Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UMLS:C0024141 (systemic lupus erythematosus)
 44,322 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The effect of plasma exchange on CIC, anti-dsDNA and complement levels and clinical activity was studied in eight patients with SLE, one with idiopathic anaphylactoid purpura and one with mixed cryoglobulinaemia. No association existed between different tests for immune complex detection. Plasma exchange as sole therapy was effective in patients with idiopathic anaphylactoid purpura and mixed cryoglobulinaemia, but not in one SLE patient with CIC. Five SLE patients with CIC treated with corticosteroids showed improvement on plasma exchange but in two patients with and two with CIC plasma exchange was not effective.
Proc Eur Dial Transplant Assoc 1979
PMID:Plasma exchange in immune complex disease. 16 5

Patients with end-stage renal disease secondary to SLE with or without preceding nonrenal disease manifestations, should have dialysis and/or transplantation offered to them. There is no increased risk of allograft rejection. Neither does there appear to be excessive risk of recrudescence of SLE disease activity.
Proc Clin Dial Transplant Forum 1977
PMID:Renal transplantation in systemic lupus erythematosus. 35 35

Neutrophils (PMN) appear to be involved in inflammatory phenomena as a result of direct interaction with immune complexes (IC). In SLE glomerulonephritis IC are fixed in vivo on the PMN surface through the receptors for FC fragments of complexed immunoglobulins and complement. Phagocytic properties are lost and immunological lysosomal release in vitro is markedly reduced by virtue of receptor occupation. The elimination of neutrophil cationic proteins (NCP) in urine is an expression of PMN lysosomal constituent release.
Proc Eur Dial Transplant Assoc 1977
PMID:In vivo fixation of immune complexes on polymorphonuclear cells and release of neutrophil cationic proteins in systemic lupus erythematosus (SLE). 60 Sep 64

C1q deposits are usually found in association with other complement components and immunoglobulins in proliferative glomerulonephritis and may predominate in systemic lupus erythematosus (SLE). We report the clinical outcome of four patients who developed a nephrotic syndrome associated with C1q nephropathy unrelated to SLE. On presentation the mean urinary protein loss was 6.8 g/24 h (range 4-10), and renal function impaired, mean serum creatinine 201 mumol/l (150-400). Over a mean follow up period of 6.5 years (1.7-19), all four patients improved, three spontaneously and one treated with steroids and cyclosporin, to a current urinary protein loss of 0.3 g/24 h (less than 0.2-0.9) and serum creatinine 98 mumol/l (68-115). C1q nephropathy was confirmed in each biopsy by conventional immunohistology. C1q deposits were demonstrated within the glomerular basement membrane of three biopsies and the mesangium in two samples. One patient had been categorized on light- and electron-microscopy as having mesangiocapillary glomerulonephritis, one membranous glomerulonephritis, one proliferative glomerulonephritis with focal segmental glomerulosclerosis, and one diffuse proliferative glomerulonephritis with both subendothelial and mesangial dense deposits. In view of the expected progressive nature of the underlying renal histopathological appearance, the presence of predominant C1q deposits would appear to be associated with a better clinical outcome.
Nephrol Dial Transplant 1992
PMID:C1q nephropathy: do C1q deposits have any prognostic significance in the nephrotic syndrome? 132 73

Renal transplant biopsies were obtained from 16 patients with systemic lupus erythematosus 6 months to 11 years post-transplant. Eight biopsies were taken on clinical grounds while eight were elective. Histopathological findings suggesting recurrent lupus nephritis were found in seven biopsies, five of which were taken on clinical indication. By light-microscopy, five graft biopsies showed proliferative glomerulopathy and two glomerulosclerosis. Immunofluorescence was positive for IgM and C3 in a finely granular pattern in all biopsies, for C1q in three, but for IgG in only two. Electron-dense deposits were found in all seven biopsies with predominantly subendothelial location. All but one patient had clinical signs of renal involvement, but only three had extrarenal symptoms and three had serological signs of active SLE. Upon increased immunosuppressive therapy, renal and serological signs improved but one graft was later lost due to recurrent SLE nephritis.
Nephrol Dial Transplant 1992
PMID:Recurrence of SLE in transplanted kidneys: a follow-up transplant biopsy study. 133 39

A cohort of 60 stable dialysis patients (56 haemodialysis, 4 continuous ambulatory peritoneal dialysis) was followed for 1 year to determine the relationship between anticardiolipin (aCL) antibodies and lupus anticoagulant (LA), and clinical events. The outcome measures were death, arterial, venous, and fistula thromboses, and fistula repairs. At baseline 15% had antibodies (5/60 IgG aCL, 3/60 LA, and 1/60 had both); 15 patients had a history of arterial thrombosis (1 patient was aCL positive), seven venous thrombosis (1 patient LA positive), 10 fistula thromboses (1 aCL positive); and 21 had a history of fistula repairs (4 aCL positive). Renal diagnosis, age (66.78 versus 59.67 years) and duration of dialysis (38.11 versus 45.25 months) were similar in patients with and without aCL antibodies or LA. Only the sex ratio showed a female predominance in the aCL- or LA-positive patients compared to the negative patients (3M:6F versus 36M:15F), but this was not significant (P = 0.07). After 1 year there were 10 deaths (1 LA positive), 12 thrombotic events in eight patients (none aCL or LA positive), and nine fistula repairs in seven patients (1 aCL-positive patient). We are unable to show higher rates of death, thrombotic event, or fistula repair in dialysis patients with aCL antibodies or LA followed up for 1 year in one centre. The clinical importance of antiphospholipid antibodies in dialysis patients is uncertain.
Nephrol Dial Transplant 1992
PMID:Are antiphospholipid antibodies clinically relevant in dialysis patients? 133 59

