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)

From a group of 75 patients with systemic lupus erythematosus (SLE), 30 patients with lupus nephropathy presenting concomitant changes of the CIC level, of the complement system (C3 and C1q factors) and proteinuria were chosen for the study. In these 30 patients, no statistically significant correlation was observed between CIC level and the value of serum complement. Low serum complement was observed in 89% of the cases while low complement values associated with increases of the CIC level were observed only in 57.8% of the cases. From the values of the C3 and C1 complement factors it results that in 76.6% of the cases of lupus nephropathy the activation of complement was achieved in the classical way. The value of proteinuria presented no significant correlation with any of the parameters investigated. The serum immunogram presented varied aspects and the components of the CIC structure revealed a great diversity of this structure.
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PMID:Circulating immune complexes and the complements system in lupus nephropathy. 149 64

The treatment of patients with immune nephropthies is discussed: rapidly progressive nephritis, lupus nephropathy, Wegener granulomatosis, Goodpasture syndrome, Schonlein-Henoch nephritis. A combined treatment of plasmapheresis and immunosuppressants is applied. A definite result, specially with the cases of Wegener granulomatosis, is registered for certain number of the patients. Together with the usual tests: CIC, immunoglobulins, complement, etc. a method for controlling of the detoxic efficiency of the treatment is suggested. This is a biologic method- the level of paramecium caudatum in media from patients' plasma is registered in relation to time. After plasmapheresis the life of paramecium caudatum is considerably prolonged.
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PMID:Combined treatment of immune nephropathies with plasmapheresis and immunosuppressants. 325 39

The reduced level of complement receptor 1 (CR1) on erythrocytes is speculated as a key mechanism contributing to immune complex (IC) overload and exaggerated complement (C) activation in systemic lupus erythematosus (SLE). Comparatively, fewer studies documented lower levels of CR1 on leukocytes and glomerular podocytes in this disease. The decline in E-CR1 is largely believed as an acquired phenomenon caused due to the proteolytic cleavage of CR1 from erythrocyte membrane. The mechanism underlying reduced CR1 expression on nucleated cells is under constant investigation. Recently, reduced leukocytes CR1 gene transcription had been demonstrated in SLE and was suggested as the main cause of decline in leukocyte CR1 (L-CR1). The relationship of L-CR1 gene transcription with severity and pathophysiology of disease needs to be elucidated. We determined the levels of L-CR1 in 30 active SLE patients and compared with normal healthy controls (n = 30). Patients were categorized into two groups i.e., with nephritis (n = 14) or without nephritis (n = 16). The expression of L-CR1 at transcriptional level was correlated with the levels of serum CIC, C3 and anti dsDNA antibodies. The levels of L-CR1 transcription were significantly reduced in all SLE patients as compared to controls (P < 0.001). This decline in L-CR1 however, was more marked in patients with nephritis than those without nephritis. In addition, the serum levels of CIC, anti dsDNA antibodies were higher and the levels of serum C3 were lower than the normal range in the patients. The difference was much more marked in SLE patients with nephritis than those without nephritis. The levels of L-CR1 transcription correlated negatively with the levels of CIC and anti dsDNA antibodies and positively with serum C3 levels. Thus, between SLE patients with and without nephritis, we found significant difference in the levels of L-CR1 transcription (P < 0.01), CIC (P < 0.05), anti dsDNA antibodies (P < 0.01) and C3 (P < 0.01). Our findings suggest that L-CR1 is drastically reduced in patients with severe form of SLE, i.e., lupus nephritis. Determination of L-CR1 expression at transcriptional level in addition to disease hallmarks like C3, CIC and anti-dsDNA antibodies may facilitate the assessment of severity of SLE and discrimination between patients with or without renal involvement.
Lupus 2005
PMID:Association of leukocyte CR1 gene transcription with the disease severity and renal involvement in systemic lupus erythematosus. 1586 13

Thirty silent lupus nephritis (SLN) patients were compared to 16 individuals bearing overt lupus nephritis (OLN). Results included: years of systemic lupus erythematosus (SLE) diagnosis were significantly earlier (4.6 +/- 2.8 years) in SLN than in OLN (7.18 +/- 3.61) (P < 0.05). Neurological compromise, hypertension, normocitic anemia and lymphopenia were significantly prevalent in OLN than in SLN (P < 0.05). Beside normal urinary sediment and renal function tests, the SLN group showed a moderate increase of both activity (AI) and chronicity (CI) renal pathology index when compared to highly increased AI and CI in OLN (P < 0.05). Seventy percent of SLN patients were ISN/RPS Classes I (6.6%) and II (63.3%) while 81% of OLN cases were Classes III, IV (37.5%) and V. IgG, IgA, IgM, lambda chain, C3 and fibrinogen immune deposits were found in 90% or over in both SLN and OLN individuals while in 60% or over, both groups also showed kappa chain, Clq and C4 deposits. While prevalence of ANA, anti-dsDNA and anti-C1q antibodies were similar in both groups, anti-histone, anti-RNP, CIC and CH50 serum levels were significantly different in OLN versus SLN (P < 0.05). We strongly suggest that indeed SLN is the earliest stage in the natural history of lupus nephritis.
Lupus 2006
PMID:Further description of early clinically silent lupus nephritis. 1721 89