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Query: UMLS:C0409974 (lupus)
22,386 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Renal artery infarction is a very rare complication in patients with systemic lupus erythematosus (SLE), even in patients with antiphospholipid syndrome which often causes thromboembolism: Renal infarctions have only been reported in 4 SLE patients with antiphospholipid antibodies (aPL). Here we report a case of SLE without aPL who accompanied by renal and cerebral infarctions. A 42-year old Japanese woman with 8 year history of SLE manifested by arthralgia, central nervous system symptoms, positive-antinuclear and anti-DNA antibodies was admitted to our hospital for the treatment of progressive lupus nephritis. Physical examinations revealed hypertension (130-160/80-110 mmHg) without pitting pretibial edema. Laboratory evaluations showed proteinuria (3.7 g/day), normal serum creatinine level (0.9 mg/dl), low serum albumin level (2.3 g/dl) and high cholesterol level (317 mg/dl). Old cerebral infarctions were recognized by magnetic resonance imaging. However, hematological and immunological studies revealed that this case has neither a prolonged activated partial thromboplastin time, lupus anticoagulant nor anticardiolipin antibodies. Prednisolone was increased from 30 mg/every other day to 30 mg/day, and oral azathioprine, 50 mg/day, was started for the treatment of lupus nephritis. On the 11th day, she suddenly complained severe abdominal pain, which gradually localized on the right side. Computed tomography of the kidney suggested right renal infarctions, and arteriography of right renal artery confirmed both an obstruction of the ventral branch and a narrowing of the dorsal branch of right renal artery. No intra-cardiac thrombus was demonstrated by echocardiography. Following to the treatment with fibrinolytic agent and anticoagulant, her symptoms have improved.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Renal and cerebral infarctions in a patient with systemic lupus erythematosus without antiphospholipid antibodies]. 823 16

The significance of interstitial inflammatory and chronic tubulointerstitial lesions was studied in relation to the severity of glomerular lesions in 62 patients with lupus nephritis and 88 with IgA nephropathy. Severe interstitial inflammatory and chronic tubulointerstitial lesions were found in patients with severe glomerular lesions in both lupus nephritis and IgA nephropathy. In such cases, the serum creatinine levels at biopsy were high and the renal prognosis was poor regardless of the underlying disease (lupus nephritis or IgA nephropathy). No IgA nephropathy patients with nil or mild glomerular lesions had moderate or severe interstitial inflammatory and/or chronic tubulointerstitial lesions. In contrast, predominantly severe interstitial inflammatory lesions were found in 36% of lupus nephritis patients with nil or mild glomerular lesions. The prevalence of interstitial immune complexes deposition was markedly high in those with predominant interstitial inflammatory lesions. However, the severity of chronic tubulointerstitial lesions was mild and renal function did not deteriorate in the mean follow-up periods of 68.6 months. It is suggested that, besides the tubulointerstitial lesions attributable to the severe concomitant glomerular damage, the interstitial deposition of immune complexes per se plays a pathogenic role in the interstitial inflammatory lesions in lupus nephritis. Its prognostic significance, however, was considered to be minor.
Lupus 1993 Aug
PMID:Interstitial inflammatory and chronic tubulointerstitial lesions in lupus nephritis: comparison with those in IgA nephropathy. 826 75

The antiphospholipid syndrome is usually defined by the association of a clinical manifestation (recurrent venous and/or arterial thrombosis, recurrent spontaneous miscarriages) and a biological abnormality (anticardiolipin antibody, lupus anticoagulant). We retrospectively analyzed the records of 5 patients (4 females, 1 male, aged 30 +/- 12 years) with antiphospholipid syndrome, primary (n = 1) or secondary to systemic lupus erythematosus (n = 4), who developed malignant systemic hypertension with renal insufficiency, in the absence of lupus nephritis. Before the episode of malignant hypertension, all patients had normal systemic blood pressure and renal function. During malignant hypertension the systolic pressure was 206 +/- 39 mmHg and the diastolic pressure 130 +/- 25 mmHg, peak serum creatinine was 204 +/- 95 mumol/l, daily proteinuria was 1.1 +/- 0.8 gr, and complement serum levels were normal in all patients. Renal angiography found normal proximal renal arteries. Renal biopsy showed ischaemic glomeruli without proliferative lesions (n = 5), focal intimal fibrosis either isolated (n = 3) or associated with thrombosis (n = 2) of the intrarenal vessels, and the absence of vasculitis. Immunofluorescence study did not reveal typical lupus deposits. Patients were treated with antihypertensive agents, increasing doses of prednisone (n = 3), and anticoagulant (n = 2) or anti-aggregant therapy (n = 1). After a mean follow-up of 6.8 +/- 5.2 years, 4 patients were still alive with normal blood pressure and renal function, whereas 1 patient died of a probable catastrophic antiphospholipid syndrome. Patients with antiphospholipid syndrome, primary or secondary to systemic lupus erythematosus, may develop malignant hypertension with renal insufficiency and intrarenal vascular lesions, in the absence of lupus nephritis.
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PMID:Malignant hypertension in antiphospholipid syndrome without overt lupus nephritis. 827 82

