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)

Recently a role of the upregulation ofcyclooxygenase isoforms in renal injury and modulation the severity of the inflammatory reactions is suggested. Cyclooxygenase exists as two isoforms COX-1 and COX-2 which are poorly understood with regard to their roles in renal function. Thereby, the present study was undertaken to ascertain the immunoexpression of cyclooxygenase-1 (COX-1) and cyclooxygenase-2 (COX-2) in lupus (LMGN) and nonlupus (NLMGN) membranous glomerulopathy and to examine the possible relationship between this immunoexpresion and inflammatory infiltrates. Eleven renal biopsy specimens from patients with class V lupus glomerulopathy and 16 from patients with primary (nonlupus) membranous glomerulopathy were examined by percutaneous renal biopsy. As a control 10 biopsy specimens of the kidneys removed because of trauma were used. In each specimen staining intensity of COX-1 and COX-2 in glomeruli, tubuli, arterioles and interstitial cells were recorded semiquantitatively whereas CD68+ cells, CD3+ cells and CD20+ cells were assessed quantitatively using computer image analysis system. Our study revealed that the mean scores of COX-1 immunoexpression did not differ significantly in all groups investigated whereas immunoexpression of COX-2 in LMGN was significantly stronger as compared with both NLMGN and controls. Moreover, in LMGN a significant positive relationship was noted between COX-2 immunoexpression and CD 68+ cells. In NLMGN and controls the correlations between COX-2 immunoexpression and CD 68+ cells were positive, but they have not reached statistical significance. In conclusion, our findings point that glomerular inflammation in lupus and non-lupus membranous glomerulopathy have different signalling pathways and suggest that in lupus nephritis COX-2 and monocytes/ macrophages but not COX-1 isoform are involved in the inflammatory process.
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PMID:Analysis of renal immunoexpression of cyclooxygenase-1 and cyclooxygenase-2 in lupus and nonlupus membranous glomerulopathy. 1845 55

A 61-year-old Japanese woman with both Takayasu's arteritis (TA) and systemic lupus erythematosus (SLE) presented with proteinuria due to glomerulopathy associated with podocytic infolding. She presented with unequal pulses in the upper extremities at 38 years old. TA was diagnosed on the basis of angiographic identification of stenosis in the left subclavian artery. Eight years after onset of TA, SLE was diagnosed on the basis of clinical and laboratory findings, including proteinuria, hematological and immunological abnormalities, high titer of antinuclear antibody, and a positive lupus band test on the skin. A renal biopsy showed lupus nephritis coexisting with podocytic infolding associated with TA, which has rarely been reported. After low-dose prednisolone therapy and immunosuppressive therapy by cyclosporine for 14 years, proteinuria has persisted without deterioration of serum creatinine levels.
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PMID:A case of lupus nephritis coexisting with podocytic infolding associated with Takayasu's arteritis. 1894 9

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

Renal transplantation (Tx) is the treatment of choice for end-stage renal disease. The incidence of acute rejection after renal Tx has decreased because of improving early immunosuppression, but the risk of disease recurrence (DR) is becoming relatively high, with a greater prevalence in children than in adults, thereby increasing patient morbidity, graft loss (GL) and, sometimes, mortality rate. The current overall graft loss to DR is 7-8%, mainly due to primary glomerulonephritis (70-80%) and inherited metabolic diseases. The more typical presentation is a recurrence of the full disease, either with a high risk of GL (focal and segmental glomerulosclerosis 14-50% DR, 40-60% GL; atypical haemolytic uraemic syndrome 20-80% DR, 10-83% GL; membranoproliferative glomerulonephritis 30-100% DR, 17-61% GL; membranous nephropathy approximately 30% DR, approximately 50% GL; lipoprotein glomerulopathy approximately 100% DR and GL; primary hyperoxaluria type 1 80-100% DR and GL) or with a low risk of GL [immunoglobulin (Ig)A nephropathy 36-60% DR, 7-10% GL; systemic lupus erythematosus 0-30% DR, 0-5% GL; anti-neutrophilic cytoplasmic antibody (ANCA)-associated glomerulonephritis]. Recurrence may also occur with a delayed risk of GL, such as insulin-dependent diabetes mellitus, sickle cell disease, endemic nephropathy, and sarcoidosis. In other primary diseases, the post-Tx course may be complicated by specific events that are different from overt recurrence: proteinuria or cancer in some genetic forms of nephrotic syndrome, anti-glomerular basement membrane antibodies-associated glomerulonephritis (Alport syndrome, Goodpasture syndrome), and graft involvement as a consequence of lower urinary tract abnormality or human immunodeficiency virus (HIV) nephropathy. Some other post-Tx conditions may mimic recurrence, such as de novo membranous glomerulonephritis, IgA nephropathy, microangiopathy, or isolated specific deposits (cystinosis, Fabry disease). Adequate strategies should therefore be added to kidney Tx, such as donor selection, associated liver Tx, plasmatherapy, specific immunosuppression protocols. In such conditions, very few patients may be excluded from kidney Tx only because of a major risk of DR and repeated GL. In the near future the issue of DR after kidney Tx may benefit from alternatives to organ Tx, such as recombinant proteins, specific monoclonal antibodies, cell/gene therapy, and chaperone molecules.
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PMID:Disease recurrence in paediatric renal transplantation. 1924 94

