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Query: UMLS:C0020538 (hypertension)
 170,190 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Twenty five patients with renal vasculitis presenting over an eight year period were reviewed. Ten had microscopic polyarteritis, 6 classic polyarteritis, 5 overlap syndrome, 2 Churg-Strauss syndrome and 2 Wegener's granulomatosis. Clinical features included hypertension, pulmonary involvement, neurological involvement and arthralgia. Serum creatinine was over 500 umol/l in 13 patients, 10 of whom required dialysis. Visceral angiography was positive in 80% of those studied, Focal and segmental necrotising glomerulonephritis was the commonest renal lesion. Treatment consisted of corticosteroids and cytotoxic agents in most cases. Plasmapheresis was used for rapidly progressive renal failure, severe pulmonary haemorrhage or cerebral vasculitis. Improvement or stabilisation of renal function was seen in 68% of patients treated. There were 4 early deaths and one late death. The diagnosis, histology, treatment and outcome of renal vasculitis is discussed. The importance of early diagnosis and treatment is emphasised in this potentially reversible cause of acute renal failure.
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PMID:Systemic vasculitis with renal involvement--a review. 269 9

In the case we have reported, there is a combination of factors that can be attributed to SLE and its associated complications, which may explain the transient hypodensities seen on cranial CT scan. Vasculitis and uncontrolled hypertension lead to arterial spasm, ischemia, and increased vascular permeability, all of which eventually cause cerebral edema. This edema may manifest itself clinically as profound but transient neurologic deficits.
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PMID:Reversible profound neurologic deficits associated with transient cranial CT abnormalities and systemic lupus erythematosus. 271 92

Three patients aged over 60 with endocapillary proliferative glomerulonephritis and nephrotic syndrome were reported. Immunofluorescence and electron microscopical findings were similar in all of them: granular deposits of IgG and C 3 along the capillary loops, electron dense deposits in the subendothelial area, and partial mesangial interposition. The levels of CH 50 were slightly suppressed in two of them, but neither preceding infection nor elevation in ASLO were noticed. None of then responded to steroid therapy. One patient fell in renal failure in spite of intensive steroid therapy, and died of bronchopneumonia. In another patient, proteinuria was remitted with systemic treatment against high blood pressure. The remaining patient took a favorable course during the admission without any special treatment, but proteinuria recurred after the discharge. These clinical manifestations and clinical courses were not compatible with the diagnoses of acute glomerulonephritis, mesangiocapillary glomerulonephritis, or vasculitis. We concluded that the endocapillary proliferative glomerulonephritis in adults over 60 years might be different form of glomerulonephritis from that of AGM, MPGN, and vasculitis, in which diffuse endocapillary proliferative changes in the glomeruli are seen in younger people.
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PMID:[Three elderly cases of endocapillary glomerulonephritis and nephrotic syndrome]. 273 23

A 40 year old man with a history of myocardial infarction and hypertension presented with transient cerebral ischaemic attacks, aortic regurgitation, a raised erythrocyte sedimentation rate, and thrombocytopenia. The anticardiolipin syndrome was diagnosed and he was treated with prednisolone and warfarin. He died two years later after the development of acute heart failure. At necropsy his heart showed widespread arteriolar thrombosis without vasculitis, recanalised large vessel occlusion, and a "post-inflammatory" valvulitis of the aortic valve.
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PMID:Findings at necropsy in the heart of a patient with anticardiolipin syndrome. 275 75

Traditional thinking suggests that pleural fluid develops on the basis of systemic venous hypertension or a primary pleural process. Recent investigations, however, indicate that both acute lung injury and pulmonary venous hypertension can be important in the pathogenesis of pleural effusions. To evaluate the role of acute lung injury in the formation of pleural effusions, we developed a model of acute, reversible lung injury in NZW rabbits. Intravenous ethchlorvynol (ECV), known to produce permeability edema in humans, was used to produce permeability pulmonary edema in rabbits. The injury was examined over 14 days with bronchoalveolar lavage, pleural fluid analysis, and morphologic analysis. Ethchlorvynol injection (40 mg/kg) produced a PMN-predominant, exudative alveolitis (2 h), alveolar hemorrhage (6 to 10 h), and pleural effusions by 2 h (peak, 10 h). Pathologic findings included a patchy, subpleural, hemorrhagic PMN inflammatory response, which peaked by 24 h, and an acute PMN vasculitis of small arterioles and capillaries; these changes resolved in 5 to 7 days. No parietal pleural abnormalities were observed. We conclude that ECV induces an acute, reversible parenchymal lung injury resulting in a capillary leak and that fluid moves from the interstitium of the lung into the pleural space along a pressure gradient through a relatively permeable mesothelium. The data support the concept that diffuse or localized lung injury can result in pleural effusions.
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PMID:Pleural effusions associated with ethchlorvynol lung injury result from visceral pleural leak. 278 46

