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)

Lupus anticoagulant (LAC) is an acquired inhibitor of prothrombin activator complex, which probably interferes with the phospholipid portion. Characteristically, LAC prolongs the partial prothrombin time, but only slightly prolongs the prothrombin time. It is a paradoxical fact that LAC is characterized by thrombosis. It was initially described in patients with SLE, but recently, it has been described as occurring with other autoimmune disorders. Patients with LAC have been treated with steroid and aspirin, anti platelet agents or warfarin. Steroid and aspirin therapy has been reported useful for habitual abortion associated with LAC. In our study, 11 patients, whose prior pregnancies resulted in habitual abortion (41 abortions), received intentional prednisolone (40 mg/day) and aspirin (81 mg/day) therapy before further pregnancies. The doses of both agents were decreased gradually, and the therapy with prednisolone (10-15 mg/day) and aspirin (40.5 mg/day) was maintained during the pregnancy period. The outcome of pregnancy was successful in 7 out of 10 pregnancies. To evaluate the relationship between LAC and glomerulopathy, we examined the renal biopsy from 5 LAC cases without SLE. In pathological findings, there were 3 of with mild proliferative GN and 2 cases of minor glomerular abnormality. There were no characteristic findings in LAC nephropathy.
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PMID:[Lupus anticoagulant]. 130 2

A previously healthy 34-year-old woman, was diagnosed as having systemic lupus erythematosus (SLE), with membranous glomerulopathy which improved rapidly. Neither lupus anticoagulant nor anticardiolipin antibodies were detected in her plasma. After three months of total remission, she developed a severe pulmonary thromboembolism for which no specific biological cause was found. Her plasma was analysed for different antiphospholipid antibodies: lupus anticoagulant and anticardiolipin antibodies were again negative. Using an ELISA prepared with either five different anionic phospholipids or zwitterionic phosphatidylethanolamine, solely an anti-phosphatidylethanolamine IgG was discovered in her plasma. In lupus patients, the presence of antiphospholipid antibodies is now well recognized as a high risk factor for repeated thrombosis and/or recurrent abortions. This case suggests that the presence of antiphosphatidylethanolamine antibody should be investigated in cases of unexplained thrombosis in SLE, where the usual clinical and biological investigations have failed to shed light.
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PMID:Antiphosphatidylethanolamine antibody as the sole antiphospholipid antibody in systemic lupus erythematosus with thrombosis. 148 13

Excretion patterns of kidney related urinary proteins such as lysosomal beta-N-acetylglucosaminidase (beta NAG), brush-border Ala-(Leu-Gly)-aminopeptidase (AAP), gamma-glutamyl transpeptidase (GGT), and alkaline phosphatase (AP) as well as of IgG, albumin, and alpha-1-microglobulin, were assessed in patients with chronic glomerulonephritis (n = 53), pyelonephritis (n = 27), systemic lupus erythematodes (n = 5), and patients with essential arterial hypertension (n = 18). Excretion of tubular marker enzymes and serumproteins (related to urine creatinine concentration = protein creatinine index) in spontaneously voided second morning urine was significantly higher as compared to the controls (n = 2). Alpha-1-microglobulin was markedly elevated in both pyelonephritis and glomerulonephritis indicating disturbance in tubulointerstitial handling of microglobulins also in cases with primary glomerulopathy. Rise of albumin, IgG, and alpha-1-microglobulin as well as of tubular kidney markers AAP, AP, GGT, and beta NAG in cases with arterial hypertension without preexisting nephropathy support the hypothesis of a defect in charge and size permselectivity in these patients which is probably due to an increase in glomerular capillary perfusion pressure and hyperfiltration.
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PMID:Kidney- and serum derived proteins in urine of patients suffering from renal diseases or arterial hypertension. 247 9

