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

A patient with hypertension of sudden onset and with segmental renal ischemia due to an aneurysm in a renal artery branch underwent a nephrectomy which apparently cured his arterial hypertension. The nephrectomy specimen was studied to determine the activity of the juxtaglomerular cells and the concentration of prostaglandins in both ischemic and normal renal tissue. As compared with the normal tissue, the ischemic cortex had an increased number of heavily granulated juxtaglomerular cells. Interstitial fibrosis in the ischemic segment was associated with considerably lower tissue concentration of both prostaglandins A2 and E2 when compared with surrounding normal medulla. These findings appear to correlate well with present theories that consider renal ischemia to be associated with decreased production or response of prostaglandins that normally would counteract the effects of angiotensin.
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PMID:Renins and prostaglandins in segmental renal artery aneurysm associated with accelerated hypertension. 84 14

Two cases of renal arterial aneurysm or diffuse renal arterial dilatation are presented. Frequency, pathogenesis, clinical appearance, and prognosis of this disorder are discussed. Major complications include rupture or thrombosis of the renal artery, and hypertension due to renal ischemia; the latter is best diagnosed by renin determination in renal venous blood collected by selective catheterization.
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PMID:[Renal arterial aneurysms--diffuse renal arterial ectasia. (Review and case histories) (author's transl)]. 84 59

The role of some mechanisms in the development of hypertension due to unilateral renal artery stenosis is influenced by the presence or absence of the intact opposite kidney. In this paper: a) the cardiovascular reactivity (CR) to norepinephrine (NE) and b) the effect of a ganglionic blocker (pentolinium, P) during the early (first two weeks) and later periods (ten weeks) of hypertension elicited by unilateral renal ischemia in the presence of the untouched contralateral kidney in the rat have been reported. Neither the threshold doses nor the dose-pressor response curves have shown a greater reactivity of the cardiovascular system to NE in this specific type of renovascular hypertension. An increase in the activity of the nervous system apparently contributes in early and late periods to the fuller development of high arterial pressure (AP).
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PMID:Cardiovascular reactivity and neurogenic tone in unilateral renovascular hypertension in the rat. 103 58

Information defining the renin-angiotensin-aldosterone axis as a control system concurrently regulating salt balance and blood pressure has been applied to examine the role of renin in the causation of experimental and clinical forms of renovascular and renal hypertension and thence to develop criteria for differentiating these entities. Experimantally there are two models of renovascular hypertension, one characterized by excess renin with reduced sodium (vasoconstrictor form) and the other by excess sodium with reduced renin (volume form). But with sodium depletion, the volume form switches to a vasoconstrictor form, illustrating how the two factors coordinate to maintain blood pressure. Human renovascular and renal hypertensions appear to be sustained by the same two mechanisms. Experimental and clinical studies both indicate that curable renal hypertension is in fact a renin-dependent vasoconstrictor hypertension. Three criteria, derived from four renin measurements, identify this situation: (1) Hypersecretion of renin is reflected by a high peripheral level when referenced against sodium excretion. (2) Lacteralization of renin secretion with contralateral suppression rules out occult bilateral disease. It is indicated by V-A = 0 from the uninvolved kidney. (3) A third criterion, (V-A)/A greater than 48 per cent from the ipsilat-eral kidney, identifies renal ischemia. These three criteria, when taken together in a combined scoring analysis, provide high precision in identifying the patient with the vasoconstrictor form of renal hypertension that is potentially reversible by appropriate surgery. Absence of these criteria identifies hypertension associated with either occult or overt bilateral renal disease. In these patients, the volume factor often predominates and is expressed by some suppression of plasma renin levels. Here, removal of renal tissue is contraindicated. Corroborative evidence to support these three criteria can be developed from the blood pressure response to angiotensin blocking drugs or to anti-renin therapy with propranolol. Thus in all of these renal hypertensions, the vasoconstrictor and volume factors can be identified using renin measurements and pharmacologic interventions.
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PMID:New concepts of the renin system and of vasoconstriction-volume mechanisms. Diagnosis and treatment of renovascular and renal hypertensions. 109 53

A case is reported of documented renovascular hypertension due to traumatic occlusion of the main renal artery in a double renal artery system. Emphasis is placed on the value of the oblique renal arteriogram in assessing segmental vasuclature prior to surgical intervention. Oblique arteriography may also aid in the preoperative evaluation of patients with segmental renal ischemia due to other causes.
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PMID:Renovascular hypertension. Secondary to traumatic occlusion of supplemental renal artery. 111 29