OBJECTIVES--To investigate urine neopterin as a parameter of disease activity in an unselected group of patients with systemic lupus erythematosus (SLE) and to study the relation between urine neopterin and certain patterns of organ disease and differing drug regimens in the treatment of SLE. METHODS--Neopterin was determined by high performance liquid chromatography in 115 early morning urine samples from 68 patients with SLE. Serum soluble interleukin 2 receptor (sIL-2R) and antibodies to double stranded DNA (dsDNA) were determined by enzyme linked immunosorbent assay (ELISA), and the erythrocyte sedimentation rate (ESR), plasma C3, C4, and C3 degradation products (C3dg) were measured in corresponding blood samples. Disease activity was scored using the British Isles Lupus Assessment Group (BILAG) index. RESULTS--Urine neopterin was significantly increased in patients with active and inactive SLE compared with the control group and was significantly higher in patients with active than in those with inactive SLE. Urine neopterin did not distinguish between subsets of patients with SLE with particular patterns of organ disease, as defined by the BILAG index, nor was its level primarily influenced by differing drug regimens. Levels of serum sIL-2R, antibodies to dsDNA, the ESR, and plasma C3, C4, and C3dg were also significantly different between the patients with active and inactive SLE. Unlike urine neopterin there was considerable overlap in the values of these parameters between the two activity groups. Highly significant correlations found between urine neopterin and serum sIL-2R, ESR, and plasma C3, C4, and C3dg suggest the close association of neopterin with clinical activity in SLE. Multivariate logistic regression analysis showed that urine neopterin > 300 mumol/mol creatinine was a highly significant predictor of disease activity with an odds ratio of 3.51. CONCLUSIONS--Determination of urine neopterin, a non-invasive, relatively simple and inexpensive measurement, appears to be the best parameter for assessing and monitoring disease activity and treatment in patients with SLE.
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PMID:Urine neopterin as a parameter of disease activity in patients with systemic lupus erythematosus: comparisons with serum sIL-2R and antibodies to dsDNA, erythrocyte sedimentation rate, and plasma C3, C4, and C3 degradation products. 832 94

Our objective was to determine the effects of fish oil on renal function, symptoms, and serum lipids in patients with lupus nephritis. A double-blind, randomized crossover trial of fish oil versus placebo (olive oil) was done on 26 patients with confirmed systemic lupus; 21 completed the study. Intervention was fish oil or placebo, 15 g/day, for one year followed by a 10 week wash-out period, and then the reverse treatment for one year. At baseline and six month intervals, we measured platelet membrane fatty acids, indices of renal function, a disease activity index, serum lipid levels, blood pressure, serum viscosity and red cell flexibility. We found that platelet membrane phospholipids were uniformly affected by fish oil supplementation (P < 0.001) but with significant carry-over effects despite a 10 week wash-out period. Glomerular filtration rate and serum creatinine were not affected. A non-significant reduction in mean (SE) 24-hour proteinuria occurred, from 1424.1 mg (442.7) on placebo to 896.7 mg (352.2) on fish oil (P = 0.21). Fish oil lowered serum triglycerides from 1.89 (0.25) mmol/liter to 1.02 (0.11) mmol/liter (P = 0.004). VLDL cholesterol decreased markedly whether patients initially received fish oil or placebo (P = 0.004). The size of the reduction was affected by the order of treatment (P = 0.03), but parallel comparisons were significant before the crossover (P = 0.0006). With the possible exception of bleeding time, no other treatment effects were shown with fish oil. However, treatment order effects were seen in urinary IgG excretion (P = 0.03), whole blood viscosity (P < 0.0001), red cell flexibility (P = 0.004), and bleeding time (P = 0.06). In conclusion, one year of dietary supplementation with fish oil in patients with stable lupus nephritis did not improve renal function or reduce disease activity, but did alter some lipid parameters. Hitherto unreported carry-over effects and treatment order effects caused by the olive oil created a risk of type II error, and bear methodologic consideration in the design of future studies.
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PMID:Fish oil in lupus nephritis: clinical findings and methodological implications. 835 69

