[Clinical picture, diagnosis and therapy of renovascular hypertension].
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Antihypertensive Agents↗
Biomedical subjects
J Furrer
Publications and source records attributed to J Furrer.
[Experiences with a new hypouricemic diuretic (tienilic acid): comparison with hydrochlorothiazide].
A new hypouricemic diuretic (tienilic acid) was compared with hydrochlorothiazide in a double-blind study in 8 patients with mild essential hypertension. After a two-week placebo period the patients received either 250 mg tienilic acid or 50 mg hydrochlorothiazide in a single daily dose for 3 weeks. After a second placebo period of 2 weeks the patients received, in a crossover design, either tienilic acid or hydrochlorothiazide for a further 3 weeks. The reduction of blood pressure and of body weight was similar for both drugs. When treatment was started diuresis and natriuresis increased with tienilic acid and with hydrochlorothiazide. Whereas serum sodium levels showed only minor variations, serum potassium levels fell with both diuretics and urinary potassium excretion increased. Urinary calcium excretion decreased and serum calcium levels slightly increased under both treatments. Both diuretics induced similar increases of plasma renin activity, plasma aldosterone concentration and aldosterone-18-glucuronide excretion. Blood urea nitrogen and, to a lesser extent, serum creatinine levels were raised slightly under both drug regimens. Whereas the serum uric acid level rose and remained elevated for the duration of hydrochlorothiazide treatment, it fell significantly and remained lowered during treatment with tienilic acid. Uric acid clearance was about twice as high with tienilic acid as with hydrochlorothiazide. Tienilic acid therefore appears to be a therapeutic alternative to thiazides and other hyperuricemic diuretics in hypertensive patients in whom hyperuricemia should be avoided or corrected.
Adult↗
[Renovascular hypertension: therapy by means of percutaneous transluminal dilatation of renal artery stenoses].
Percutaneous transluminal dilatation was performed in 5 patients with unilateral atherosclerotic renovascular disease and one patient with occlusion of a renal artery. Hemodynamic activity of the stenosis was documented by determination of pre- and poststenotic blood pressure values and by measurement of renal plasma flow. Flowing transluminal dilatation all patients showed a significant drop in blood pressure and antihypertensive treatment could be reduced or even discontinued. Only one patient became hypertensive again 3 months after the dilatation procedure. In this patient both the reduction of renal plasma flow and the delayed nephrographic effect on the stenotic side in the intravenous urogram were interpreted as symptoms of a recurrence of significant renal artery stenosis. In 2 of the six patients with impaired kidney function glomerula filtration are increased, as documented by a decrease in serum creatinine values. The results show that percutaneous transluminal dilatation may be a valuable method in the management of renovascular hypertension.
Creatinine↗
Primary aldosteronism: inability to differentiate unilateral from bilateral adrenal lesions by various routine clinical and laboratory data and by peripheral plasma aldosterone.
In 31 patients with primary aldosteronism routine clinical and laboratory data, the effect of orthostasis on plasma aldosterone (PA), plasma renin activity (PRA) and cortisol (PC), effect of fludrocortisone or high sodium intake on basal PA and night-day fluctuations of basal PA and PC with and without suppression of pituitary ACTH by dexamethasone were determined to differentiate patients with a unilateral aldosterone producing tumour (adenoma, APA, n=20; carcinoma, CA, n=1) from those with idiopathic bilateral adrenal hyperplasia (IAH, n=10). Mean systolic and diastolic blood pressure, age, serum potassium and urinary excretion of sodium and potassium were not significantly different in both groups of patients. Normokalaemic primary aldosteronism occurred both in patients with APA (n=2) and in patients with IAH (n=1). Mean basal PA and mean urinary excretion rate of aldosterone-18-glucuronide were higher though not significantly different in patients with APA or CA than in those with IAH. A substantial number of the patients with APA (n=5) and with IAH (n=3) showed urinary excretion rates of aldosterone-18-glucuronide less than 13 microgram/24 h. Mean PA and PRA significantly increased (P less than 0.025) in patients with IAH in response to posture. However, these changes also occurred at times in some patients with APA. Both fludrocortisone and high sodium intake produced a variable and no group-specific effect on basal PA. Night-day variations in PA were positively correlated with those in PC in all patients with APA (n=12) and in 5 of 8 patients with IAH. A dissociation of PA and PC, however, was only observed in patients with IAH. Finally, the effect of dexamethasone on plasma aldosterone curves was variable in both groups of patients. Our results indicate that under the described conditions analysis of routine clinical and laboratory data and of peripheral PA, PRA and PC are of limited value in differentiating patients with APA or CA from those with IAH.