A total of 411 children, aged from 0.3 to 18 years, suffering from glomerular diseases, were studied by renal biopsy between 1976 and 1985. The clinical presentation included nephrotic syndrome (79% of cases), renal failure (43%), and arterial hypertension (38%). In all, 177 cases presented with primary nephrotic syndrome; all had complicated courses and most were either corticosteroid-dependent or -resistant. Only 26.6% had minimal change disease on renal biopsy; 56.5% had focal-segmental sclerosis; and immunofluorescent deposits were observed in half of the group. Acute poststreptococcal (36 cases), mesangiocapillary (80 cases), and lupus (34 cases) glomerulonephritis occurred frequently; IgA glomerulopathy (10 cases) and haemolytic uraemic syndrome (6 cases) were uncommon. Glomerular crescents were observed in 71 cases. These observations illustrate the types of glomerular diseases seen in Iranian children.
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PMID:Glomerular diseases in children. "The Iranian experience". 270 71

The ddY mice are known to develop spontaneous glomerulonephritis resembling human IgA nephritis after 40 weeks of age. A sharp rise of circulating polyclonal IgG and IgA is also observed at this stage. Since these overproduced immunoglobulins seem to be related to the development of murine glomerulopathy, antigen-antibody interactions between renal tissue proteins and serum immunoglobulins were analyzed by Western blotting in ddY mice before and after 40 weeks of age. Serum IgG at 50 weeks reacted with an 18-kDa renal tissue protein which was identified as histone H3, as well as with histone H1. Renal histones were extracted along with IgG from the murine kidney at 50 weeks in a high salt soluble fraction. Serial studies of anti-histone antibodies by enzyme-linked immunosorbent assay showed that IgG class antibodies markedly increased after 40 weeks of age. IgA class antibodies mildly increased after 56 weeks of age. Anti-DNA antibodies were not detected. These results demonstrate that ddY mice also develop mainly IgG class and partly IgA class anti-histone autoantibody after 40 weeks of age, and that histone-anti-histone complexes may contribute to the development of murine glomerulopathy. Although anti-histone antibodies have been reported in lupus mice, ddY mice differ from these mice in that no anti-DNA antibodies develop.
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PMID:Anti-histone autoantibodies in ddY mice, an animal model for spontaneous IgA nephritis. 273 9

The renal glomeruli are vulnerable to injury by a number of drugs and other toxic agents. These agents may lead to damage by one of two basic mechanisms: direct, dose-related toxic injury; indirect, immunologically mediated injury, largely dose-independent. Proteinuria is the simplest and most important functional indicator of glomerular injury. It occurs almost immediately in direct toxic injury, but there is a latent period of weeks to months with immunologically mediated processes. Of the two mechanisms, the second is by far the more common in clinical settings. The best studied experimental agent causing direct toxic injury is the aminonucleoside of puromycin. Clinically, perhaps the most important agent is Cyclosporine A. Although this agent is usually thought of primarily as a tubular toxin, it is capable of giving rise to a microangiopathic glomerular lesion similar to that in the hemolytic uremic syndrome. The classic model for immunologic glomerular lesion is Heymann nephritis, which produces a membranous glomerulopathy. Clinically, most drug mediated glomerulopathies also take the form of a membranous nephropathy, usually with a frank nephrotic syndrome. Among the more common offenders are penicillamine, gold salts used in rheumatoid arthritis, and captopril used in hypertension. The other common type of drug-related glomerulopathy occurs as part of a lupus-like syndrome induced by a variety of drugs, including hydralazine, procainamide, and penicillamine. All of these give rise to a variety of antibodies, most prominently antinuclear antibodies, and in the more severe cases there may be lupus-like glomerular lesions as well.
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PMID:Drug-associated glomerulopathies. 294 Jun 67

