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)

The local graft-versus-host reaction (GVHR) following intradermal injection of peripheral blood lymphocytes (PBL) in Lewis rats was examined in order to test the cell-mediated immunity (CMI) in 31 patients with renal disease and in healthy controls. It was found that patients with lipoid nephrosis (LN) in the nephrotic stage and systemic lupus erythematosus (SLE) had less mean lesion of the local GVHR and a smaller proportion with positive reactions as compared to normal subjects. This abnormality in LN patients was correlated well with the degree of delayed hypersensitivity skin test responses to purified protein derivative (PPD) and improved with the onset of clinical remission. In contrast, the mean lesion in PBL from LN patients without nephrotic syndrome (NS) and from chronic mesangial proliferative glomerulonephritis (CGN) did not differ from the normal subjects. These findings raise the question of a selective defect in CMI in LN patients with NS. Our studies also indicate that the local GVHR represents a rapid, clinically useful test for assessing cellular immunocompetence in renal disease.
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PMID:Depression of local graft-versus-host reaction in patients with lipoid nephrosis. 387 48

The T-colony-forming capacity was examined in 13 normal subjects and 14 patients with biopsy-proven lipoid nephrosis (LN). Eighteen additional patients with other well-defined forms of glomerulonephritis were studied as a disease control. Significantly fewer T lymphocyte colonies were found in LN patients and the nephrotic syndrome (NS) than in normal controls. A similar change could be observed in the groups with other types of NS. LN patients with NS had the lowest values of T-colony-forming cells (TCFC), but there was no statistically significant difference between the groups of nephrotic subjects. It was also of interest that peripheral blood lymphocytes (PBL) from 3 patients with lupus nephritis (SLE) produced significantly low levels of TCFC. The lower levels of TCFC in LN could be enhanced when exogenous interleukin 2 (IL 2) was added to the system. We also examined the production of T-colony-stimulating factor (TCSF). The TCSF production by stimulated PBL from LN patients was lower than in normal subjects. To explain our observations, we presumed that the T colony dysfunction seen in LN patients with NS might in part be due to the decreased TCSF activity.
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PMID:Impaired T-lymphocyte colony formation in lipoid nephrosis. 387 48

Four of 10 children with SLE kept under observation over the past nine years have developed avascular necrosis (AN) of the femoral head. The symptoms of AN are insidious and unpredictable and predate the radiologic diagnosis by weeks to months. In a comparison of these children with SLE, with and without AN, with a group of patients with nephrosis treated with corticosteroids and a group with glomerulonephritis treated with azathioprine, AN was related to the duration of daily steroid therapy rather than the total duration of steroid treatment; this was not true for azathioprine. The occurrence of AN in our patients while they were on alternate-day steroid therapy, or coincident with a relapse, suggests that its development is determined by underlying disease.
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PMID:A vascular necrosis of the femoral head in childhood systemic lupus erythematosus. 442 18

In this study, three kinds of monoclonal antibodies directed at human T lymphocytes, produced by mouse hybridomas and termed OKT3, OKT4, and OKT8, were used in an indirect immunofluorescence assay, to analyze the distribution of peripheral T lymphocyte subsets in 41 patients with glomerulonephritis (GN) and 11 patients with systemic lupus erythematosus (SLE). As assessed by functional studies, OKT4 and OKT8 defined the helper and cytotoxic/suppressor T lymphocytes subsets, respectively, whereas OKT3 recognized all peripheral T-cells. Among GN patients, the ones presenting membranous GN (MGN), IgA disease, and lipoid nephrosis associated with segmental and focal hyalinosis (FGS) showed significant decrease of their peripheral cytotoxic/suppressive T cells. On the contrary, no significant alteration was found in the peripheral T cell distribution of patients with membranoproliferative GN (MPGN) and lipoid nephrosis associated with minimal-change GN (MCGN). Unexpectedly, there was a tendency for peripheral cytotoxic/suppressive T lymphocytes to be high in the majority of SLE patients, and only two of these subjects exhibited a relative decrease in peripheral OKT8 marked cells. The steroid therapy received by our patients might account for this discrepancy with previous reports of altered suppressor function in active SLE.
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PMID:Abnormalities of T-cell subsets in glomerulonephritis and systemic lupus erythematosus. 645 2

In order to elucidate their role in mediating renal immune injury in man, the glomerular C3b receptors have been analyzed in frozen sections of 205 kidneys biopsied from 199 patients affected by various well-defined renal diseases. Using fluoresceinated C3b-coated bacteria as the indicator system, the receptor activity has been compared with that found in 10 normal human kidneys. In 76 out of 98 cases (77%) of glomerulonephritis (GN) with capillary wall abnormalities, a significant loss of receptor activity has been observed. No difference was present between the 89 patients affected by GN presumably due to immune complexes (ICX) parietal deposition (membranoproliferative, membranous, acute poststreptococcal GN and proliferative GN of SLE and cryoglobulinemia) and the 9 patients affected by GN presumably due to anti-GBM antibodies (Goodpasture's syndrome and extracapillary GN). In the group of ICX-GN, no correlation could be demonstrated between inhibition of C3b receptors and the presence of parietal C3 deposits. A significant loss of receptors activity has been also demonstrated in 12 out of 13 patients with amyloidosis or diabetic glomerulosclerosis. On the contrary, inhibition of C3b receptors has been observed in only 3 out of 20 patients with nonglomerular renal diseases (interstitial and vascular nephropathies) and in only 11 out of 57 patients (19%) affected by mesangial GN with no capillary wall abnormalities (Berger's disease, Henoch-Schonlein purpura and mesangial GN of SLE). C3b receptors were normal in 13 out of 17 patients affected by lipoid nephrosis (minimal change GN or focal glomerulosclerosis). In conclusion, the analysis of C3b receptors in renal diseases do not support the hypothesis of their involvement in parietal localization of C3b-bearing ICX: these results rather suggest that the receptors become undetectable in many glomerular diseases (immune-mediated or not) with lesions of capillary walls, because of the loss of integrity of C3b receptor-bearing visceral epithelial cells.
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PMID:Significance of glomerular C3b receptors in human renal diseases. 645 26