Sera from 45 patients with lupus nephritis (LN), 63 patients with immunoglobulin A nephropathy (IgA N), and 71 glomerulonephritic controls (including 44 mesangial proliferative glomerulonephritis cases, 14 membranous glomerulonephritis cases, and 13 focal segmental glomerular sclerosis cases), and from 33 normal control subjects were tested by a cellular enzyme-linked immunoabsorbent assay for their anti-endothelial cell antibody (AECA) activity. Compared with normal controls, AECAs of the IgG subtype (AECA-IgG) were detected in LN (P < 0.001) and AECAs of the IgA subtype (AECA-IgA) were detected in both IgA N and LN (P = 0.018 and P < 0.001, respectively). Binding activity of AECA to endothelial cells was inhibited by endothelial cell lysate and fibroblast lysate but not by lymphocyte lysate, double stranded-DNA, or bovine serum albumin. Anti-endothelial cell antibody-positive sera also reacted with fibroblasts. In IgA N, associations were found between the presence of AECA and younger age (P = 0.036), proportion of crescents greater than 10% (P = 0.016), fibrin crescents (P = 0.016), and focal and segmental necrotizing lesions (P = 0.047). In LN, inverse associations were found between the presence of AECA and the duration of disease (P = 0.021), elevated serum creatinine levels (P = 0.020), decreased creatinine clearance (P = 0.043), and frequency of chronic renal failure (P = 0.036). Positive associations were observed between the presence of AECA and active lupus (P = 0.017), anti-nuclear antibodies (P = 0.015), and anti-DNA antibodies (P = 0.041). Our results suggest that AECA may be linked with the pathogenesis of LN and IgA N.
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PMID:Clinicopathologic associations of anti-endothelial cell antibodies in immunoglobulin A nephropathy and lupus nephritis. 837 32

The role of intravenous and oral cyclophosphamide in treating systemic lupus and Wegener's granulomatosis was examined in several large studies during the past year. Oral cyclophosphamide for 2 months followed by prednisone alone was relatively ineffective in preventing disease progression in lupus nephritis patients with initially abnormal serum creatinine values. A controlled trial in which three regimens for treating lupus nephritis were compared resulted in superiority of long-term intravenous cyclophosphamide therapy over pulse prednisone or short-term intravenous cyclophosphamide. Two open studies describe treatment of neuropsychiatric lupus with pulse cyclophosphamide. Patients with clinical evidence of inflammatory disease of the central nervous system appeared to respond to this therapy even if antiphospholipid antibodies were present. Analysis of a large cohort of patients with Wegener's granulomatosis showed a high incidence of cancer at long-term follow-up as well as a high incidence of recurrence, often several years after induction of remission with cyclophosphamide plus prednisone. Much progress was made in defining the mechanisms of action of cyclosporine. Additional studies examine the role of cyclosporine in necrotizing scleritis complicating rheumatoid arthritis. Concomitant administration of nonsteroidal anti-inflammatory drugs and cyclosporine to rheumatoid arthritis patients resulted in increased short-term deterioration of renal function. Studies of patients with various autoimmune diseases showed an association of the mean, maximal, and cumulative doses of cyclosporine with biopsy-proven nephropathy. Cytarabine was tried at low doses in the treatment of rheumatoid arthritis with improvement in some patients.
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PMID:Immunosuppressive drug therapy for rheumatic disease. 851 65

Predominant tubulointerstitial lupus nephritis is rare. Only eight cases have been described in the literature. We report the case of a 59-year-old man with systemic lupus erythematosus who presented with acute renal failure. On renal biopsy, he was found to have chronic tubulointerstitial nephritis with a mononuclear infiltrate. The immunofluorescence showed immune deposits in the tubular basement membranes, interstitium, and glomerular capsule. The glomeruli were minimally involved. He was initially treated with high-dose corticosteroids and supported with hemodialysis. Renal function improved and dialysis was discontinued after three treatments. The corticosteroid dosage was gradually tapered. Renal function after 72 months of follow-up has remained stable (serum creatinine, approximately 1.9 mg/dL) and except for one relapse, there has been no clinical or serologic evidence of lupus activity. Furthermore, 24-hour urinary protein excretion has remained within the normal range.
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PMID:Predominant tubulointerstitial lupus nephritis. 865 6

