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

The course of mean arterial pressure was compared in two series concerning 18 primary or tumoral hyperaldosteronism and 8 idiopathic ones. Identification of the nature of the hyperaldosteronism should not yet motivate a decision on principle, surgical in case of tumor, medical in an idiopathic case. In the latter case cooperation and tolerance of medical treatment, severity of hypertension also come into consideration. A positive spirolactone test, a hypertension course of less than six years were in our experience a good indication of successful surgery, as opposed to a normal unilateral renal biopsy. In case of operation, the removal protocol should adapt to the peroperative findings; 80% adrenalectomy is the most common procedure, except in the case of isolated adenoma of more than 10 mm diameter.
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PMID:[Primary and idiopathic hyperaldosteronism. Course 1 year after operation. Apropos of 28 cases]. 82 53

The clinical presentations and renal biopsy specimens of 18 patients with primary aldosteronism were reviewed to determine the characteristic pathologic features of the kidney in this syndrome. All patients were hypertensive with a mean blood pressure of 192 nm. Hg systolic and 122 mm. Hg diastolic. The average duration of hypertension was 6.88 years. The mean serum potassium was 2.88 mEq. per l. and the mean plasma carbon dioxide was 31.4 mEq. per l. A significant history of urinary tract disease was noted in 8 patients. Laboratory and diagnostic studies evaluating renal structure and function were abnormal in 11 patients. Renal biopsies from all 18 individuals showed evidence of parenchymal damage. Hypertensive and hypokalemic changes were the most significant abnormalities and were considered moderate to severe in 78 and 89 per cent of the patients, respectively. Histologic evidence of pyelonephritis was noted in 2 patients only and no renal specimens contained characteristic changes of metabolic alkalosis. The preoperatively hypertensive and renal evaluations did not reflect the severity of the renal changes noted histologically. The extent of renal injury caused by hypertension and hypokalemia in these patients emphasizes the consequences of primary aldosteronism. Early diagnosis and treatment of this disorder are essential if these consequences are to be avoided.
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PMID:Renal changes in primary aldosteronism. 83 53

Previous studies have reported an exaggerated natriuresis in hypertensive man; however, a systematic appraisal of this response in various forms of hypertension has not been made. We measured fractional excretion of sodium (FENa) during a four hour intravenous infusion of 2 liters normal saline in 162 normal subjects and 120 hypertensives. Of these, 13 had primary aldosteronism (ALDO), 19 high renin (HRH), 30 low renin (LRH), and 57 normal renin (NRH) essential hypertension. FENa for normals (1.42%), NRH (1.57%), and HRH (1.46%) was similar. That for LRH (2.56%) and ALDO (4.18%) was elevated compared to the other three subgroups (P less than 0.001). Although the four hour FENa during saline infusion was associated with mean atrterial blood pressure (MABP) within the entire hypertensive population (r = 0.51), when the subgroups of the hypertensive patients were considered separately no association between FENa and MABP was identified. Moreover, the MABP of subjects with HRH was greater (P less than 0.05) than in those with NRH, although the FENa of the two subgroups was similar. Patients with ALDO and LRH have a greater natriuretic response to a salt load than do other subgroups of essential hypertension or normal subjects. The exaggerated natriuresis appears to be a feature of hypertension with renin suppression. The degree of exaggerated natriuresis in not solely a function of an elevated mean arterial blood pressure.
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PMID:Natriuretic response to saline infusion in normotensive and hypertensive man. The role of renin suppression in exaggerated natriuresis. 84 36

In a Zurich outpatient clinic in 1975 hypertension was found in 10.4% of 8228 patients (3657 females and 4571 males). Essential (primary) hypertension was found in 92.9% of all hypertensives. Among secondary forms of hypertension (7.1%) renal hypertension was the most common (5.8%) with 4.9% for hypertension of renal parenchymatous origin, .8% renovascular hypertension, and .1% hypertension associated with unilateral hydronephrosis. In 2 patients (.2%) the underlying disease was primary aldosteronism and in 5 (.6%) coarctation of the aorta. In 4 females (.5%) hypertension was caused by oral contraceptives. Patients with essential hypertension had higher body weight than those with normal blood pressure. These differences were statistically significant in young and middle-aged patients. The percentage of primary hypertension was significantly high. In only 18 (2.1%) of 854 hypertensives was a curable form of high blood pressure found (hypertension caused by renal artery stenosis, hydronephrosis, aldosterone-producing adenoma of the adrenal gland, and oral contraceptives). The very low percentage of curable forms of high blood pressure should be kept in mind when deciding on expensive procedures in a search for secondary forms of high blood pressure.
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PMID:[Primary and secondary hypertension in polyclinical patients]. 85 17

