Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0033687 (proteinuria)
 24,015 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Anticardiolipin antibodies (aCL) were recently discovered to recognize a complex consisting of phospholipids and apolipoprotein H (apo H). In this study, we determined the serum apo H levels in 36 systemic lupus erythematosus (SLE) patients with or without antiphospholipid antibodies (aPL), including aCL and lupus anticoagulants, to clarify the possible effects of aPL on apo H levels in vivo. The apo H levels were low in SLE patients as compared with 22 healthy controls. However, no associations were found between apo H levels and circulating aPL or clinical features of the antiphospholipid antibody syndrome. A secondary hyperlipidemic state, which probably related to lupus nephritis (proteinuria) and/or prednisolone treatment, increased apo H levels in SLE patients.
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PMID:Serum apolipoprotein H levels in systemic lupus erythematosus are not influenced by antiphospholipid antibodies. 130 75

Our objective was to define the renal involvement in primary antiphospholipid syndrome (APS). We studied 20 patients with primary APS. Fourteen were women, mean age 34.4 years. None met ARA criteria for systemic lupus erythematosus. All patients underwent complete renal function studies. The presence of hypertension was also investigated. Renal disease was found in 5 patients, and was characterized by proteinuria, hypertension and renal failure. Kidney biopsy was performed in these 5 patients, showing thromboses of the microvasculature, mesangiolysis, mesangial interposition, electron lucent subendothelial material and ischemic obsolescence of glomeruli. Arterioles showed luminal narrowing due to medial hypertrophy, mucoid thickening of the intima, thrombosis and fibrosis. We found renal disease in 25% of our patients with primary APS. Biopsy findings were consistent with a thrombotic microangiopathy involving both arterioles and glomerular capillaries.
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PMID:Renal involvement in primary antiphospholipid syndrome. 815 77

A 23-year-old woman, who had nonbullous congenital ichthyosiform erythroderma since her childhood, was diagnosed as nephrotic syndrome caused by systemic lupus erythematosus (SLE). She was pregnant but experienced fetal loss at the age of 25. Although 10 mg/day of oral prednisolone was administered, low levels of serum complement, proteinuria, thrombocytopenia (6.0 x 10(4)/mm3) and biological false positive for STS continued. When she was 27 years old, right hemichorea developed. She was admitted to our hospital at the age of 28 because of low levels of serum complement, high titers of anti ds-DNA antibody, profuse proteinuria, gingival bleeding and thrombocytopenia (1.5 x 10(4)/mm3). The nephrotic syndrome gradually improved after 1 g/day of methylprednisolone for 2 days and the oral prednisolone dosage was then increased up to 40 mg/day, and was tapered to 10 mg/day. Epileptic attack (minor seizure) occurred at the age of 29. Continuous low levels of serum complement and high titers of anti ds-DNA antibody were improved by adding 50 mg/day of cyclophosphamide. However, high levels of beta 2 GPI dependent anticardiolipin antibody and lupus anticoagulant activity were observed throughout the study. Our patient was a very rare case of congenital ichthyosis with typical antiphospholipid antibody syndrome and SLE. A few cases of acquired ichthyosis associated with SLE has been reported, and ichthyosis developed only in active stage of SLE. However, our patient's ichthyosiform lesions were not changed throughout the course.
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PMID:[Systemic lupus erythematosus and antiphospholipid antibody syndrome in a patient with congenital ichthyosiform erythroderma]. 748 67