To evaluate the results, the long-term prognosis and the rates of complication of an immunosuppressive regimen with corticosteroids and cyclophosphamide in the treatment of the nephritis of systemic lupus erythematosus, 21 patients with lupus glomerulonephritis were studied. Renal biopsies were performed in 17/21 of them and indicated diffuse proliferative (6 patients), diffuse mesangial (4) and membranous (7) glomerulonephritis. Treatment was structured in 4 phases: 1) induction with methylprednisolone 250 mg i.v. for 7-14 days, and cyclophosphamide 100-200 mg p.o., q.d., or 20 mg/kg i.v. every 28 days; 2) maintenance with prednisone p.o., 2 mg/kg q.o.d. for 45 days, and cyclophosphamide as before; 3) tapering, with reduction of prednisone by 15% each month for 4 months; 4) indefinite maintenance with prednisone slowly tapered to the least effective q.o.d. dose and cyclophosphamide discontinued after six months of treatment. This cycle was repeated in the event of a relapse. After a first immunosuppressive cycle, 20/21 patients achieved remission of glomerulonephritis. Plasma creatinine fell from 97 +/- 6 to 80 +/- 3 microMol/l (p < 0.01). Proteinuria fell from 2.1 +/- 0.4 to 0.2 +/- 0.4 g/d (p < 0.0001) and the nephrotic syndrome, present in 8 patients, disappeared. After an average of 20 +/- 7 months, 8 patients relapsed: all remitted again after a repeat cycle, but 1 later progressed to end-stage renal failure during pregnancy. After an average of 56 months 4 out of these 8 patients relapsed again: 1 progressed to end-stage renal disease following an abortion and 3 remitted completely after a third cycle. Thus, 18 out of 21 patients are presently in remission with an average dose of prednisone of 13.7 mg/day after an average follow-up of 52 +/- 38 months (range 2 to 156). Three patients are presently off treatment. In 16 patients with extended follow-up of 2 to 13 years, anti-nuclear antibodies, anti-DNA antibodies, albuminuria and cylindruria fell below post-cycle levels (p < 0.001 for all). We conclude that intensive immunosuppression with steroids and cyclophosphamide can achieve excellent long-term results in the treatment of systemic lupus with glomerulonephritis.
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PMID:Immunosuppressive treatment of the glomerulonephritis of systemic lupus. 871 48

Abnormalities of prostanoid metabolism, which may affect renal function, were studied in lupus nephritis. The subjects were 31 patients with lupus nephritis, ten with non-renal SLE, and four with renal, non-SLE collagen disease. Urinary levels of various prostanoids, thromboxane B2(TXB2), 11-dehydro-TXB2, 6-keto-PGF1 alpha,2,3-dinor-6-keto-PGF1 alpha and PGE2, and plasma level of 11-dehydro-TXB2, were determined. The effects of four days' dosing of a selective thromboxane A2 (TXA2) synthetase inhibitor, DP-1904 (DP), on prostanoid metabolism, were also studied. Urinary excretion of TXB2, which reflects the renal production of TXA2, was significantly increased in patients with lupus nephritis as compared with non-renal SLE (p < 0.05). The urinary TXB2/6-keto-PGF1 alpha ratio was also increased in lupus nephritis as compared with non-renal SLE or healthy controls (p < 0.01), indicating a prostanoid imbalance, which may lead to impaired renal function and subsequent pathology. The urinary TXB2/6-keto-PGF1 alpha ratio in these lupus nephritis patients showed negative correlations with Ccr and positive correlations with anti-DNA antibody titer (p < 0.001). DP was administered orally (400 mg/day, given in two divided doses) for four days to eight lupus nephritis patients. The urinary excretion of TXB2 and urinary TXB2/6-keto-PGF1 alpha ratio were decreased after one to two days of treatment in all patients. An increase in creatinine clearance used as a measure of renal function was observed in four of eight patients. Furthermore, no side effects were elicited during the four days of treatment. The conclusion reached were that the abnormal prostanoid metabolism observed in lupus nephritis could aggravate renal function through hemodynamic mediation, and that the deviated metabolism was reversible and, at least partially, corrected by a TXA2 synthetase inhibitor.
Lupus 1996 Apr
PMID:Abnormal prostanoid metabolism in lupus nephritis and the effects of a thromboxane A2 synthetase inhibitor, DP-1904. 874 26


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