Adenoma↗
Congenital pseudohypoaldosteronism: case report and review. Effect of indomethacin during sodium chloride depletion.
A newborn boy (birth weight 2550 g) presented from the first days of life with poor drinking, moderate vomiting and persistent weight loss. On hospital admission at age 4 weeks, there were severe dehydration, dystrophy and electrolyte disturbances (Na 107, Cl 80, K 5,4 mval/l). The usual causes of salt wasting were excluded, but plasma renin activity, plasma aldosterone and urinary aldosterone-18-glucuronide were markedly increased. DOCA had no salt-retaining effect, but a sodium chloride supplement of 3 g per day improved the clinical condition dramatically and normalized the electrolyte values. With this treatment, plasma renin activity and aldosterone were normal or almost normal beyond the age of 6.5 months, but urinary aldosterone-18-glucuronide remained slightly increased. Considerable augmentation of the plasma renin activity and of urinary aldosterone-18-glucuronide, but no clear salt loss were induced by spironolactone. With salt restriction, there was evidence for marked salt loss. Its progress could be inhibited by administration of indomethacin. Since indomethacin inhibits the synthesis of prostaglandins with saluretic activity, it is probable that the prostaglandins participate in the pathogenesis of the salt wasting in pseudohypoaldosteronism.
Adrenal Insufficiency↗
[Effect of long-term hemodialysis on renin activity, aldosterone, cortisol, serum potassium, serum sodium and blood pressure].
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Aldosterone↗
[Aldosterone and renin in liver cirrhosis with ascites].
Supine plasma aldosterone and plasma renin activity were determined in patients with cirrhosis of the liver and ascites (n = 10). Most of the patients initially showed an increase in plasma aldosterone and plasma renin activity. However, values within the normal range were observed (plasma aldosterone, n = 3; plasma renin activity, n = 4). In the ascitic fluid renin activity could not be detected, whereas aldosterone concentrations correlated significantly with the respective plasma levels (r = 0.8, p less than 0.01). During therapy with spironolactone alone (n =2) or in combination with furosemide (n = 4), diuresis and natriuresis showed no correlation with changes in plasma aldosterone and/or plasma renin activity. Our results suggest that other factors than renin and aldosterone secretion may be important in the formation of ascites in patients with cirrhosis of the liver. In addition, the inverse correlation between mean arterial blood pressure and plasma renin activity (r = -0.65, p less than 0.05) found in our patients supports the assumption that the increase in renin secretion is probably induced by changes in (renal) hemodynamics.
Aldosterone↗
[Studies on the differential determination of renin activity in renal venous blood in renal artery stenosis].