Pulmonary hypertension due to vasculitis is a rare complication of rheumatoid arthritis (RA). We describe 2 patients with RA and pulmonary hypertension who died with a clinical diagnosis of idiopathic pulmonary hypertension. In each case postmortem examination revealed severe pulmonary vasculitis as the actual cause of the hypertension. Subclinical systemic vasculitis was found in one case and hepatic nodular regenerative hyperplasia in both cases. Pulmonary vasculitis must be included in the differential diagnosis of pulmonary hypertension associated with RA. Open lung biopsy should be considered in this clinical setting in an attempt to identify this potentially treatable cause of pulmonary hypertension.
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PMID:The association of pulmonary hypertension with rheumatoid arthritis. 281 Feb 87

We placed 20 bypass grafts to the lateral plantar artery in 18 extremities to salvage feet with wet (12) or dry (six) gangrene; 15 grafts were implanted in men (75%), and five were implanted in women (25%). The median age was 65 years. All except two patients had diabetes; eight were treated with insulin. One patient had Buerger's disease, and another had vasculitis with chronic lymphocytic leukemia. History of smoking (65%), hypertension (53%), heart disease (71%), and osteomyelitis in the foot (35%), were noted. Cultures were positive in 15 gangrenous feet, 11 with gram-negative bacilli. Four long femoroplantar bypasses were placed. Ten short grafts were placed from the popliteal artery, and six jump grafts were placed distal to a femoropopliteal or tibial bypass. Hospital stay ranged from 8 to 38 days (median 16 days), and there were two in-hospital deaths. Transmetatarsal or button toe amputations were performed in nine feet. There were two below-knee amputations, one with a patent graft, for a foot salvage rate of 89% at 2 months. In four instances the gangrenous ulcers took longer than 6 months to heal; all other wounds healed within 6 months. The primary and secondary patency rates were 85% at 1 month, and 73% at 3 months and thereafter. Four of five graft failures occurred in the two legs with repeat bypass graftings. All patients with successful revascularization are able to walk, and seven returned to work full time.
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PMID:Lateral plantar artery bypass grafting: defining the limits of foot revascularization. 281 May 37

Cardiovascular manifestations develop in the majority of SLE patients at some time during the course of their illness, the most common being acute fibrinous pericarditis and pericardial effusion. Echocardiography has demonstrated an increased incidence of pericardial effusion, even in those who have minimal symptoms. Chronic adhesive pericarditis, pericardial tamponade, and constrictive pericarditis occur rarely. While myocarditis is commonly noted at autopsy, it is often silent clinically. Diagnosis during life can be confirmed only by endomyocardial biopsy. Electrocardiographic changes are often nonspecific. Endocarditis with superimposed nonbacterial verrucous vegetations (Libman-Sacks) is noted in more than 40% of hearts at autopsy, but is rarely diagnosed during life. Valve dysfunctions, such as aortic stenosis, aortic insufficiency, mitral stenosis, and mitral insufficiency, occasionally manifest during life and rarely may necessitate surgery. Atrial and ventricular arrhythmias, first degree AV block, and acquired CHB occur in association with pericarditis, myocarditis, vasculitis, and myocardial fibrosis, respectively. CCHB developing in newborns of mothers with SLE, particularly those who have an antibody to soluble tissue ribonuclear protein RO(SS-A), is increasingly being appreciated by both pediatric cardiologists and rheumatologists. Recently, severe coronary atherosclerosis resulting in angina pectoris and/or myocardial infarction in young adults has been noted, particularly in those who had developed risk factors such as hypertension and hyperlipidemia while receiving prolonged corticosteroid therapy. Rarely, coronary arteritis may produce similar symptoms. Congestive heart failure of either single or multiple etiologies carries an ominous prognosis. It remains a cause of high morbidity and mortality unless recognized early and treated properly. Extracardiac vascular manifestations of SLE include telangiectasia, vasculitis, livedo reticularis, Raynaud's phenomena, and thrombophlebitis, all of which may occur either alone or in different combinations. Evidence is now slowly accumulating that substantiates that immune complex deposition, complement activation and subsequent inflammatory reaction is responsible for the majority of the cardiovascular manifestations of SLE, for example, pericarditis, myocarditis, endocarditis, coronary arteritis, coronary atherosclerosis, and systemic and pulmonary vasculitis.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Cardiovascular manifestations of systemic lupus erythematosus: current perspective. 286 Jun 99

Epididymitis is an uncommonly recognized complication of systemic necrotizing vasculitis. We report 2 cases in which epididymitis heralded the onset of more severe visceral organ involvement. Early biopsy of atypical epididymitis in patients with hypertension or constitutional symptoms is important if effective therapy is to be instituted before irreversible organ damage occurs.
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PMID:Systemic necrotizing vasculitis presenting as epididymitis. 287 98

Although uncommon, a wide variety of ocular manifestations can be seen in polyarteritis nodosa. These occur as a result of the arteritis or secondary to the associated renal induced hypertension. A case of biopsy documented polyarteritis nodosa is reported in which the patient presented with bilateral iritis, vitritis, and a retinal vasculitis involving both the retinal arteries and veins, a feature not described previously. Patients with this potentially fatal disorder may initially present with ocular involvement; thus ophthalmologists should be familiar with the clinical features of this disease.
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PMID:Retinal vasculitis in polyarteritis nodosa. 288 10


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