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

Twenty-six patients with the syndrome of inappropriate secretion of antidiuretic hormone were reviewed. The underlying diseases were bronchogenic carcinoma (12 cases); myxoedema (five cases); diseases of the nervous system (five cases); bronchopneumonia, carcinoma of the oesophagus, acute intermittent porphria and chlorpropamide therapy (each one case). Serum sodium levels ranged between 104 and 125 mEq per litre. Eighteen patients presented neurological manifestations, which in 14 were considered to be due to hyponatraemia. Neurological signs included disorders of consciousness (stage I and II coma), extrapyramidal signs, asterixis and epileptic seizures. An hyponatraemic coma was the first manifestation of the syndrome in five cases. In all cases where the EEG was recorded it showed non-specific signs of metabolic coma. The fundi never showed signs of intracranial hypertension. Blood urea and creatinine levels were invariably low in the euthyroid patients; these values were normal or elevated in patients with myxoedema and hyponatraemia. Hypokalaemia was frequent, and hypocalcaemia constant. In eleven cases an excess of water intake revealed the clinical syndrome: six patients were excessive beer drinkers and five had received extensive intravenous infusions. In one case the deleterious effect of diuretics was evident, and in another, the syndrome became evident during radiotherapy of an oesophageal tumour. Treatment of the syndrome was successful in all cases. A review of the literature concerning the various pathogenic mechanisms corresponding to the different underlying diseases is presented. The concept of aberrant hormonal production by a tumour is illustrated by an electron microscopic study.
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PMID:Clinical, biological and pathogenic features of the syndrome of inappropriate secretion of antidiuretic hormone. A review of 26 cases with marked hyponatraemia. 100 53

1. A cross-over study was done in twenty patients with hypertension to compare the effects of chlorothiazide (0-5 g twice daily) and metolazone (5 mg daily) in combination with other anti-hypertensive agents. 2. Compared with absence of diuretic therapy, chlorothiazide and metolazone both produced significantly lower blood pressures. 3. Blood pressures on metolazone tended to be lower than on chlorothiazide but this difference was not statistically significant. 4. Both diuretics significantly lowered serum potassium concentrations and total body potassium to a similar degree, but the serum potassium did not fall below the normal range in any patient and no potassium supplements were needed. No electrocardiographic changes suggestive of hypokalaemia were noted. 5. Small but significant increases in serum bicarbonate, calcium, urea and acid were observed with both diuretics. 6. Patient acceptance was excellent and no adverse effects were encountered.
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PMID:A comparison of the effects of chlorothiazide and of metolazone in the treatment of hypertension. 107 94

The aim of this study was to evaluate the number, outcome, survival time, and causes of death of patients with severe arterial hypertension who were admitted to the Department of Medicine at Landspitalinn (National Hospital) in Reykjavik during the years 1957 to 1971. During this period 117 patients were found to have severe arterial hypertension (12.6% of all cases of hypertension diagnosed) according to the grading of Keith and Wagener, 20 patients with grade IV retinopathy and 97 patients with grade III. The case histories were analysed according to age and sex distribution, blood urea, electrocardiographic changes, heart size by X-ray at the time of diagnosis and final outcome. The survival calculations were done by the decrement method (life tables) and aim taken from patient age 65 years and less. Relatively fewer patients with severe arterial hypertension were admitted during the last five year period (1967-1971) than during the two previous five year periods. The main causes of death were cerebrovascular accidents (26.6%), myocardial infarctions (22.8%), and renal failure (22.8%). Approximately 50% of the men and 60% of the women survived five years. Elevated blood urea values and signs of left ventricular hypertrophy on ECG at the time of diagnosis carried a more sinister prognosis.
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PMID:Severe arterial hypertension (grade III and IV). 107 39

1. A group of patients with essential hypertension was divided into three categories on the basis of the plasma renin activity. 2. There was no correlation between the plasma renin activity categorized as high, normal or low and the duration of hypertension, the incidence of left ventricular enlargement, the blood urea nitrogen, serum creatinine, cholesterol or uric acid respectively. 3. Analysis of data showed that the incidence of cardiovascular events in the hypertensive population correlated with the plasma renin activity only in combination with known risk factors.
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PMID:Plasma renin activity and cardiovascular disease. 107 64