Antiphospholipid antibodies (aPL) are associated with thrombosis, thrombocytopenia and recurrent fetal loss in humans and in some animal models. Immunization with beta 2 glycoprotein I (beta 2GPI) induced aPL production in normal rabbits and mice. However, the association of these antibodies with disease manifestations remains controversial. To determine whether induction of aPL by beta 2GPI immunization in an autoimmune strain of mice (MRL/++) would result in acceleration of clinical and serological autoimmune disease manifestations, three groups of 8-week-old female mice were studied. One group was immunized with beta 2GPI, and one with ovalbumin (OVA); the third was not immunized. After two booster injections, sera were analysed for the presence of anticardiolipin (aCL) and anti-DNA by ELISA and anti-nuclear antibody (ANA) by immunofluorescence. Mice were studied for thrombocytopenia, proteinuria, fecundity rates, litter sizes and the development of central nervous system dysfunction. Elevated levels of aCL, anti-DNA and ANA were detected in all beta 2GPI-immunized, in three OVA-immunized, and in none of the unimmunized mice. The anti-DNA antibodies were inhibited by CL micelles, suggesting cross-reactivity between aCL and anti-DNA. Platelet counts, fecundity rates and litter size were reduced in beta 2GPI-immunized but not in OVA-immunized or unimmunized mice. None of the mice developed neurological dysfunction or significant proteinuria over a 10-week period post-immunization. These findings suggest that beta 2GPI immunization induces aPL in MRL/++ mice associated with accelerated autoimmune manifestations resembling the antiphospholipid syndrome.
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PMID:Early onset of autoimmunity in MRL/++ mice following immunization with beta 2 glycoprotein I. 762 96

A 42-yr-old woman with hypertension and renal involvement due to systemic lupus erythematosus (SLE) developed unilateral headache followed by the sudden onset of confusion and a grand mal convulsion. Cerebral computed tomography was normal. A magnetic resonance imaging angiogram revealed cerebral venous thrombosis and a venous infarct. Nephrotic syndrome had resulted in an acquired protein S deficiency. A review of previous cases suggests that either renal disease with proteinuria or features of the antiphospholipid syndrome are prerequisites for the development of cerebral venous thrombosis in SLE. Low free-protein S levels may be an additional risk factor. Furthermore it is likely that this condition is underdiagnosed.
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PMID:Cerebral venous thrombosis and acquired protein S deficiency: an uncommon cause of headache in systemic lupus erythematosus. 763 1

Antiphospholipid antibodies are associated with fetal distress and fetal death. Although different therapeutic regimens have been used, the incidence of fetal growth retardation varies between 30 and 60 per cent of reported cases. We report the evolution of fetal growth in patients with antiphospholipid antibody syndrome treated with high-dose intravenous immunoglobulins (IVIG). Fourteen patients with a history of recurrent spontaneous abortion and immunological diagnosis of antiphospholipid syndrome were followed longitudinally. Intravenous immunoglobulin at a dose of 0.5 g/kg body weight for two consecutive days was started from the fifth week of pregnancy and repeated every 4 weeks until the 33rd week of gestation. Fetal biometry was evaluated longitudinally from the appearance of the gestational sac at 4 weekly intervals. In the period between 26 and 34 weeks, the frequency of evaluation was increased to every 14 days. Data obtained were compared with a control group of 70 fetuses with uneventful pregnancies matched for gestational age. Neonatal weight is shown in relation to the centiles for the normal population. One patient out of 14 (7.1 per cent) developed gestational hypertension and abruptio placentae. No other pregnancy complications were seen. No proteinuria was found. The mean maternal age was 31.2 +/- 3.8 years. Median birth weight was 3433 g +/- 287. The median centile of the birth weight was 65.3 +/- 18.6. Mean gestational age at delivery was 1.3 weeks. No fetal or neonatal growth retardation was seen.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Normal fetal growth in women with antiphospholipid syndrome treated with high-dose intravenous immunoglobulin (IVIG). 765 85

