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Biomedical subjects

F C Reubi

Publications and source records attributed to F C Reubi.

At least 55 records · Page 3Linked to original sources
PubMed1978

Pathogenesis and renal function in acute toxic nephropathies.

Acute toxic nephropathy may be produced by a variety of poisons and drugs. Cellular poisons, such as mercuric bichloride, produce tubular necrosis. Many drugs induce an immunologically mediated response presenting as interstitial nephritis, glomerulonephritis or angiitis. Substances, which are not primarily nephrotoxic but induce dehydration, shock, hemolysis, rhabdomyolysis and/or electrolyte disturbances may also lead to secondary acute renal failure. Reduced renal blood flow, suppressed glomerular filtration, increased tubular pressure due to obstruction, and tubular leakage are responsible for the functional breakdown. In addition, specific tubular functions may be impaired. Complete or incomplete recovery is the rule.

Acute Kidney Injury↗
PubMed1977

Interrelations between age and plasma renin, aldosterone and cortisol, urinary catecholamines, and the body sodium/volume state in normal man.

Interrelations between age and plasma renin, aldosterone and cortisol levels, urinary catecholamiens, plasma and blood volumes, exchangeable body sodium and blood pressure wwere studied in 28 young (19 to 29 years), 16 middle-aged (32 to 58 years) and 15 elderly (60 to 74 years) healthy subjects. Supine and upright plasma renin and supine aldosterone levels decreased while urinary noradrenaline excretion rate increased progressively with aging (r= greater than 0.34; p less than 0.05), with significant differences in mean values between young and elderly subjects (p less than 0.02). There was also an age-related decrease in upright plasma aldosterone concentration, although this was no statistically significant. Furthermore, mean plasma cortisol concentrations increased in response to upright posture in elderly ( + 50%; p less than 0.02), but not in young ( --10%) or middle-aged ( --8%) subjects. Blood pressure correlated with age ( r =0.35; p less than 0.05) or noradrenaline excretion rate ( r= 0.34) in the entire study population and with blood volume in the elderly ( r = 0.68), but not in the young or middle-aged study. Groups. There were no significant age-related differences in the body sodium/volume state, basal plasma cortisol levels or urinary adrenaline excretion rate, and plasma renin or aldosterone levels did not correlate with these parameters or with blood pressure. It is concluded that the influence of age on plasma renin or aldosterone levels, plasma cortisol responsiveness to upright posture, and urinary noradrenaline excretion should be taken into consideration, whenever these factors have to be interpreted in patients with arterial hypertension or other clinical disorders. Further more, these data are conssitent with the possiblity that in normal man increases in supine blood pressure with aging may be related at least partly to concomitant changes in free peripheral noradrenaline.

Adult↗
PubMed1977

[Correlations between blood pressure, blood volume and plasma renin during therapy with diuretics in essential hypertension. Comparison between the mineralocorticoid antagonist spironolactone and the "loop" diuretic mefruside].

35 patients with benign essential hypertension were treated for 6 weeks with high doses of the mineralocorticoid-antagonist spironolactone (400 mg/day), or with the "loop-diuretic" mefruside (mean maximal dose 110 mg/day). Spironolactone caused greater reductions in blood pressure and blood volume and a more marked increase in plasma renin activity (PRA) than mefruside (p less than 0.05). It appears possible that he weaker antihypertensive effect of mefruside may relate partly to its lesser influence on circulatory volume. With both diuretics, mean decreases in blood pressure were greater in patients with low pre-therapeutic PRA than in patients with normal or high PRA. However, the diuretic-induced changes in blood pressure did not correlate with the associated variations in blood volume or PRA. Thus, the increased blood pressure sensitivity to diuretics in patients with low-renin essential hypertension did not appear to be volume or renin-dependent. Under normal conditions, the maintenance of a constant blood pressure during volume depletion may partly depend on compensatory activation of the sympathetic nervous system. Moreover, patients with low-renin essential hypertension have been found to have decreased adrenergic activity. It seems possible, therefore, that the marked blood pressure sensitivity to diuretic treatment in such patients may be the result of an impaired compensatory sympathetic response to sodium and volume depletion. Analysis of the literature suggests that the diuretic furosemide, a structural relative of mefruside, may also have less blood pressure lowering efficacy in patients with essential hypertension than the distally-acting thiazides, chlorthalidone or spironolactone. Consideration of possible differences in the blood pressure reducing potential of certain diuretics thus appears to be necessary in planning the pharmacotherapy of essential hypertension.

Blood Pressure↗
PubMed1977

Interrelations among blood pressure, blood volume, plasma renin activity and urinary catecholamines in benign essential hypertension.