Utilizing transmission electron microscopy we have found multiple cilia with a 9 + 2 microtubular pattern (the same type found in the bronchial tree) in the renal tubules of four adults with the nephrotic syndrome. Each patient had a different pathologic diagnosis: amyloidosis, lipoid nephrosis, membranoproliferative glomerulonephritis, and focal segmental glomerulosclerosis. Previously, multiple renal tubular cilia with 9 + 2 architecture had been reported in patients with Burnett's syndrome, systemic lupus erythematosus, and congenital nephrotic syndrome. Additionally, we found multiple cilia in the metanephric tubules of 4 of 4 human fetuses. Pathologists should be aware that cilia with various microtubular patterns occur in human adult kidneys.
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PMID:Cilia in the human kidney. 648 21

Plasma protein loss via gastrointestinal tract was determined in 24 patients with clinical and laboratory data for manifested nephrosis syndrome, 21 of them being with various histological forms of chronic glomerulonephritis, 2--with disseminated lupus erythematosus and 1--with renal amyloidosis. Isotope labelled chromium trichloride was intravenously applied, marking the albumin pool in a dose of 0.5 micro curie (20 KBq/kg body weight). In four patients an increased fecal radio-activity was established amounting to 1.00 to 2.63 per cent of the injected dose for 96 hours. The possible causes for that phenomenon are discussed as well as its significance in the advancement of nephrosis syndrome.
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PMID:[Plasma protein loss via the gastrointestinal tract in nephrotic syndrome patients]. 667 79

Lactic acid (LA) concentrations in the pleural fluid of 75 patients were determined by the Monotest Lactate Kit (MLK). Lactic acid values in 18 cases of bacterial or tuberculous pleural infection were strikingly higher (mean 81 mg%, range 45-200 mg%), than in 42 cases with pleural effusion due to congestive heart failure, hepatic cirrhosis, nephrosis, trauma, and systemic lupus erythematosus (SLE; mean 19 mg%, range 6-47 mg/). High levels of LA were also found in the pleural fluid of 15 patients with malignancy of pleural cavity. Determination of LA can be an additional rapid tool in the differentiation between bacterial pleural inflammation and pleural effusion of various forms except in cases with malignancy of the pleural cavity.
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PMID:Measurement of lactic acid in pleural fluid. 722 Dec 2

Clinical manifestations and immunological characteristics in a series of 15 patients with systemic lupus erythematosus and renal involvement are presented. These findings have been correlated to different pathologic lesions and compared to another series of patients without renal involvement. The overall rate of renal involvement was 25 percent, with ages ranging from 14 to 47 years. A female predominance was noticed. Histopathologic findings were as follows: focal glomerulonephritis (five cases), and minimal changes (one case). Under a histological glomerulonephritis (two cases); membranous glomerulonephritis (one case), and minimal change (one case). Under a histological standpoint the earliest lesions had the worse prognosis. Patients with diffuse glomerulonephritis showed a high degree of renal function impairment. Urinary infection was present in half of the cases. A significant hyperlipidemia was found in patients with nephrosis. Proteinuria and abnormal urinary sediment were common findings in all histologic types. Antinuclear antibodies, were positive in 14 cases, with statistical significant high titres in diffuse glomerulonephritis. Serum immunoglobulins IgG and IgA were elevated. Decrease of serum complement levels (C3, C4, C3PA and C5) were found in patients with renal involvement.
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PMID:[The spectrum of lupus nephropathy]. 742 56

Seven patients suffering from systemic lupus erythematosus (SLE) were treated by cyclosporin A (CSA) plus corticosteroids. The indications for treatment were: lupus nephritis refractory to treatment with corticosteroids and cyclophosphamide (one patient), nephrosis syndrome or lupus nephritis associated with severe cytopenia and refractory to corticosteroid treatment (5 patients), severe thrombocytopenia refractory to conventional treatments (one patient). The treatment for 6 months of this latter patient resulted in complete remission, lasting for at least 1.5 years. Patients with kidney involvement also responded to therapy. The response manifested within 1 month. Treatment lasted for a mean of 5.1 months (the treatment of one patient was interrupted after 1 month because of lack of cooperation). There were no side effects. CSA treatment in combination with corticosteroids, when properly indicated, may be beneficial in SLE.
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PMID:[Cyclosporin therapy of patients with systemic lupus erythematosus]. 782 58


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