Plasma renin activity (PRA) was determined in both renal veins of 37 patients with angiographically proven renal artery stenosis. Renal venous PRA was determined in 17 patients without furosemide stimulation and in 20 patients before and 15 and 30 min after intravenous injection of 40 mg furosemide. 21 of 37 patients showed abnormally high peripheral PRA. In the 17 patients in whom renal venous PRA was measured without stimulation, 11 showed a PRA ratio (PRA stenotic side/PRA unaffected side) greater than or equal to 1.5. The 20 patients in whom stimulation with furosemide was performed were divided into 2 groups each containing 10 patients: The first group was characterized by an increase in PRA ratio after furosemide stimulation, while in the second group this PRA ratio decreased. In the first group mean duration of hypertension was 4.5 years compared to 7.5 years in the second group. In 17 of 37 patients renal artery stenosis was corrected by surgery. After operation 12 patients became normotensive and in 2 patients hypertension improved. There was no effect of renovascular surgery on blood pressure in only 3 patients. None of these patients showed an increasing ratio in response to furosemide. Our results suggest that the validity of renal venous PRA measurements is enhanced when the procedure is performed before and after administration of furosemide.
Furosemide↗
[Effect of the angiotensin antagonist saralasin on blood pressure and hemodynamics in patients with terminal renal insufficiency].
The angiotensin antagonist saralasin was infused both before and 10 hrs after dialysis in 10 hypertensive and 4 normotensive patients hemodialyzed for terminal renal failure. A significant increase in mean arterial pressure (MAP) and total peripheral resistance (TPR) without change in cardiac output measured by impedance cardiography were observed during the first few minutes of saralasin infusion. MAP and TPR decreased during the second half of the infusion in 4 hypertensive patients and remained at the preinfusion levels in 6 hypertensive and 4 normotensive patients. Plasma renin activity (PRA) was significantly higher in patients in whom MAP fell both before and after hemodialysis. There was a significant correlation between PRA before saralasin and the fall in MAP and TPR. The fall in MAP in 4 of 10 hypertensive patients demonstrates that inappropriately high renin and angiotensin levels are involved in the pathogenesis of hypertension in some patients with terminal renal failure. Volume factors are probably of primary importance in the other patients.
Adult↗
Control of plasma aldosterone during hemodialysis in patients with terminal renal failure.
The control of plasma aldosterone during hemodialysis was investigated in 31 patients with terminal renal failure. While before hemodialysis renin predominantly influenced aldosterone, this effect dissipated during hemodialysis. In addition, no relationship was observed between changes in aldosterone and those in sodium, potassium and plasma cortisol. In a group of 10 patients isokalemic and isonatremic hemodialysis failed to document an effect sodium or potassium on hemodialysis induced changes in aldosterone. Our data suggest that none of the four factors - renin, ACTH, sodium and potassium - had constantly caused the observed changes in aldosterone during hemodialysis.
Aldosterone↗
[Spironolactone-induced changes of the renin-angiotensin-aldosterone system and blood pressure lowering in essential hypertension].
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Aldosterone↗
[Endocrine hypertension in primary aldosteronism and in Cushing's syndrome].
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Adenoma↗
[Effect of the angiotensin antagonist saralasin (1-sar-8-ala-angiotensin II) on the blood pressure in secondary hypertension].
The angiotensin antagonist saralasin (1-sar-8-ala-angiotensin II) was given to 27 patients with different forms of secondary hypertension. The blood pressure fell in 6 of 7 patients with renal artery stenosis and in 4 of 10 patients with terminal renal failure on regular hemodialysis. No change or a rise in blood pressure was observed in 3 patients with Cushing's syndrome, 4 patients with primary aldosteronism, 3 patients with hypertension and a unilateral small kidney of other than renovascular origin, and 6 patients with terminal renal failure. It can be concluded from the results that angiotensin II is involved in the pathogenesis of renovascular hypertension and in some cases of hypertension accompanying chronic renal failure.
Angiotensin II↗
Hypotension during angiotensin blockade with saralasin.
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Adult↗
[Blood pressure and renin activity in essential hypertension under pindolol].
