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)

Renal disease, a major feature of systemic lupus erythematosus (SLE), rarely occurs in drug-induced SLE. Immune complex glomerulonephritis has been demonstrated in a few cases of SLE following procainamide or anticonvulsant therapy but has not been documented in association with hydralazine-induced SLE despite the recognition of this syndrome 30 years ago. We report the clinical and renal pathologic findings in a patient with hydralazine-induced lupus nephritis and review the renal pathologic material in earlier reports of hydralazine-induced SLE.
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PMID:Immune complex glomerulonephritis in hydralazine-induced SLE. 622 78

Systemic lupus erythematosus (SLE) is a chronic systemic autoimmune disease characterized by the production of antibodies directed against self antigens. Immune complex glomerulonephritis (GN) is one of the most serious complications of this disorder and can lead to potentially fatal renal failure. The aetiology of SLE is complex and multifactorial, characterized by interacting environmental and genetic factors. Here we examine the nature of the renal pathology in mycobacteria-treated non-obese diabetic (NOD) mice, in order to assess its suitability as a model for studying the aetiopathogenesis of, and possible treatment options for, lupus nephritis (LN) in humans. Both global and segmental proliferative lesions, characterized by increased mesangial matrix and cellularity, were demonstrated on light microscopy, and lesions varied in severity from very mild mesangiopathic GN through to obliteration of capillary lumina and glomerular sclerosis. Mixed isotype immune complexes (IC) consisting of immunoglobulin G (IgG), IgM, IgA and complement C3c were detected using direct immunofluorescence. They were deposited in multiple sites within the glomeruli, as confirmed by electron microscopy. The GN seen in mycobacteria-treated NOD mice therefore strongly resembles the pathology seen in human LN, including mesangiopathic, mesangiocapillary and membranous subclasses of LN. The development of spontaneous mixed isotype IC in the glomeruli of some senescent NOD mice suggests that mycobacterial exposure is accelerating, rather than inducing, the development of GN in this model.
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PMID:Mycobacteria, an environmental enhancer of lupus nephritis in a mouse model of systemic lupus erythematosus. 1251 5

Immune complex glomerulonephritis is a common diagnosis in renal biopsy series of human immunodeficiency virus (HIV)-infected patients. There are a variety of glomerulonephritides associated with HIV infection, including IgA nephropathy, membranoproliferative glomerulonephritis, membranous nephropathy, lupus-like glomerulonephritis, immunotactoid glomerulopathy, and fibrillary glomerulonephritis. In addition, HIV-related proteins may be implicated in circulating immune complexes directly related to a response to the infection. In some cases, the relationship of the HIV infection to the glomerulonephritis is unclear. HIV infection is associated with the development of polyclonal hypergammaglobulinemia, which can promote the development of circulating immune complexes. It is not clear if HIV-associated glomerulonephritis is caused by the passive trapping of these circulating immune complexes or the in situ deposition of antibodies binding to HIV viral antigens. Some renal lesions that are seen in the setting of HIV infection more likely may be related to the presence of a co-infection such as hepatitis C virus infection. The optimal therapy for immune complex glomerulonephritis in the setting of HIV infection is unknown. Because of the underlying immunosuppressed state of many HIV-infected patients, caution with traditional cytotoxic therapies is advised. The role of antiretroviral therapy in modifying the course of these renal lesions is unclear.
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PMID:Immune complex renal disease and human immunodeficiency virus infection. 1901 24