Fibrillary glomerulonephritis (FGN) is a rare immune-mediated glomerulopathy characterized by randomly arranged immunoglobulin (Ig) deposits on electron microscopy. Only seven pediatric cases have been reported, and the incidence in adults is about 1.5%. A 12-year-old boy presented with systemic lupus erythematosus (SLE) with World Health Organization Class IV lupus nephritis. A repeat biopsy carried out due to a poor response to standard immunosuppressive therapy and worsening renal functions revealed diffuse proliferative glomerulonephritis with fibrillary deposits. Despite aggressive immunosuppression with plasmapheresis and rituximab, the patient developed end stage renal disease. This is an atypical pediatric case characterized by SLE-associated FGN and a poor prognosis.
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PMID:Fibrillary glomerulonephritis and renal failure in a child with systemic lupus erythematosus. 1930 60

The aim of this study was to compare the clinical characteristics of recurrent and de novo membranous glomerulopathy (MG) among a cohort of 614 recipients transplanted between 1989 and 2006. Lupus nephritides were excluded. The diagnosis was established on protocol biopsies performed 1, 2, 4, or 8 years after transplantation or because of proteinuria/nephrotic syndrome and/or an increased serum creatinine level. HCV infection, cryoglobulinemia, monoclonal gammopathy, skin cancers, Kaposi sarcoma, diabetes mellitus, anti-HLA antibodies, and graft survival were not significantly different between the groups. Seventeen MG were diagnosed in 15 patients (2.45% of the whole group), including 6 recurrent MG (35%) and 11 de novo MG (75%). Recurrent MG occurred earlier than de novo MG (15.58 +/- 19.13 vs 49.27 +/- 32.71 months). Recipients with de novo MG were more frequently infected with HCV, which seemed to be the main etiologic factor for de novo MG, and may be linked to a Th2 polarization of the immune response.
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PMID:Recurent and de novo membranous glomerulopathy after kidney transplantation. 1932 52

Autoimmune disorders encompass a wide spectrum of diseases that progress with several clinical findings. They can be organ-specific (such as Hashimoto's thyroiditis) or they can involve multiple organs (such as SLE). The common characteristic of all these disorders is the production of different autoantibodies against various autoantigens along with inflammation. IgA nephropathy is the most common non-lupus glomerulopathy. It rarely coexists with SLE and has never been reported to coexist with Hashimoto's thyroiditis. In this case report, a female patient diagnosed with SLE and Hashimoto's thyroiditis and whose renal biopsy revealed IgA nephropathy is presented.
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PMID:Coexistence of systemic lupus erythematosus, Hashimoto's thyroiditis and IgA nephropathy in the same patient. 2073 88

Collapsing glomerulopathy is a rare form of glomerular injury, characterized by segmental or global collapse of the glomerular capillaries, wrinkling and retraction of the glomerular basement membrane, and marked hypertrophy and hyperplasia of podocytes. Prognosis is usually poor, with most cases developing end-stage renal disease, in spite of treatment. The association of collapsing glomerulopathy and systemic lupus erythematosus is very unusual. In this report, we describe the first case of a simultaneous diagnosis of collapsing glomerulopathy and diffuse proliferative lupus nephritis. The case presented with acute kidney injury and nephrotic syndrome and evolved with partial remission of nephrotic syndrome and recovery of renal function after aggressive treatment with intravenous cyclophosphamide and methylprednisolone.
Lupus 2011 Jan
PMID:Collapsing glomerulopathy associated with proliferative lupus nephritis: reversible acute kidney injury. 2107 65

C1q nephropathy is a rare idiopathic glomerulopathy characterized by mesangial deposition of immunoglobulin and complement with C1q dominance or co-dominance, and the absence of clinical and laboratory evidence of systemic lupus erythematosus. Its clinical course is unpredictable and the response to corticosteroid or cytotoxic treatment is variable. Here, we report two cases of C1q nephropathy, one in a child and one in an adult, both presenting with impaired renal function and massive proteinuria. Both patients failed to respond to immunosuppressive medications; however, rituximab, an anti-CD20 antibody, was effective in preserving renal function in one patient and eliminating the need for hemodialysis in the other. In one patient, histologic regression of abnormalities was documented over 3 years post-treatment. Both patients have remained off other immunosuppressive medication for a prolonged period with stable renal function. These cases are, to our knowledge, the first reported successful treatment of C1q nephropathy with rituximab.
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PMID:Resolution of clinical and pathologic features of C1q nephropathy after rituximab therapy. 2110 33

Human immunodeficiency virus (HIV) involves glomerular, tubulointerstitial, and vascular compartments of the kidney. The most common glomerular lesion is HIV-associated focal segmental glomerulosclerosis (FSGS) and related mesangiopathies collectively termed HIV-associated nephropathy (HIVAN). A variety of immune-complex mediated glomerular diseases such as membranoproliferative glomerulonephritis (MPGN), IgA nephropathy, and lupus-like glomerulonephritis also occur. HIVAN is restricted to patients presenting with proteinuria and progressive reduction of renal function and with distinctive but not pathognomonic pathology (FSGS often coexisting with glomerular collapse and tubular microcystic dilatations). The worldwide incidence of collapsing glomerulopathy (CG) in HIV-positive patients is high in Americans. But in India and other Asian countries, other forms of kidney diseases are more commonly seen. We report the first case of CG in the state of Jammu and Kashmir which also happens to be a very low incidence belt for HIV.
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PMID:Collapsing glomerulopathy in an HIV-positive patient in a low-incidence belt. 2120 85


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