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)

Primary antiphospholipid antibody syndrome (APS) is characterized by abortion, thrombosis, thrombocytopenia and/or valvular disease and it is liable to complicate systemic lupus erythematosus (SLE). We carried out a study to investigate the clinical and renal pathological findings in five patients with APS, but not SLE. In the clinical findings, the patients had negative tests for proteinuria and hematuria, and their renal function and tubular function were within normal limits. In the light microscopic findings, three patients exhibited mild mesangial hypercellularity, and two had minor glomerular abnormalities. In immunofluorescent study, there were IgM and/or C3 depositions in the mesangial area in some cases, and in electron microscopic study, there were no special findings other than mesangial hypercellularity. In conclusion, nephropathy is a rare complication in patients with APS, unlike systemic lupus erythematosus.
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PMID:[Nephropathy in patients with primary antiphospholipid antibody syndrome]. 813 48

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 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

We report a case of secondary antiphospholipid syndrome (APS) occurring in a progressive systemic sclerosis (PSS) patient who took herbal medication. Clinical findings compatible with APS included positive IgM anticardiolipin antibody (ACL), thrombocytopenia, and obstruction of the left radial artery on digital subtraction angiography (DSA). Clinical findings compatible with PSS included sclerodactyly and digital ulcers, Raynaud's phenomenon, pulmonary fibrosis and pulmonary hypertension, proteinuria and renal mesangial reaction, and myocarditis.
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PMID:Antiphospholipid syndrome associated with progressive systemic sclerosis. 867 27

We described a 10-year-old girl with SLE complicated with anticardiolipin antibody, who showed bleeding tendency since infant. Her platelet was 6 x 10(3)/microliter. The APTT was remarkably prolonged. The platelet count was normalized after steroid treatment. A false positive Venereal Disease Research Laboratory (VDRL) test, lupus anticoagulants and anticardiolipin antibodies (IgG and IgM) were positive. Her symptoms and the laboratory data fulfilled the criteria of antiphospholipid syndrome. Renal biopsy was performed because of proteinuria, hematuria and the positive of anti-nuclear antibody. The pathology of kidney showed that of lupus nephritis (diffuse membranous glomerulonephritis), and she was diagnosed SLE. She showed no laboratory findings of hyperfibrinolysis and no symptoms of thrombosis under the steroid treatment for 3 years.
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PMID:[A 10-year-old girl with anticardiolipin antibody, who showed bleeding tendency]. 881 May 51

A 33-year-old man presented malar rash in April, 1992. The rash had gradually developed and he was admitted to our hospital in February, 1994. Laboratory findings showed proteinuria of 0.5-0.8 g/ day, thrombocytopenia (4.8 x 10(4)/mm3), false positive serologic test for syphilis, anti-nuclear antibody with a speckled type at a titer of 1 : 80. Activated partial thromboplastin time was prolonged (41.3 s), and anti-beta 2-GPI antibody was strongly positive (56.6 U/ml on enzyme linked immunosorbent assay). The diagnosis of systemic lupus erythematosus with antiphospholipid syndrome was made and prednisolone 60 mg/day improved his manifestations. He could be discharged in July, 1994. Nine months after the discharge he developed dyspnea, and he was admitted to our hospital again. On admission the blood pressure was 212/170 mmHg, Levine III/VI systolic murmur was noted at the apex of heart. Significant laboratory findings showed as follows: WBC 15, 110/mm3 (Neu 73%, Lym 18%), RBC 380 x 10(4)/mm3, Hb 10.2 g/dl, Plt 20.0 x 10(4)/mm3, GOT 23 IU/l, GPT 21.
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PMID:[Acute cardiac failure due to dilated cardiomyopathy in systemic lupus erythematosus with antiphospholipid antibody]. 912 25

A case of SLE is reported in a 43-year-old female who had initial signs of the disease 10 years before (exudative pleuritis). SLE ran chronically with spontaneous remissions. Insolation in 1985 provoked exacerbation and further progress. The progression was accompanied with appearance of antiphospholipid syndrome (APS): habitual miscarriage, livedo, Raynaud's [correction of Raunald's] syndrome, recurrent thrombophlebitis. Aortic valve disease was more likely to be consequent to non-infectious endocarditis while arterial hypertension as well as proteinuria could be caused by renal thromboangiopathy. This case demonstrates not only a wide spectrum of SLE and APS symptoms but also difficulties which may be faced in the choice of the treatment policy.
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PMID:[The late diagnosis of systemic lupus erythematosus with the antiphospholipid syndrome]. 948 49

Renal involvement in antiphospholipid syndrome (APS) is increasingly reported. So far, massive proteinuria as the principal feature of primary APS (PAPS) has not been well documented. We describe 3 patients with PAPS and massive proteinuria. Renal biopsy was performed in all 3, and features consistent with membranous and focal segmental glomerulopathy were disclosed. These histological lesions were not yet reported in PAPS. We conclude that the spectrum of renal lesions in PAPS is diverse and that it should be considered in the differential diagnosis of patients with massive proteinuria.
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PMID:Massive proteinuria as a main manifestation of primary antiphospholipid syndrome. 957 67

Even 10 yr after the identification of the antiphospholipid syndrome (APS), renal involvement in the course of APS is still relatively unrecognized, and is probably underestimated. The association of anticardiolipin antibodies and/or lupus anticoagulant with the development of a vaso-occlusive process involving numerous organs is now confirmed. In a multicenter study, 16 cases of "primary" APS (PAPS) were found and followed for 5 yr or more, all with renal biopsy. In all 16 cases of PAPS, there was a vascular nephropathy characterized by small vessel vaso-occlusive lesions associated with fibrous intimal hyperplasia of interlobular arteries (12 patients), recanalizing thrombi in arteries and arterioles (six patients), and focal cortical atrophy (10 patients). In combination, these led to progressive destruction of the kidney, accelerated by acute glomerular and arteriolar microangiopathy in five patients. Focal cortical atrophy is a distinctive lesion, present in 10 biopsies, and likely represents the histologic and functional renal analogue to the multiple cerebral infarcts detected on imaging studies. The clinical hallmark of this vascular nephropathy in PAPS is systemic hypertension, only variably associated with renal insufficiency, proteinuria, or hematuria. The ensemble of histologic renal lesions defined in this study should aid in the separation of the lesions found in cases of secondary APS, especially systemic lupus erythematosus, into those lesions related to APS and those related to the underlying disease.
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PMID:The intrarenal vascular lesions associated with primary antiphospholipid syndrome. 1007 1

We report a rare case with multiple renal infarction associated with lupus anticoagulant and SLE. A 20-year old woman presented with remitent fever, butterfly rash and, abdominal pain. Laboratory findings showed leukopenia, positive antinuclear and anti-DNA antibodies, and biological false positive for syphilis. Despite a therapy with prednisolone 25 mg/day, the patient showed hypocomplementemia, high titer of anti-DNA antibody and a development of proteinuria and an elevation of serum creatinine. Renal biopsy revealed no abnormalities. She presented abdominal pain with an elevation of serum LDH. Abdominal dynamic computed tomography demonstrated multiple perfusion defects in both kidneys indicating multiple renal infarction. Brain MRI showed multiple micro infarction in the anterior lobes. She was treated with 80 mg of aspirin and have been in remission for two years. Although there have been reported 18 cases with renal infarction associated with antiphospholipid syndrome, this is the first report in Japan. Renal infarction should be differentiated from renal involvement in patients with SLE who have antiphospholipid antibodies.
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PMID:[Multiple renal infarction associated with lupus anticoagulant in a patient with systemic lupus erythematosus]. 1043 52


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