Available clinical evidence indicates a high prevalence of hyperuricemia in patients with essential hypertension; this becomes accentuated with diuretic therapy. Since there is an association of hyperlipidemia with hyperuricuria and hypertension and since hyperuricemia is a feature of diuretic therapy, we explored whether these relationships might be provoked by prolonged diuretic therapy. Eighteen male patients with uncomplicated essential hypertension of mild severity were treated for 9 months with hydrochlorothiazide and supplemental potassium chloride, 100 mg and 45 mEq/day, respectively. Arterial pressure, renal function, and serum electrolyte, uric acid, blood glucose, and lipid concentrations were measured several times before and during therapy. Arterial pressure remained significantly reduced during therapy (P less than 0.001); this was associated with reduced serum potassium (P less than 0.01) and increased blood glucose and serum uric acid concentrations (P less than 0.005, P less than .025, respectively). Blood urea nitrogen, serum creatinine, sodium, cholesterol and triglyceride levels did not significantly change with treatment. Thus, although diuretics increase serum uric acid and blood glucose, their effect on serum lipid concentration is negligible.
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PMID:Effects of diuretics on lipid metabolism in patients with essential hypertension. 107 5

Our objective was to produce reductions in the luminal volume of Henle's loop and increases in linear flow velocity through the loop. We did this in a recollection micropuncture study by collecting fluid with and without suction from early distal tubules. With suction, transit time of fast green dye through the loop decreased by 34%, calculated loop volume decreased by 28%, and fractional water reabsorption fell from 73.6 to 70.3% (p smaller than 0.025) in water diuretic rats. Absolute water reabsorption did not decrease significantly. In urea-saline dieuretic rats transit time decreased 25%, calculated loop volume decreased 22%, fractional reabsorption fell from 59.0 to 51.7% (smaller than 0.001), and absolute reabsorption decreased by 2.3 nl/min (p smaller than 0.025). Single nephron glomerular filtration rate, distal tubular sodium concentration, and osmolality were unaffected. The less pronounced effect of collection with suction in water diuretic rats may be related to the lower medullary fluid osmolality, which was 338 plus or minus 9 (S.E.) mOsmol/kg as compared to 497 plus or minus 35 in urea saline diuretic rats. Collecting fluid with suction from late proximal tubules did not alter glomerular filtration rate or fractional water reabsorption. Stumpe et al. ((1970) J. Clin. Invest. 49, 1200-1212) noted an inverse correlation between fluid reabsorption from Henle's loop and flow velocity in rats with hypertension or congestive heart failure. One can reproduce this correlation by artificially altering the transmural pressure gradient in the loop.
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PMID:Physical factors influencing fluid reabsorption from Henle's loop. 113 20

Measurement of the increase in area of the renal silhouette, as it appears on radiographs following the administration of water-soluble contrast medium and certain diuretics, seems to be useful in the diagnosis of renovascular hypertension. In order to assess the optimal technique for such measurements, washout urography was performed in 32 hypertensive patients in two consecutive examinations so that the distensive effect of etacrynic acid, furosemide and hypertonic mannitol, respectively, were compared with that of urea in the same patients. In spite of their stronger diuretic effect, none of the above-mentioned diuretics caused a greater renal distension than urea, the maximum increase in area of the renal silhouette being about 7 to 20%, average about 11%. Since urea is probably the best siuted diuretic for the washout test, it seems to be the drug of choice for these diagnostic procedures.
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PMID:Renal distension in response to water-soluble contrast medium and various diuretics. 114 41