We have conducted an immunocytochemical analysis to investigate the presence of the recently described vascular cell adhesion molecule-1 (VCAM-1) in human kidney, using the anti-VCAM-1 monoclonal antibody 1.4C3. In normal control tissue VCAM-1 was present on some (but not all) parietal epithelial cells lining Bowman's capsule. Forty-nine of fifty clinical biopsy specimens were characterised by the additional presence of VCAM-1 on proximal tubular cells. This was most marked in biopsies of patients with interstitial nephritis or systemic vasculitis with crescentic nephritis, but was also observed in biopsies with minimal change, IgA or lupus nephropathy, or from patients with diabetic nephropathy, amyloid, or gout. Proximal tubule VCAM-1 correlated significantly with the number of transferrin-receptor-positive leukocytes (r = 0.607, p less than 0.0001) in the interstitium, but not with expression of HLA-DR by tubular cells. Surprisingly, VCAM-1 was not observed on vascular endothelial cells in these biopsies, even in the presence of a marked infiltrate; this contrasts with other tissues (e.g. skin and synovium). The presence of VCAM-1 on tubular cells in the inflamed kidney indicates the potential for these cells to interact with mononuclear cells, either as accessory cells or as cytotoxic targets. The unexpected absence of VCAM-1 in renal vascular endothelial cells suggests local differences in the endothelial cells of this organ.
Nephrol Dial Transplant 1991
PMID:Expression of VCAM-1 in the normal and diseased kidney. 172 89

Sixteen human renal biopsies taken from patients suffering from systemic lupus erythematosus nephritis were examined using an immunohistochemical method which allows the localisation of IgG at both light and electron-microscopical levels. The tissue was embedded in the hydrophilic resin lowicryl K4M and sections were stained using gold-labelled antibodies. On routine light microscopical examination the biopsies were diagnosed as: 1 case of WHO type II, 3 type III, 9 type IV, 2 type V, and 1 type III/V. Using light microscopy, IgG was localised in the glomerulus using the IGSS staining method. In some cases staining was seen within the glomerular epithelial cell cytoplasm. At the ultrastructural level the presence of IgG was demonstrated within vesicles in the cytoplasm of the epithelial cells in 0/1 type II, 2/3 type III, 8/9 type IV, 1/2 type V, and 1/1 type III/V cases: in some vesicles deposits of immune material were electron-dense but in others immune material was electron-lucent. Our results suggest that the human glomerular epithelial cell can endocytose IgG and that this may be part of a clearance mechanism acting within the glomerulus.
Nephrol Dial Transplant 1991
PMID:Glomerular epithelial cell endocytosis of immune deposits in human lupus nephritis. 187 Jul 47

Ten patients with rapidly progressive glomerulonephritis and acute renal failure were treated with extracorporeal immunoadsorption, prednisolone, and cyclophosphamide. Three patients had systemic lupus erythematosus, five had microscopic polyarteritis and two had Wegener's granulomatosis. All ten patients were dialysis-dependent prior to immunoadsorption. Nine of ten patients rapidly regained renal function and seven continue to have independent renal function between 9 and 30 months after immunoadsorption. Three patients at presentation were not dialysis dependent. Despite treatment with methylprednisolone, cyclophosphamide, and oral prednisolone, renal function continued to deteriorate and they required dialysis. Immunoadsorption was then started without alteration in baseline immunosuppression. Within a mean of 4.6 days, range 3-7 days, renal function improved and the patients no longer required dialysis. Antineutrophil cytoplasmic antibodies and double-stranded DNA antibodies were rapidly removed by immunoadsorption. Only one patient with systemic lupus erythematosus and two with microscopic polyarteritis had significant resynthesis of antibody at 1 month post-immunoadsorption. Renal biopsy before and after immunoadsorption and immunosuppressive therapy showed resolution of glomerular crescents and no evidence of active disease. Immunoadsorption coupled with prednisolone and cyclophosphamide may be of value in the treatment of rapidly progressive glomerulonephritis.
Nephrol Dial Transplant 1991
PMID:Treatment of rapidly progressive glomerulonephritis by extracorporeal immunoadsorption, prednisolone and cyclophosphamide. 195 51

Anticardiolipin antibodies are autoantibodies clinically associated with hypercoagulability. Systemic thrombosis and thrombosis of the vascular access for haemodialysis coexist with immunoregulation abnormalities in end-stage renal disease (ESRD). The aim of the present study was to analyse the incidence of thrombotic episodes and the presence of anticardiolipin antibodies and lupus anticoagulant in 73 patients with ESRD--51 on haemodialysis and 22 on conservative treatment. Four (18%) patients on conservative treatment had IgG-anticardiolipin, three of them also having lupus anticoagulant. Sixteen (31%) patients on haemodialysis showed IgG-anticardiolipin and 11 (22%) lupus anticoagulant; overall, 19 (37%) patients on haemodialysis had IgG-anticardiolipin and/or lupus anticoagulant. This greater incidence in haemodialysis was associated with a more frequent use of cuprophane membranes (68% versus 34%, P less than 0.05). Six patients with ESRD--one on conservative treatment--met criteria for the diagnosis of primary antiphospholipid syndrome, clinically characterised by thrombosis of the vascular access. IgG-anticardiolipin and/or lupus anticoagulant are frequently found in ESRD and their incidence increases with haemodialysis, probably due to some kind of membrane bioincompatibility. IgG-anticardiolipin and lupus anticoagulant can be associated with thrombotic episodes, being constituents of an ESRD-related antiphospholipid syndrome.
Nephrol Dial Transplant 1991
PMID:Anticardiolipin antibodies and lupus anticoagulant in end-stage renal disease. 195 52


1 2 3 4 5 6 7 8 9 Next >>