Serial measurements of urinary sodium excretion, sodium space, plasma volume, and plasma renin concentration were made during the development of hypertension in patients who were exposed to an excess of endogenous or exogenous mineralocorticoid activity. Five patients with primary aldosteronism due to adenoma were followed during spironolactone treatment, for 35-55 days after the drug had been stopped, and finally, after surgery. Blood pressure rose continuously after stopping spironolactone. Sodium balance, however, showed an initial phase of sodium gain, followed by a phase of gradual sodium loss. Sodium space and exchangeable sodium rose by 5.0 +/- 0.48 liters/1.73 m2 of body surface area (BSA) (P less than 0.005) and by 865 +/- 97 mEq/1.73 m2 BSA (P less than 0.005), respectively; the values were maximal after 10-15 days, declined afterward, but remained higher than during spironolactone treatment. Plasma and blood volumes rose by 624 +/- 90 ml/1.73 m2 BSA (P less than 0.005) and by 327 +/- 74 ml/1.73 m2 BSA (P less than 0.01), respectively; they were maximal after 20-25 days, and then returned to their initial values. Exchangeable sodium, during the phase of sodium loss, was inversely correlated with the rise in blood pressure (P less than 0.01). Renin fell during the phase of sodium gain, and remained low afterwards. Blood pressure and sodium space declined after surgery, but plasma volume showed no change. The postsurgery values of these parameters were not significantly different from those measured during spironolactone treatment. Two subjects with adrenocortical insufficiency, who were followed for 45-60 days during treatment with dexamethasone and 9alpha-fluorocortisol acetate, also showed a transient rise in sodium space and plasma volume. The results suggest a redistribution of body fluids during development of hypertension. They also suggest that the tendency of body fluid volumes to return to normal is pressure-dependent. The long-term effects of mineralocorticoid excess on the interrelations between pressure, volume, and renin bear some resemblance to the pattern observed in patients with established essential hypertension, i.e., pressure remains elevated despite a decrease of volume, and renin is "inappropriately" suppressed in relation to the sodium and volume status.
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PMID:Volume-pressure relationships during development of mineralocorticoid hypertension in man. 85 75

The symptoms and clinical course of chronic hypokalemic nephropathy are described in 21 patients with longstanding potassium deficiency. In 14 patients (group A) the potassium depletion was caused by malnutrition and/or abuse of laxatives and/or diuretics. 7 patients (group B) suffered from primary (6 cases) or secondary (1 case) aldosteronism. The average duration of potassium depletion was 8.8 years in group A and 3.4 years in group B. Depending on the duration of potassium depletion, chronic renal disease develops which may end in terminal renal failure. Urinalysis is non-specific or negative. The clearance of creatinine slowly decreases. Metabolic alkalosis is a constant finding and in group A occurs with a tendency to hyponatremia and hypochloremia, with the development of metabolic acidosis only in advanced renal insufficiency. In contrast to patients of group B, patients of group A have normal or low blood pressures converting to hypertension, if at all only in the late phase. The cases of group A had secondary aldosteronism (and, correspondingly, a hyperplastic juxtaglomerular apparatus). Although urinary tract infection is a regular finding in advanced stages, the clinical, radiological and histological evidence suggests that bacterial pyelonephritis, if occurring at all, is rather a complication than the cause of the disease. In 5 patients 7 instances of acute renal failure of unknown origin were observed which was lethal in one case. Another patient died from terminal renal failure, a third from an intercurrent pneumonia. Renal histology obtained from 13 patients showed the picture of diffuse chronic abacterial interstitial nephritis.
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PMID:Symptoms and course of chronic hypokalemic nephropathy in man. 87 Feb 67

