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

38 cases of severe hypertension due to a vascular abnormality of the renal pedicle were studied in children under 16 years of age, 18 boys and 20 girls. The most common presentation was at routine clinical examination. The diagnosis of an abnormality of the renal artery was suggested by the appearances of intravenous urography. There were many causes; 4 aneurysms of the renal artery or its branches, 4 fibromuscular dysplasias with one case of bilateral fibromuscular dysplasia, 4 idiopathic stenoses, 2 endarteritis, and 6 thromboses revascularised to variable degrees (2 after umbilical vein catheterisation and one due to DLE). In three cases the hypertension was related to compression of the pedicle by a tumour of haematome, and 14 cases had multiple arterial lesion. In the latter group, 6 cases of neurofibromatosis, 2 cases of William and Beuren's disease, 1 case of generalised Elastorhexia, 2 cases of aortic medio stenosis, probably Takayashu's disease, and 3 unidentified conditions. Surgery was performed on 29 patients, 21 of whom had unilateral lesions and were definitively cured of hypertension. Of the 8 cases with multiple lesions, only 2 were completely corrected with cure of their hypertension.
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PMID:[Arterial hypertension caused by anomaly of the renal artery or its branches in children]. 11 10

The authors report the case of a young woman with Sneddon's syndrome and expose literature review. This rare entity is characterized by idiopathic livedo reticularis, ischemic stroke, and occasionally, mild arterial hypertension. Skin biopsy shows endarteritis obliterans of deep dermal arteries. The pathogenesis of this disorder is still unknown and the treatment is not clearly established.
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PMID:[Sneddon's syndrome: review of the literature apropos of a case]. 209 37

In order to evaluate whether immunoglobulin deposition in vessels plays some role in the development of vascular lesions in severe hypertension, an immunohistochemical study was performed in spontaneously hypertensive rats (SHRs), to which deoxycorticosterone acetate (DOCA) and salt were administered. DOCA and salt rapidly induced severe hypertensive vascular lesions, including necrotizing arteriolitis and productive endarteritis. In these rats, considerable deposits of IgG and IgM were found in the small arteries and arterioles of the kidneys. These deposits were accompanied by complement (C3), and could be eluted by acid incubation. They were localized in periodic acid-Schiff-positive insudative lesions, which were thought to be an early phase of the hypertensive vascular lesions. These results suggest that the immunoglobulins might be bound to an unknown antigen in the vascular lesions and that some immunological mechanism mediated by the immunoglobulins is involved in the development of vascular lesions in severe hypertension.
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PMID:Immunohistochemical study of vascular lesions in severe hypertension induced by DOCA and salt administration to spontaneously hypertensive rats. 226 Nov 49

Two cases in the same sibship are reported. The elder patient, who had posterior dislocation of the lens resulting in glaucoma and significant psychomotor retardation, died at the age of 13 with malignant arterial hypertension. Death was caused by thrombotic events (left carotid artery, coronary vessels, renal arteries and arterioles with fibrous endarteritis). The sister, aged 10, had psychomotor retardation and anomalies of both lenses. Chromatographic studies of serum and urine amino acids confirmed the diagnosis of homocystinuria. The form was pyridoxine-sensitive as shown by the results of therapy with pyridoxine and folates. We suggest that homocystinuria, although infrequent, should be routinely looked for in every child with a thrombotic event since a pyridoxine-folate combination is successful in half the cases, preventing the development of complications especially when initiated early.
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PMID:[2 familial cases of homocystinuria one of which revealed by fatal hypertensive encephalopathy]. 235 Jan 47

This article has reviewed the involvement of the kidney as a target organ of essential hypertension. Since Bright first made the association of renal disease and hypertension in 1836, the nature of this relationship has been debated. Although there is evidence implicating abnormalities of renal function in the pathogenesis of essential hypertension, hypertension frequently precedes histologic evidence of alterations in renal structure. Nephrosclerosis, or hardening of the kidney, is the term used to describe the histologic changes occurring in the kidney as the result of hypertension. It can be though of as an acceleration of the normal aging process of the renal vasculature. Glomerular and tubular changes have been traditionally thought to be ischemic in origin. Experimental evidence supports the notion that, as renal function is lost, intraglomerular hypertension develops and may be responsible for additional nephron loss in hypertension. This idea may have therapeutic implications for hypertensive patients with renal insufficiency in that agents that reduce both systemic and intraglomerular pressure may be preferable. Hemodynamically, early hypertension is often characterized by normal peripheral and renal vascular resistance and an increased cardiac output. In established hypertension, cardiac output is usually normal, and peripheral and renal vascular resistances are increased. Renal blood flow is reduced, glomerular filtration rate is maintained, and the filtration fraction rises. In the absence of an accelerated malignant phase, renal failure is uncommon in essential hypertension. Males and blacks are most sensitive to the vascular damage of essential hypertension. Essential hypertension remains an important cause of end-stage renal disease, especially in blacks. Atherosclerotic obstruction of the renal arteries may be a more common cause of renal failure in patients with essential hypertension than has been previously recognized. There are few sensitive markers of early renal involvement in essential hypertension. Several studies of sensitive markers are promising and may detect patients who are prone to renal injury and deserve more aggressive treatment. Malignant hypertension is characterized pathologically by vascular changes of proliferative endarteritis and fibrinoid necrosis. Fortunately, its frequency is decreasing because of early identification and effective treatment of essential hypertension. Effective treatment of severe and malignant hypertension clearly leads to stabilization (and occasionally improvement) of renal function.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Renal parenchymal involvement in essential hypertension. 330 6

