Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0020538 (hypertension)
 170,190 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 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 describe a 22-year-old woman with renovascular hypertension, stroke, and left renal infarction. She had markedly elevated antiphospholipid antibodies without evidence of systemic lupus erythematosus, other autoimmune or rheumatic disorders. Selective renal angiogram revealed lack of perfusion to the lower pole of left kidney and her left renal vein renin level was elevated. She represents an example of primary antiphospholipid antibody syndrome resulting in renal infarction and hypertension.
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PMID:Primary antiphospholipid antibody syndrome, renal infarction and hypertension. 837 Dec 24

This study was undertaken to determine if there is an association between increased titers of five different antiphospholipid antibodies (aPLA) in young patients' sera and the occurrence of acute myocardial infarction (AMI). Antibodies to anticardiolipin (aCL), anti-phosphatidylserine (aPS), antiphosphatidylinositol (aPI), anti-phosphatidylcholine (aPC), and anti-phosphatidylethanol amine (aPEA) were measured in 214 patients (102 patients, 102 healthy controls and 10 patients with antiphospholipid syndrome). These antibodies were measured twice (within 4h of onset of acute myocardial ischemic chest pain and 3 months after the myocardial infarction) by enzyme linked immunosorbent assay (ELISA). Elevated titers of four different aPLA were detected in 6.9% of all patients with AMI on hospitalization. Titers of aPLA in AMI were elevated in the younger age group < 50 years old (P < 0.001) and in men only (not statistically significant). No correlation was found between the presence of aPLA and cardiovascular risk factors (smoking, hypertension, diabetes mellitus and hyper-cholesterolemia). Three of the seven patients with increased titers of aPLA did not have any other cardiovascular risk factors. The titers of aPLA were within normal range 3 months after AMI. Evidence of significantly elevated titers of different aPLA at the early stage of AMI suggests that these autoantibodies are present before the AMI and are not secondary to them. The disappearance of the elevated aPLA 3 months after AMI may be due to an absorption effect or possibly a cyclic phenomenon similarly found in other autoimmune diseases. aPLA may be an additional risk factor for AMI, and should especially be considered in a patient of the younger age group without apparent cardiovascular risk factors.
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PMID:The presence of antiphospholipid antibodies in acute myocardial infarction. 852 29

Benign intracranial hypertension is a rare complication of systemic lupus erythematosus often attributed to cerebral sinus thrombosis which impairs venous drainage and cerebrospinal fluid outflow. We report the case of a woman with a primary antiphospholipid syndrome who developed benign intracranial hypertension with no actual evidence of venous cerebral thrombosis and with no other possible cause for this clinical manifestation than high titres of anticardiolipin antibodies and a lupus anticoagulant.
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PMID:Benign intracranial hypertension: a non-thrombotic complication of the primary antiphospholipid syndrome? 852 33

A case of rapidly progressive nephritis is reported in a female patient having systemic lupus erythematosus (SLE) with antiphospholipid syndrome. Clinical presentation of progressive lupus nephritis with intensifying renal insufficiency, arterial hypertension, hematuria, nephrotic syndrome was associated with unusual morphological manifestations of mesangiocapillary glomerulonephritis with advanced vasculitis. The authors attribute a malignant nephritis course atypical for patients with antiphospholipid syndrome to development of renal vasculitis. The discussion covers lupus genesis of vascular involvement, a probable triggering role of antibodies to phospholipids in impairment of endothelial cells.
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PMID:[The characteristics of kidney involvement in a female patient with systemic lupus erythematosus and the antiphospholipid syndrome]. 857 27

Renal manifestations of the "primary" antiphospholipid syndrome are rare. We report the case of an athletic 35-year-old man with an unremarkable medical history who suddenly developed hypertension and a renal infarction. Laboratory and radiological investigations showed a complete thrombosis of the infrarenal aorta, extensive collateral circulation arising from the superior mesenteric artery, and the primary antiphospholipid syndrome. Eight cases of renal infarction have previously been reported in the primary antiphospholipid syndrome. To our knowledge, this represents the first case of an infrarenal aortic thrombosis attributable to this syndrome.
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PMID:Renal infarction and thrombosis of the infrarenal aorta in a 35-year-old man with primary antiphospholipid syndrome. 862 34

Aspirin, an inhibitor of cyclo-oxygenase, is prescribed in a number of conditions related to abnormal production of prostaglandins including gravidic hypertension. Results of the most recent trials demonstrate that in patients with a past history of pre-eclampsia or intra-uterine growth retardation, a pathological Doppler examination of the uterus, a pathological angiotensin test or an antiphospholipid syndrome, prescription of aspirin at the dose of 100 mg/day can prevent recurrence or development of pre-eclampsia or intra-uterine growth retardation. Treatment should begin as soon as possible during pregnancy, certainly before development of clinical manifestations. After history taking and identification of possible contraindications, bleeding time (Ivy method) is recorded before and after prescription and should be lower than 8 minutes. In case bleeding time exceeds 10 minutes 10 to 15 days after initiating aspirin, doses may be reduced to 50 mg per day or even 50 mg every two or three days to reach the target level. Treatment should generally be continued up to 36 weeks gestation.
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PMID:[Aspirin during pregnancy. Indications and modalities of prescription after the publication of the later trials]. 872 90

Antiphospholipid syndrome (APLS) is defined as a symptom complex characterized by arterial and venous thromboses, obstetric abnormalities, thrombocytopenia and hyperproduction of antiphospholipid antibodies. APLS may be primary and secondary developing in the presence of autoimmune disorders, SLE in particular. At examination of 28 patients with primary and secondary APLS 14 patients proved hypertensive. Renal pathology was absent. Arterial hypertension appeared often in combination with microthrombi of the skin and affections of peripheral vessels. Arterial hypertension as a cardiological sign of APLS occurs more frequently than other symptoms.
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PMID:[Arterial hypertension and the antiphospholipid syndrome]. 877 55

Vascular damage in systemic lupus erythematosus (SLE) occurs through vasculitis, premature atherosclerosis, and hypercoagulability (predominantly due to the antiphospholipid antibody syndrome). In the Hopkins Lupus Cohort, a prospective cohort study, the incidence of thrombosis is 2 per 100 person-years of follow-up. Markers of immune-complex mediated injury (high anti-dsDNA and low C3), atherosclerosis (hypertension, hyperlipidemia, homocysteine) and antiphospholipid antibodies (lupus anticoagulant or anticardiolipin) are independent predictors of thrombosis. Hydroxychloroquine use is protective against future thrombosis.
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PMID:Thrombosis and systemic lupus erythematosus: the Hopkins Lupus Cohort perspective. 879 94


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