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)

We report the case of a young woman with primary antiphospholipid syndrome (APS), which presented with acute renal failure, hypoproteinemia, hypoalbuminemia and nephrotic proteinuria. Investigations showed total infarction of right kidney by extensive arterial and vein thrombosis and presence of anticardiolipin antibodies IgG isotype (anti-beta2-glycoprotein I-positive). She was submitted to right nefrectomy and initiated anticoagulant therapy. After nefrectomy, the postoperative period was marked by the development of arterial hypertension and persistence of nephrotic syndrome. Hypertension was treated with antihypertensive drugs (IECA, beta-blocker and calcium antagonist). As the nephrotic syndrome persisted despite anticoagulant and antihypertensive therapy, the patient was treated with oral corticosteroids. Her renal function improved, hypoproteinemia and hypoalbuminemia corrected to normal values and proteinuria decreased to subnephrotic value. We discuss the unusual presentation of this case of primary antiphospholipid syndrome with total unilateral renal thrombosis and nephrotic syndrome that respond to anticoagulant, antihypertensive and corticosteroid therapy.
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PMID:Primary antiphospholipid syndrome presented by total infarction of right kidney with nephrotic syndrome. 1044 98

Antiphospholipid antibodies (APA) were studied in 30 women with a history of recurrent fetal losses. An increased level of anticardiolipin antibodies was found in 7(23.3%) of them, being high and moderate in 4 women. Lupus anticoagulant was present in 9(30.0%) examinees. None cases of SLE were diagnosed. Diagnostically significant APA levels were associated with moderate symptomless thrombocytopenia. 12 of 13 women with antiphospholipid syndrome markers had definite (livedo reticularis, damage of cardiac valves, recurrent thrombophlebitis, leg ulcers, stroke, migraine) and possible (moderate arterial hypertension, proteinuria, retina angiopathy) extragenital features of this disorder. The most serious vascular complications took place in the group with high and moderate levels of anticardiolipin antibodies IgG.
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PMID:[Antiphospholipid syndrome in females with recurrent fetal losses]. 1048 65

Some features of the vascular and glomerular pathology of primary antiphospholipid syndrome (APS) are well recognized, but we describe novel glomerular ultrastructural changes that we consider to be pathognomonic of APS. Renal biopsies from eight patients with APS were examined by light and electron microscopy. All had anti-cardiolipin antibodies, and the clinical presentation ranged from fulminant multi-system disease to isolated proteinuria. By light microscopy, the hexamine silver stain showed a combination of glomerular basement membrane wrinkling and reduplication. By electron microscopy, redundant, wrinkled segments of basement membrane were accompanied by a 'new' straighter thin basement membrane adjacent to the endothelium. In two cases the presence of these antibodies was not suspected clinically, and there was no clinical history or evidence of a thrombotic microangiopathy. We describe a distinctive glomerular lesion that represents an unexplained form of endothelial injury in this syndrome.
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PMID:The renal pathology of primary antiphospholipid syndrome: a distinctive form of endothelial injury. 1087 55

A 30-year-old woman with primary antiphospholipid syndrome (PAPS) presented with cerebral ischemia, thrombocytopenia, anemia and proteinuria. Administration of warfarin potassium, without concomitant corticosteroid administration, significantly improved all of these symptoms along with a decrease in the titers of antiCL-beta2-GP-I antibodies and a shortening of prolonged APTT. Therefore, the antiphospholipid antibodies in this patient could have been evoked by vitamin-K-dependent coagulation factors or plasma proteins which are assumed to undergo conformational changes exposing cryptic epitopes. This case report provides clues to the mechanisms underlying the production of antiphospholipid antibodies in patients with PAPS.
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PMID:Primary antiphospholipid syndrome presenting with cerebral ischemia, thrombocytopenia, anemia and proteinuria successfully treated with warfarin potassium. 1096 8

The effect of dietary modifications has been extensively studied in lupus animal models. Calorie, protein, and especially fat restriction, caused a significant reduction in immune-complex deposition in the kidney, reduced proteinuria and prolongation of the mice's life span. The addition of polyunsaturated fatty acids (PUFAs), such as fish oil or linseed oil, was also related to decreased mice morbidity and mortality in animal models of lupus and of antiphospholipid syndrome. PUFAs such as eicosapetaenoic acid (EPA) and docosahexaenoic acid (DHA) competitively inhibit arachidonic acid with a resultant decrease in inflammatory eicosanoids and cytokines. Human studies support the effect of a PUFAs-enriched diet, both scrologically and clinically. Large scale clinical studies are needed to confirm the primary results.
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PMID:Diet and lupus. 1131 62