Among the atypical pictures of primary aldosteronism, sometimes, normal blood and urine concentration of aldosterone have been observed in association with an adrenal aldosterone-producing adenoma. Here we report a case of atypical primary aldosteronism so characterized: -- the patient had the typical clinical findings of aldosteronism (hypertension, hypokalemic alkalosis, polyuria, etc). -- the patient exhibted all the biochemical abnormalities of primary aldosteronism: increase of exchangeable Na and of plasma volume, decrease of exchangeable K, etc. -- the patient had normal blood and urine levels of aldosterone. -- the patient's blood and urine aldosterone concentration increased following sodium depletion and K administration. Such increase was comparable with that obtained in normal subjects after the same tests. However, at the end of these tests, the patient was still in potassium depletion and sodium repletion. Therefore, it was concluded that the secretion of aldosterone, although normal in absolute values, was inappropriate to the metabolic status of the patient, since such "normal" values were found in association with conditions that should have produced an inhibition of aldosterone production. The catheterization of adrenal veins demonstrated the existence of a right adrenal adenoma. The blood pressure and the biochemical parameters of the patients have been normalized by right adrenalectomy.
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PMID:[Physiopathological and functional semeiologic considerations in a case of primary normoaldosteronemic hyperaldosteronism]. 88 97

We have reported tissue distribution studies in rats and dogs with a new adrenal imaging agent. 131I-6beta-iodomethyl-19-nor-cholesterol (NP-59). This agent concentrated five times higher in the adrenal cortex than 131I-19-iodocholesterol without increased concentration in non-adrenal tissues. We now report in 34 patients, the findings on scintigraphy with NP-59 compared with angiograms and/or adrenal vein hormone levels and histopathology, including 13 patients with hypercortisolism, 12 with primary aldosteronism, 2 with low renin hypertension, 5 with catecholamine excess, 1 with a liver metastasis from an aldosterone producing adrenal cortical carcinoma, and 1 with anaplastic adrenal cortical carcinoma. NP-59 adrenal cortical uptake was more rapid and intense and background activity was less prominent, allowing earlier and more definite interpretation of images than was possible with 131I-19-iodocholesterol.
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PMID:A new and superior adrenal imaging agent, 131I-6beta-iodomethyl-19-nor-cholesterol (NP-59): evaluation in humans. 88 97

Described herein is an autopsy case of a 16-year-old female with severe hypertension, hyperreninemia and secondary aldosteronism. She had had a progressively growing tumor of her right orbita from the age of 4. The tumor was partially excised 13 months before death. A high content of a renin-like material was detected in the excised tumor, which was histologically a hemangiopericytoma. Bowie stain revealed some granules in small number of tumor cells and electron microscopic study showed some cytoplasmic granules. Following the operation, hypertension was somewhat improved, but the levels of plasma renin activity and plasma aldosterone concentration remained elevated, because the tumor was partially resected. At autopsy, the tumor invaded into the cranial base and right frontal lobe, and metastasized to the lungs. In the present case, renal renin-secreting tumor, malignant hypertension and renovascular hypertension were ruled out by the clinical and pathological studies.
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PMID:Extrarenal renin-secreting tumor associated with hypertension. 91 Jun 30

Primary hyperaldosteronism is a potentially curable cause of hypertension, and much interest has been shown in methods of diagnosing the associated hypokalaemic hypertension and localising the adrenal adenoma. In two patients the diagnosis of primary aldosteronism was confirmed by colonic potential measurement and the adenoma localised by a new subtraction technique for early adrenal imaging applied to the use of 131I-19-iodocholesterol. Both patients underwent adrenalectomy and in each case an adenoma was removed. Blood pressure and electrolyte levels returned to normal after operation. In one patient bilateral adrenal phlebography had failed to show the tumour, and sampling of aldosterone concentrations in the adrenal veins had been unsatisfactory.
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PMID:Adrenal aldosterone-producing adenoma: use of colonic potential in diagnosis and subtraction scanning technique for localisation. 93 76


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