Peripheral plasma renin activity (PRA) is not invariably elevated in patients whose ischemic renal lesion is causing hypertension. Infusions of an angiotensin II antagonist, 1-sar-8-ala-angiotensin II (P-113), have been used to determine whether the blood pressure responses might indicate angiotensin dependence in 221 consecutive hypertensive patients. In 32 patients P-113 infusion reversibly reduced blood pressure, and almost all of these "P-113 responders" had elevated renal vein and/or peripheral PRA levels, together with evidence of renal ischemia. Among the 189 "P-113 nonresponders," peripheral PRA was elevated in seven (3.8%), and renal vein PRA ratio was abnormal in two patients, who might represent exceptions to the otherwise successful record of the P-113 response in identifying "angiotensinoginic" hypertensives.
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PMID:Identification of angiotensinogenic hypertension in man using 1-sar-8-ala-angiotensin II (Saralasin, P-113). 113 74

It is apparent that the split function study and renal vein renin determination are complementary and afford valuable information for selecting patients with potentially curable renovascular hypertension. The split function study, when interpreted with the recently defined split function ratio, offers the clinician a highly accurate means of diagnosing significant renal ischemia. Because the split function ratio shows the disparity between the ischemic and contralateral kidney to a greater degree, the chance of misdiagnosis due to laboratory or physician error is minimized. The split function study, however, is of limited value in patients with pyelonephritis since the water- and salt-losing characteristics of the pyelonephritic kidney may mask significant renal ischemia. In these patients, as well as those with a nonfunctioning kidney or hydronephrosis, the renal vein renin determination is the test of choice. In addition, the added morbidity of the split function study is not warranted in a patient with an elevated peripheral renin which, for interpretation, requires an accurate 24 hour urine for sodium, a renal vein renin ratio outside the range of patients with essential hypertension (renal vein renin ratio greater than 1.7) and evidence of suppression of renin secretion from the contralateral kidney. If, however, the renin determination does not afford convincing evidence of significant renal ischemia in a patient with radiographic evidence of renal arterial stenosis, a split function ratio definitely should be determined to more completely define the pathology. The attendant morbidity of a carefully performed split renal function study does not approach the morbidity and mortality associated with unnecessary surgery or inadequately treated hypertension.
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PMID:Ureteral catheterization studies. 115 55

A case of renin elevated hypertension cured by cyst decompression is presented. The proposed mechanism is segmental renal ischemia produced by the cyst. Renal cyst evaluation should include renin studies if hypertension is present.
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PMID:Simple renal cyst and high renin hypertension cured by cyst decompression. 125 97

This article reports the case of a rapidly severe stenosis of the right renal artery, causing uncontrolled hypertension. After failure of a percutaneous transluminal renal angioplasty, which provoked the thrombosis of the vessel, a surgical revascularization was performed after +/- eighteen hours of renal ischemia. Blood pressure, blood urea nitrogen and serum creatinine returned to normal values. A dramatic improvement of the right renal function was attested at the hippuran scintigraphy after a dose test of captopril. The results of renographic studies obtained in this clinical case underline the role of the captopril radionuclide test in detection and follow-up after treatment of renovascular hypertension.
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PMID:Role of the captopril test in renovascular hypertension: a case report. 144 67

The term nephrosclerosis is customarily used to designate a pathological entity that tends to characterize subjects with high blood pressure; it refers to a condition of diffuse fibrous replacement of renal substance secondary to ischemia from hypertension-related vascular injury. The features of parenchymal fibrosis can be distinguished from those of vasculopathies in tissue sections, parenchymal fibrosis being measured by assessing the degree of interstitial fibrosis and by counting obsolete glomeruli, while vasculopathies are measured by determining arterial intimal fibroplasia and by counting hyalinized arterioles. A series of 166 autopsies in subjects aged 25 to 92 years, selected because ample documentation of blood pressure was available, was assessed. One form of vasculopathy, arterial fibroplasia, is a better correlate of high blood pressure than is parenchymal fibrosis in this body of data. Cases with much vasculopathy and little parenchymal fibrosis occurred frequently, and these subjects were usually hypertensive. Cases with little vasculopathy and much parenchymal fibrosis were also encountered, but these subjects were usually not hypertensive. The suggested conclusion is that blood pressure relates less to the renoprival state of nephron loss than it does to renal ischemia in patients with nephrosclerosis.
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PMID:Blood pressure related separately to parenchymal fibrosis and vasculopathy of the kidney. 149 64


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