Activation and proliferation of lymphocytes requires the active signal transducer Ras. Activation of lymphocytes, associated with autoimmunity, may therefore be modified by S-farnesylthiosalicylic acid (FTS), a synthetic substance that detaches Ras from the inner cell membrane and induces its rapid degradation. The MRL/lpr mouse is a genetic model of a generalized autoimmune disease sharing many features and organ pathology with systemic lupus erythematosus (SLE) and the primary antiphospholipid syndrome (APS). The objective of the present study was to examine the effect of FTS on laboratory and clinical pathology in the MRL/lpr mouse. Female MRL/lpr (n = 50) and MRL/++ control (n = 35) mice were treated intraperitoneally with either FTS (5 mg/kg/day) or saline between 6 and 18 weeks of age. The mice were weighed, tested for proteinuria and lymphadenopathy, lymphocyte proliferation, antibodies, grip strength and behaviour in an open field. FTS treatment resulted in a 50% decrease in splenocyte proliferation to ConA, LPS and a disease specific antigen, beta(2)-glycoprotein-I, and in a significant decrease in serum antibody levels against cardiolipin and dsDNA. Proteinuria and grip strength were normalized and lymphadenopathy and postmortem lymph node and spleen weights were significantly reduced in FTS treated MRL/lpr mice. These findings indicate that modulation of Ras activation has a significant impact on the MRL/lpr model and may represent a new therapeutic approach for the treatment of systemic autoimmune diseases such as SLE and APS.
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PMID:Treatment of MRL/lpr mice, a genetic autoimmune model, with the Ras inhibitor, farnesylthiosalicylate (FTS). 1173 78

A case of antiphospholipid syndrome (APS) is reported. A 48-year-old man visited our hospital because of proteinuria. He had suffered from thrombosis and had high titers of antibodies to beta2-glycoprotein I (abeta2GPI) and anticardiolipin antibodies (aCLIgG) and thrombocytopenia. We started anticoagulation therapy using warfarin combined with prednisolone. Although platelet count was improved, the titers of anti-beta2GPI and aCLIgG still remained high. Therefore, double-filtration plasmapheresis (DFPP) was carried out to remove the antibodies. After the treatment with DFPP, cyclophosphamide was administered. These therapies resulted in lower titers of abeta2GPI and aCLIgG and no more thrombosis occurred. A combination therapy using warfarin, prednisolone, cyclophosphamide and DFPP might be effective for the treatment of patients with APS.
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PMID:Antiphospholipid syndrome treated with prednisolone, cyclophosphamide and double-filtration plasmapheresis. 1232 1

We report here two interesting cases of systemic lupus erythematosus(SLE) accompanied by antiphospholipid syndrome nephropathy(APSN). These cases satisfied the criteria for SLE established by the American College of Rheumatology 1997 and also satisfied the criteria for antiphospholipid syndrome (APS) established by the Sapporo International Workshop of APS 1998. Both cases had high blood pressure with elevated plasma renin activity, proteinuria and renal dysfunction. Their biopsied renal specimens showed the characteristic findings for APSN, such as mesangial proliferation, double contours, thickening of the capillary loops, and intimal hyperplasia, but there was no evidence for immune complexes in the glomeruli, which were examined by the indirect immunofluorescence methods and the electron microscopy method. These results indicated that their renal dysfunction was caused by APSN, but not by immune complex nephritis. In addition to treatment with prednisolone, they were administered anticoagulants(warfarin, or aspirin, or heparin) for APSN and an angiotensin II receptor blocker, candesartan, for the hypertension. Subsequently, their conditions recovered with the improvement of renal function and hypertension. Our experiences suggest that anticoagulant therapy in addition to corticosteroids offers advantages in the treatment of patients with SLE accompanied by APSN and renal dysfunction.
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PMID:[Two cases of systemic lupus erythematosus accompanied by antiphospholipid syndrome nephropathy without immune complex nephritis]. 1260 72

Antiphospholipid syndrome spans many medical disciplines. Classic criteria include the presence of anticardiolipin antibody or lupus anticoagulant with typical complications of thrombosis or pregnancy loss. Other common associated manifestations include livedo reticularis, thrombocytopenia, valvular heart disease, and nephropathy with renal insufficiency, hypertension, and proteinuria. Treatment of serious complications with anticoagulation is standard; generally warfarin for thrombosis and aspirin/heparin for pregnancy prophylaxis. Detailed recommendations regarding precise intensity and duration of anticoagulation are still a subject of debate.
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PMID:Antiphospholipid syndrome: review. 1600 69

This case report is about a past smoker who presented with history of recurrent ulcers and digital gangrene with claudication pain of the left foot for the past fifteen years. Clinical examination and angiogram showed disease involving the peripheral vessels of lower limb. This patient had been labeled as Buerger's disease 15 years ago based on clinical and demographic profile of the illness. We felt that the progression of the disease despite the patient having stopped smoking 15 years ago along with the presence of elevated inflammatory markers in the blood with proteinuria was not in keeping with the nature of the disease. Further evaluation revealed that the patient had systemic lupus erythematosus with antiphospholipid antibody syndrome. This case highlights the need for a careful search for diseases, which can mimic Buerger's disease in young smokers who present with peripheral vascular disease and who have an atypical clinical presentation or progression.
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PMID:Systemic lupus erythematosis with antiphospholipid antibody syndrome: a mimic of Buerger's disease. 1667 78


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