1. The acute malignant phase of hypertension in rats with an untouched contralateral kidney is characterized by salt and fluid loss, increased fluid intake, decrease in body-weight gain, and reduced food consumption. Plasma concentrations of sodium and potassium were reduced, and plasma angiotensin II rose to about four times normal. 2. To investigate the significance of an untouched contralateral kidney for the development of the acute malignant phase in renal hypertensive rats, comparative studies were undertaken in unilaterally nephrectomized rats with stenosis of the remaining renal artery and in rats with bilateral renal artery stenosis. In addition, the effect of declamping one renal artery in rats with bilateral stenosis was studied. 3. In unilaterally nephrectomized rats, no signs of sodium and fluid loss were demonstrable, despite marked increase in blood pressure. Similarly, rats with bilateral renal artery stenosis had no acute malignant phase of hypertension. 4. In hypertensive rats with bilateral stenosis, removal of the clip from one renal artery was followed by an immediate fall in blood pressure and a subsequent gradual increase. Eleven of sixteen rats lost salt and fluid and developed an acute malignant phase. Plasma angiotensin II was high and serum urea elevated. 5. Consumption of 2% saline in addition to water as drinking fluid had a beneficial effect, since only five of fourteen rats showed signs of the acute malignant phase, which were milder than in rats on water only. 6. It is concluded that the untouched contralateral kidney is responsible for the negative salt and water balance and its consequences, which are characteristic of the acute malignant phase of experimental renal hypertension.
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PMID:Salt loss as a possible mechanism eliciting an acute malignant phase in renal hypertensive rats. 114 33

Twenty-six uremic patients - serum urea nitrogen (SUN) 110 MG/100 ml plus or minus 22.8 (mean plus or minus SD), serum cretinine (S-Creat) 13.2 mg/100 ml plus or minus 2.27, ratio SUN/S-Creat 8.6 plus or minus 2.26, and endogenous creatinine clearance (Ccr) 3.86 plus or minus 1.41 ml/min - were treated for three months or longer with an unselected protein-poor (16-20 g protein/day) diet with oral supply of the essential amino acids including histidine in high doses as coated tablets. The amino acids were instituted after an initial diet only period (mean 0.4 months). The average treatment time was 8.4 months (range 2.7-33.6). An improvement of the general condition was obtained, persisting for several months. SUN and SUN/S-Creat decreased on the diet alone, continued to decrease after one month, and increased slightly again after three months of treatment, but did not reach the initial levels for several months in spite of an almost doubled nitrogen intake. S-Creat increased after six months indicating a further deterioration of the renal function. In patients with initially low serum total protein (smaller than 6.5 g/100 ml, 9 patients), albumin (smaller than 3.5 g/100 ml, 10 patients), and total iron-binding capacity (smaller than 260 mug/100 ml, 11 patients) the values increased after one month on amino acids and were thereafter stable. No signs of bleeding tendency, progressive muscle atrophy, or progressive peripheral neuropathy were observed. - Five patients died due to cardiovascular maladies. A further 13 patients were withdrawn for medical reasons (overhydration, 4 patients; hypertension, 1 patient; nausea and vomiting, 7 patients; and pericarditis, 1 patient). - The renal function improved in one patient. Four patients received home dialysis training, three a kidney transplant. - The results indicate that it is possible to keep severely uremic patients free from uremic symptoms, counteract protein depletion, and even improve the nutritional status during long-term treatment with an unselected protein-poor diet supplementd with essential amino acids.
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PMID:Treatment of chronic uremic patients with protein-poor diet and oral supply of essential amino acids. II. Clinical results of long-term treatment. 114 44

The experiments we described in this paper demonstrated that the myocardiac lesions without hypertension could be produced by renal failure in rabbits; after this experimental renal failure, increase in blood urea nitrogen and various functional and morphological changes suggestive of heart lesions appeared. The main structural changes in the heart were cellular edema with dilatation of the sarcotubular system, destructive changes of the mitochondria and contractile elements, and coagulative degeneration. These myocardiac lesions are induced by renal failure, and are probably caused by electrolyte imbalance, metabolic disorder, and/or hemodynamic abnormality rather than by hypertensive or toxic factors.
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PMID:Myocardiac changes in experimental renal failure--a light and electron microscopic study. 115 92


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