Malignant hypertension was induced in Wistar rats of both sexes by complete aortic ligature just above the origin of the left renal artery. An acute and a late phase of hypertension, 4 days and 28 days after the aortic ligature respectively, were defined to study the relationship between the severity of hypertension and injury of the small arteries and myocardial necrosis. The most frequent finding in the heart was the presence of right ventricular infarction. In acute-phase hypertension most of the animals showed acute infarction of the right ventricle, but only focal left ventricular infarction was found. Lesions in the large coronary arteries were not observed. However, the small arteries and arterioles of the right ventricle presented fibrinoid necrosis lesions. In late-phase hypertension, the intramyocardial small vessels showed proliferative endarteritis and fibrinoid necrosis lesions, but this time they appeared in both ventricles. The severity of the myocardial infarcts and the percentage of small arteries and arterioles injured in the right ventricle were significantly higher than in the left ventricle despite the maintenance of blood pressure almost to the same level. No changes in the right ventricular pressure were observed in either phase. These observations suggest that in malignant renovascular hypertension the intramyocardial arteriolar lesions appear to be an important factor in the production and the severity of myocardial infarcts with predominance in the right ventricle.
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PMID:Predominant right ventricular infarction in malignant renovascular hypertension in rats. 359 33

A retrospective analysis of 66 adult patients diagnosed as having IgA nephropathy by renal biopsy revealed that 24 (36%) were hypertensive when first seen. Of these hypertensive patients, 10 (15%) had malignant or accelerated hypertension. All patients but one were male and had no knowledge of their renal disease and sought medical advice for symptoms due to hypertension. Five patients had no history of gross hematuria. Histological vascular findings showed, in three proliferative endarteritis and fibrinoid necrosis, in five arteriolosclerosis and in two vascular hypertrophy. In spite of good blood pressure control, six patients reached terminal uremia within a maximum of 14 months. In summary, the incidence of malignant hypertension in adults with IgA nephropathy is higher than previously reported, and its true incidence can only be known if more histopathologic studies of patients with malignant hypertension are performed. Patients with this association reach end stage renal failure in a short period of time.
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PMID:Malignant or accelerated hypertension in IgA nephropathy. 381 3

This paper presents 3 cases of generalized livedo racemosa and cerebral infarction in female patients ages 27, 39, and 42 years. Livedo racemosa is characterized by a broken, irregular pattern on the skin. It is probably caused by patchy impairment of cutaneous arteriolar circulation, resulting in reflectory venous dilation and stasis of blood. Livedo may accompany diseases such as atherosclerosis, diseases with intravascular occlusion, and collagen disorders, indicating a need for a careful search for an underlying condition. These 3 patients demonstrated several risk factors for atherosclerosis: hypertension (1 patient), oral contraceptive use (2 patients), and smoking (2 patients). The clinical findings in these 3 cases provide support to the theory that a chronic endarteritis obliterans of the small and medium-sized arteries is the underlying cause for the skin and neurologic manifestations in livedo racemosa associated with stroke.
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PMID:Livedo racemosa generalisata and stroke. 402 92

The authors report a cause of acute cor pulmonale caused by Schistosoma mansoni bilharziosis. The clinical feature was a collapse with right ventricular failure following a delivery. The hemodynamic exploration showed a pre-capillary and supra-systemic pulmonary hypertension. The histopathologic study in post-mortem showed pulmonary lesions of fibrosis endarteritis with granulomatosis reaction round many eggs of Schistosoma mansoni. The authors discuss the frequency of various anatomic lesions (20, 30%), hemodynamic (20%) and clinical (2,5%) of the pulmonary bilharziosis. They recall the anatomical and histological mechanisms of the pulmonary artery hypertension in this disease. They emphasize the originality of this observation which is due to its super acute character and its Schistosoma mansoni bilharziosis etiology whereas pulmonary demonstrations are usually due to Schistosoma haematobium.
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PMID:[Acute bilharzial cor pulmonale due to Schistosoma mansoni]. 652 24

Renal biopsies were carried out in 29 patients with scleroderma to study the early vascular lesions and their eventual clinical significance. Haemolytic acute renal failure was present in 9 patients. The biopsies showed early vascular lesions on interlobar arteries. The main biological change was proliferative or fibrous endarteritis. Mucoid infiltration was found in 3 biopsies. The arterioles were spared or only slightly affected without major fibrinoid necrosis. These lesions were therefore distinct from those of malignant hypertension. However, at autopsy of 2 of these cases, the vascular lesions were undistinguishable from those of malignant hypertension. The biopsies in 13 out of 14 patients with scleroderma without obvious renal involvement (9 cases) or with moderate proteinuria and/or hypertension without renal failure (5 cases) showed interlobar endarteritis with associated mucoid infiltration in 3 patients. This lesion was isolated but sometimes extensive even in young patients without hypertension. One patient died within one year, of disseminated colonic carcinoma, and 4 of cardio-respiratory failure due to scleroderma without hypertension, renal failure or proteinuria. Eight of the 9 remaining patients were traced 6 to 16 years after biopsy. Two were moderately hypertensive but none had renal failure. Cutaneous and internal organ scleroderma had regressed in the majority and proteinuria had disappeared in 3 cases.
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PMID:[Renal involvement in scleroderma]. 652 54


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