D-penicillamine (DPA) leads to side effects in different ways: collagen and elastin crosslinking are inhibited, which results in thin and vulnerable skin, cutis laxa, elastosis perforans serpiginosa, wound healing defects and embryopathy. Toxic influences effect thrombo- and leukocytopenia (incidence 5-15%), gastrointestinal disturbances (10-30%), changes or loss of taste (5-30%), loss of hair (1-2%), and partly proteinuria (5-20%). Acute hypersensitive reactions include DPA-allergy (2-10%). Severe adverse effects are autoimmune phenomena such as pemphigus, DPA-induced lupus erythematosus, polymyositis/dermatomyositis, membranous glomerulopathy and hypersensitivity pneumonitis (like Good-pasture's syndrome) and myasthenia (all less than 1%). In addition there are a number of rare side effects, often single observations. Risk factors include a genetic disposition (especially HLA-B8 and -DR3), poor sulphoxidizers and, to a certain degree, higher age. During pregnancy and in clinically relevant disturbances of bone marrow, liver and renal function DPA is contraindicated. The total incidence of side effects amounts to 30-60%, the withdrawal rate is 20-30%; therefore clear indications and a regular survey of DPA therapy are necessary.
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PMID:[D-penicillamine--side effects, pathogenesis and decreasing the risks]. 306 3

Thirty-six renal biopsies from patients with various glomerulonephritides which exhibited prominent IgA deposits were studied by indirect immunofluorescence technique utilizing monoclonal antibodies specific for alpha chain (IgA), IgA1 and IgA2 subclasses, secretory IgA, and secretory component. The ability of the IgA deposits to bind free secretory component in vitro was examined in five biopsies of IgA nephropathy of Berger and in five biopsies of lupus nephritis. All the biopsies revealed IgA1 deposits. Associated IgA2 was found in lupus nephritides and hepatic glomerulopathy. Secretory IgA and free secretory component were not detected in any biopsy. In situ free secretory component binding was demonstrated in IgA nephropathy of Berger but not in lupus nephritides. These results indicate that polymeric IgA1 molecules are the chief nephritogenic antibodies in IgA nephropathy of Berger, that there is a high frequency of association of IgA1 and IgA2 in lupus nephritides and, perhaps, hepatic glomerulopathy, and that secretory IgA does not appear to play a role in IgA-associated glomerulonephritis.
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PMID:IgA-associated glomerulonephritides: a study with monoclonal antibodies. 369 46

The frequency, distribution, and intensity of C1q localization were evaluated in 800 renal biopsy specimens, and these observations were correlated with light, immunofluorescence, and electron microscopy findings. Intense C1q immunostaining was most frequent in proliferative and membranous lupus glomerulonephritis and in a recently described form of proliferative glomerulonephritis designated "C1q nephropathy." Moderate intensity C1q immunostaining was observed in most cases of type I but not type II, membranoproliferative glomerulonephritis. Unlike lupus membranous glomerulopathy, non-lupus membranous glomerulopathy usually did not have extensive C1q localization. C1q was scanty or absent in IgA nephropathy and antiglomerular basement membrane antibody mediated glomerulonephritis. C1q, along with IgM and C3, was often present at sites of glomerular sclerosis, especially in focal segmental glomerulosclerosis. Extraglomerular C1q was most frequent and most intense in cases of lupus nephritis having extraglomerular immune deposits. The presence or absence and intensity of C1q immunostaining were shown to be useful in the differential diagnosis of some glomerulopathies.
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PMID:Immunohistopathologic evaluation of C1q in 800 renal biopsy specimens. 388 12

After using a cellular digestion technique to extract cells from the basement membranes of frozen kidney tissue, we employed scanning electron microscopy to examine the acellular glomerular basement membranes (AGBM) from normal kidneys and from kidneys of patients with idiopathic membranous glomerulopathy (MGN). This method revealed, in the AGBM, previously unrecognized three-dimensional patterns of pathologic changes. These patterns correlated with increasing MGN stage as defined by Ehrenreich and Churg. On the epimembranous AGBM surface these patterns were composed of ridge-like trabeculae, irregular plaques, and reticulated crater-like deformities. The endothelial AGBM surfaces were smooth in stages I and II MGN, but in stage III MGN the endothelial surfaces were irregular and perforated. In contrast to lupus-related MGN, where some immune-complex-like material remained after cellular extraction, epimembranous immune-complex-like material in idiopathic MGN was extracted.
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PMID:Scanning electron microscopy of the acellular glomerular basement membranes in idiopathic membranous glomerulopathy. 394 44


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