20 essential hypertension patients with diastolic blood pressure of 100-140 mm Hg were treated with increasing doses (15-45 mg/day by mouth) of pindolol for 14 weeks after an initial placebo period of 5 weeks. Systolic and diastolic blood pressure decreased significantly with as little as 15 mg of pindolol (p less than 0.001). No further changes in systolic and diastolic blood pressure were observed when the doses of pindolol were increased. Plasma renin activity (PRA) determined by radioimmunoassay did not change under increasing doses of pindolol. The blood pressure changes did not correlate with initial PRA or with individual changes in PRA under increasing doses with individual changes in PRA under increasing doses of pindolol. These results do not afford evidence for a renin-dependent hypotensive effect of pindolol.
Adolescent↗
[Primary aldosteronism].
The syndrome of primary aldosteronism is caused either by an aldosterone-producing adenoma or by idiopathic bilateral adrenal hyperplasia. Hypokalemic hypertension is the leading symptome of the disease. Diagnosis is by the combination of abnormally high and non-suppressible aldosterone values with undetectable or low renin values unresponsive to postural changes or salt restriction. Patients with aldosterone-producing adenoma normally show a fall in plasma aldosterone in response to posture and ACTH-dependent circadian rhythm of aldosterone, whereas bilateral hyperplasia is characterized by postural increases in plasma aldosterone and an ACTH-independent diurnal aldosterone rhythm. These creteria serve to differentiate between adenoma and hyperplasia. An aldosterone-producing adenoma can be localized by veinography, determination of aldosterone concentration in both adrenal veins and by 131I-cholesterol scintigraphy. In our hands the determination of aldosterone in blood from both adrenal veins is the most efficient procedure. In interpreting the results, however, rhythmic and sudden changes in adrenal hormone secretion should be considered. In cases where no adrenal venous blood is obtained, 131I-cholesterol scintigraphy may be used to localize adenoma. In patients with aldosterone-producing adenomas unilateral adrenalectomy should be performed, whereas patients with idiopathic bilateral hyperplasia should receive antihypertensive therapy. As rare instances of primary aldosteronism, a case of aldosterone-producing carcinoma of the adrenal cortex and a case of presumably unilateral adrenal hyperplasia are reported.
Adenoma↗
[Effect of saralasin on normal blood pressure and on reno-vascular hypertension (author's transl)].
The angiotensin antagonist saralasin was given intravenously to six normotensive students before and after dietary sodium restriction and to two patients with renovascular hypertension. Both patients responded to the angiotensin antagonist with a decrease of the systolic (32 and 38 mm Hg) and of the diastolic (29 and 16 mm Hg) blood pressure. The small changes in blood pressure observed in the normotensive subjects during the infusion of the angiotensin antagonist indicate that angiotensin II plays no important role in the control of normal blood pressure in recumbent men. The fall in blood pressure induced by saralasin in both patients, however, demonstrates that their hypertension was at least partly angiotensin-dependent. Renal vein renin determination led to the same conclusions. The saralasin infusion test seems to be a simple procedure to diagnose angiotensin-dependent hypertension and will probably help to identify patients with suspected renovascular hypertension.
Adult↗
Control of plasma aldosterone in terminal renal failure before and after nephrectomy and after renal transplantation.
In two patients with terminal renal failure the night-day rhythm of plasma aldosterone (PA) renin activity (PRA) and plasma cortisol (PC) were examined before and after bilateral nephrectomy and after renal transplantation. Before nephrectomy changes in abnormally high PA coincided with PC whereas no significant correlation was observed between PA and PRA. In the anephric state secretory episodes of PA occurred independent from those of PC while PRA was undetectable. After renal transplantation a lack of night-day variation in renin secretion was observed in both patients; only one of the two patients showed episodic secretion of PA while PC was suppressed in both patients probably due to the chronic administration of prednisone. Our results indicate, that before nephrectomy under the conditions described in this study plasma aldosterone was predominantly controlled by ACTH. In the anephric state and after renal transplantation other (yet unidentified) factors might have caused episodic secretion of aldosterone. Finally, the lack of night-day variation and secretory episodes in renin secretion after transplantation points to an important role of the sympathetic nervous system in the control of circadian and episodic renal renin release.
Aldosterone↗