The primary antiphospholipid syndrome and the antiphospholipid syndrome in systemic lupus erythematosus (SLE) patients (defined as secondary antiphospholipid syndrome) are characterized by the presence of anticardiolipin antibodies, thrombosis, thrombocytopenia, and recurrent fetal loss. To determine the role of anticardiolipin antibodies in the pathogenesis of antiphospholipid syndrome, monoclonal anticardiolipin antibodies were derived from mice in which experimental lupus was induced by a murine monoclonal anti-16/6 Id antibody. Two murine monoclonal anticardiolipin antibodies (2C4C2, 2C4D1) were generated and characterized. The 2C4C2, but not the 2C4D1, monoclonal antibody demonstrated remarkable lupus anticoagulant activity. Furthermore, these murine anticardiolipin monoclonal antibodies appear to recognize antigenic epitopes similar to those recognized by anticardiolipin antibodies found in sera of SLE patients. The monoclonal anticardiolipin antibody 2C4C2 was injected into naive female mice. Following immunization, the mice developed high titers of autoantibodies reacting with cardiolipin, DNA, nuclear extract, 16/6 and anti-16/6 Id, and anticardiolipin antibodies. As early as 8 weeks after immunization these mice exhibited significant leukopenia, thrombocytopenia, and proteinuria with immune complex glomerulonephritis. Moreover, mating of 2C4C2-injected mice with allogenic males resulted in low pregnancy rates and a low number of fetuses with a high percentage of fetal loss. These studies provide a new experimental model for secondary antiphospholipid syndrome demonstrating the role of anticardiolipin antibodies in the pathogenesis of this syndrome.
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PMID:Monoclonal anticardiolipin antibodies derived from mice with experimental lupus erythematosus: characterization and the induction of a secondary antiphospholipid syndrome. 768 61

A female patient with a history of migraines and chorea developed polyarthralgia at age 24 and was diagnosed with rheumatoid arthritis. In 1991 she was hospitalized because of impaired renal function and hypertension. Examination revealed thrombocytopenia and the presence of lupus anticoagulant. Antinuclear antibody was weakly positive, but anti-DNA antibody was negative, and no decrease in leukocyte count or complement level was observed. Rheumatoid arthritis with antiphospholipid syndrome was diagnosed. Renal biopsy showed renal thrombotic microangiopathy. This renal lesion was considered to be associated with antiphospholipid syndrome. Cyclophosphamide pulse therapy and anticoagulation therapy decreased proteinuria and improved renal function.
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PMID:Renal thrombotic microangiopathy in a patient with rheumatoid arthritis and antiphospholipid syndrome: successful treatment with cyclophosphamide pulse therapy and anticoagulant. 780 16

Although renal manifestations of the antiphospholipid syndrome (APS) have received scarce attention until recently, the kidney probably is a major target organ in APS. Thrombosis may develop at any location within renal vessels, ie, renal artery trunk or branches, intrarenal arteries or arterioles, glomerular capillaries, and renal vein. The clinical consequences consist of highly variable degrees of proteinuria; systemic hypertension ranging from mild to malignant; cortical necrosis; thrombotic microangiopathy, pregnancy-associated or not; and slowly to rapidly progressive renal failure that may require dialysis. These events occur mainly in the course of systemic lupus erythematosus or of "primary" APS. Renal involvement is a frequent feature of the catastrophic APS. A high prevalence of antiphospholipid antibodies has been reported recently in patients with end-stage renal failure, but their clinical significance remains to be determined.
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PMID:Renal manifestations of the antiphospholipid syndrome. 793 22

An 18-years-old female was admitted to our hospital because of severe edema, that had developed within one week, and massive proteinuria. She has been given treatment for mild proteinuria and Raynaud's phenomenon. Before the edema developed, she complained of recurrent attack of migraine associated with scintillating scotoma. At admission, she was suffering from butterfly erythema, hydropericardium and ascites. The results of tests for antinuclear antibodies and ENA antibodies were negative, but those for BFP and IgG-anticardiolipin antibody were positive, and the platelet and complement levels were low. Renal biopsy revealed typical mesangiolysis without any sign of hyperplastic nephritis. Electron microscopy demonstrated the deposition of microfibrillar structures in the mesangial areas. She was diagnosed as having SLE-antiphospholipid antibody syndrome. After the administration of prednisolone 40mg/day, the edema, Raynaud's sign and proteinuria disappeared. Migraine was improved by the additional use of warfarin, and the platelet count was normalized. These findings suggest that in this case, acute nephrotic symptom developed due to hemangioendothelial injury caused by anti-phospholipid antibody.
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PMID:[A case of anti-phospholipid antibody syndrome associated with typical mesangiolysis]. 796 76


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