studies of blood and cerebrospinal fluid were compared in an effort to discriminate between patients with membranous and vascular choroidopathy. All patients had variable neuropsychiatric symptoms and major motor seizures. While those with vascular choroidopathy had more evidence of disease activity in their sera, both groups demonstrated elevated titers of immune-complexed antinuclear antibodies in cerebrospinal fluid. Although both patterns of choroidal localization of immune aggregates were associated with neuropsychiatric dysfunction, we were unable to identify discrete clinical-symptom complexes which differentiated patients with membranous and vascular choroidopathy. These contrasting patterns of choroid plexus immunopathology suggest that factors responsible for differential localization of immune aggregates are not restricted to the renal glomerulus.
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PMID:Membranous and vascular choroidopathy: two patterns of immune deposits in systemic lupus erythematosus. 664 Oct 23

Reticuloendothelial function was assessed in 11 patients with systemic lupus erythematosus, 8 patients with Wegener's granulomatosus, and 20 patients with idiopathic membranous glomerulopathy by using autologous 99mTc-labeled heat-damaged red blood cells. With this method organ uptake could be measured by quantitative scintigraphy. There was no relation between the T1/2 of the blood disappearance curve and the T1/2 of the splenic uptake curve. The T1/2 of the blood disappearance curve was normal in all three patient groups. However, there was a significant shift from spleen to liver uptake in patients with active systemic lupus erythematosus, active Wegener's granulomatosus, and membranous glomerulopathy in comparison with a control group. There was no relation with age, level of circulating immune complexes, complement level, kidney function, or immunosuppressive treatment. We conclude that an increase of the liver component of reticulo-endothelial function may compensate abnormalities in splenic function. This stresses the importance of quantitative scanning to detect such abnormalities. The study provides evidence for disease related hyposplenism in patients with active systemic lupus erythematosus, active Wegener's granulomatosus, and membranous glomerulopathy.
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PMID:Abnormal reticuloendothelial function in patients with active vasculitis and idiopathic membranous glomerulopathy. A study with 99mTc-labeled heat-damaged autologous red blood cells. 684 Jan 27

Transformation of diffuse proliferative glomerulonephritis to membranous nephropathy 10 years later, in a patient with systemic lupus erythematosus, is reported. The original biopsy showed diffuse proliferative glomerulonephritis with epithelial crescent formation, 'wire loop' thickening of the capillary walls and moderately severe interstitial inflammation. Electron microscopy showed large subendothelial electron-dense deposits. Following treatment with a combination of prednisone and azathioprine for 2 years the 24-hour urine protein decreased from 8.8 g to 300 mg. In September, 1979, she again developed facial and pedal edema. With the exception of proteinuria of 6.0 g/24 h, the renal function remained normal. Repeat renal biopsy showed membranous glomerulopathy. On electron microscopy, electron-dense deposits were predominantly in a subepithelial position. The significance of the original biopsy as a predictor of eventual outcome and of sequential biopsies to the clinical management of patients with systemic lupus erythematosus is discussed.
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PMID:Transformation of diffuse proliferative glomerulonephritis to membranous nephritis in a patient with systemic lupus erythematosus. 726 28

We report a 16-year-old male who developed nephrotic syndrome related to membranous glomerulopathy with clinical and serological evidence of systemic lupus erythematosus after treatment with griseofulvin. To our knowledge, this is the first case of griseofulvin-exacerbated lupus in which nephrotic syndrome has been observed.
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PMID:Nephrotic syndrome related to systemic lupus erythematosus after griseofulvin therapy. 757 14

Renal biopsy specimens from 26 adult human immunodeficiency virus (HIV)-infected patients with glomerular involvement were reviewed from the files of three hospital pathology services in Northern Italy. All the patients were Italian and most (19 of 26 patients) were intravenous drug addicts. The types of glomerular lesions were as follows: minimal-change glomerulopathy (two cases), mesangial proliferative glomerulonephritis (GN) with scanty immunoglobulin deposits (four cases), and various patterns of immune complex-mediated glomerulonephritis, including postinfectious GN (six cases), membranoproliferative GN (one case), membranous GN (three cases), immunoglobulin (Ig) A nephropathy (four cases), a mixed membranous and proliferative (three cases) and diffuse proliferative lupus-like pattern with subendothelial deposits, and intraluminal thrombi (two cases) or subepithelial and subendothelial deposits (one case). None of the patients had evidence of HIV-associated nephropathy. Our study confirms previous observations on the low incidence of HIV-associated nephropathy among white HIV-infected patients in Europe, where immune complex-mediated GN seems to predominate. Apart from the frequent electron microscopic observation of endothelial tubuloreticular structures, none of the reported lesions could be distinguished on morphologic grounds from those occurring in uninfected patients. The high variability of the glomerular lesions upholds the need for accurate diagnosis for the clinician confronted with an HIV-positive patient with suspected glomerular involvement.
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PMID:Pattern of glomerular involvement in human immunodeficiency virus-infected patients: an Italian study. 764 52

Frozen samples of minimal change glomerulopathy (MCG), and of membranous, segmental and diffuse lupus glomerulonephritis (MGN, SGN, DLGN) were studied to assess the distribution of tenascin (Ten), and the extradomains A and B (EDA- and EDB-) and oncofetal (Onc-) isoforms of cellular fibronectin (cFn). Cryosections were immunostained by the ABC method with specific monoclonal antibodies. In MCG, mesangial Ten and EDA-cFn reactions were increased. In MGN, mesangial Ten and EDA-cFn staining was enhanced except in segmental scars; convincing reactions were seen in cases with membranous transformation; spikes stained strongly. In SGN, variably intense staining for Ten and all cFn isoforms was seen in glomerular necrosis, proliferation and crescents; parietal epithelium EDA-cFn staining was noted. In DLGN, strong and extensive mesangial Ten and EDA-cFn staining was seen as were focal EDB- and Onc-cFn reactions. Parietal cells with and without crescents stained variably with all Mabs. Obsolete glomeruli were unreactive save for rare periglomerular Ten rims. Interstitial inflammation and fibrosis in MGN, SGN and DLGN had moderate to strong Ten and EDA-cFn staining with rare traces of EDB- and Onc-cFn. We conclude that enhanced Ten and EDA-cFn is a potentially reversible response to glomerular injury whereas the expression of EDB- and Onc-cFn apparently result from necrosis and/or cellular proliferation which lead to scarring. And, while mesangial cells are the major source of these molecules, epithelial cells might also partake in their synthesis.
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PMID:Immunolocalization of tenascin and cellular fibronectins in diverse glomerulopathies. 768 61


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