Interrelations among blood pressure, circulatory volume, plasma renin activity (PRA) and urinary catecholamine excretion rates were studied in normal subjects and in patients with benign essential hypertension. Mean plasma or blood volumes related to lean body mass, products of blood volume and the logarithm of PRA, and catecholamine excretion rates did not differ significantly between normal and hypertensive subjects. In both normal subjects and hypertensive patients, blood pressure levels correlated positively with the noradrenaline excretion rate (r = 0.40 and 0.36, respectively; p less than 0.025) but not with adrenaline excretion, circulatory volume or the volume-renin product. The logarithm of PRA correlated inversely with mean blood pressure in normal subjects (r = 0.40; p less than 0.001) but not in hypertensive patients; however, there was no convincing evidence for an inappropriate blood pressure-PRA relationship as a prominent feature in the hypertensive patients. PRA did not correlate with blood volume. Patients with low PRA relative to sodium excretion (21 per cent of hypertensive population) were consistently normovolemic, but they tended to be older and excreted less (p less than 0.025) adrenaline than patients with normal or high PRA. The patient subgroup with high PRA relative to sodium excretion (11 per cent of population) was hypovolemic (p less than 0.02); despite this, urinary sodium output was high (172 +/- 64 meq/24 hours). These data reveal no evidence for major roles of PRA, circulatory volume and free peripheral catecholamines in the maintenance of benign essential hypertension. Essential hypertension with low PRA is usually not a hypervolemic state, but it may reflect diminished adrenergic activity, factors associated with aging and effects of a high systemic pressure. High PRA in benign essential hypertension may be at least partly a consequence of hypovolemia resulting from high blood pressure-induced sodium diuresis.

Adult↗
PubMed1977

Sodium, renin, aldosterone, catecholamines, and blood pressure in diabetes mellitus.

Interrelations among plasma renin activity (PRA), aldosterone and cortisole levels, 0lood volume, exchangeable sodium, urinary catecholamines, and blood pressure were studied in 35 normal subjects and 60 age-matched non-azotemic patients with diabetes mellitus (60% with hypertension, 15% with orthostatic hypotension). Basal PRA, plasma aldosterone, cortisol, blood volume, plasma potassium, and urinary electrolytes were comparable in diabetic and normal subjects. Diabetic patients, however, had a 10% increase in body sodium (P less than 0.01), and 8% of them showed normal postural PRA responses and subnormal aldosterone responses; 22% had subnormal PRA and normal aldosterone responses, and 17% had subnormal responses of PRA and aldosterone. Non-PRA-related aldosterone responses could not be explained by ACTH or electrolytes. Orthostatic decreases in blood pressure correlated (P less than 0.01) with both catecholamine excretion and basal PRA. This suggests that in diabetes mellitus, body sodium is increased. Basal PRA and plasma aldosterone are usually normal, but their postural responses are frequently impaired. Absent aldosterone responses, despite normal PRA responsiveness, may reflect an adrenal abnormality or an ineffective form of renin. Marked postural aldosterone stimulation, unrelated to PRA, ACTH, or electrolytes, points to a potent unknown factor in aldosterone control. Low levels of free peripheral catecholamines and PRA may be complementary factors contributing to postural hypotension.

Adult↗
PubMed1977

Curable hypertension with unilateral hydronephrosis. Studies on the role of circulating renin.

Among eight patients with unilateral hydronephrosis and hypertension, peripheral plasma renin activity was normal in seven and borderline high in one. Four patients had hydronephrotic/contralateral kidney renin ratios of greater than 1.5, suggesting excessive renin release from the diseased kidney, and ratios between contralateral kidney and peripheral blood of less than 1.2, indicating suppressed renin production in the contralateral kidney. Nephrectomy normalized blood pressure in each of these patients. Two patients had hydronephrotic/contralateral kidney renin ratios of less than or equal to 1.3 or contralateral kidney/periphery ratios of greater than 1.2, suggesting ischemia of the contralateral kidney; pyeloplasty or nephrectomy, or both, failed to improve the hypertension. Postoperative changes in blood pressure correlated with changes in peripheral renin (r = 0.90; P less than 0.01). These data suggest that hypertension associated with unilateral hydronephrosis is partly renin-dependent; and renal vein renin values are helpful in selecting patients for surgery.

Adolescent↗
PubMed1976

[Correlations between blood pressure, blood volume, plasma renin and urinary catecholamines in normal subjects and in patients with benign essential hypertension].

Interrelations between blood pressure, circulatory volume, plasma renin activity (PRA) and urinary catecholamine excretion rates were studied in normal subjects and patients with benign essential hypertension. Mean plasma or blood volumes related to lean body mass, products of blood volume and the logarithm of PRA, and catecholamine excretion rates did not differ significantly as between normal and hypertensive subjects. In both normal subjects and hypertensive patients, blood pressure correlated positively with noradrenaline excretion rate (r = 0.40 and 0.36 respectively; p less than 0.025), but not with adrenaline excretion, circulatory volume or the volume-renin product. The logarithm of PRA correlated inversely with mean blood pressure in normal subjects (r = -0.40; p less than 0.001), but not in hypertensive patients; however, there was no convincing evidence of an inappropriate blood pressure-PRA relationship as a prominent feature in the hypertensive patients. PRA did not correlate with blood volume. Patients with low PRA relative to sodium excretion (21% of hypertensive population) were consistently normovolemic, but tended to be older and excreted less (p less than 0.025) adrenaline than normal or high-PRA patients. The patient subgroup with high PRA relative to sodium excretion (11% of population) was hypovolemic (p less than 0.02); despite this, urinary sodium output was high (172 +/- 64 meq/24 hr). These data reveal no evidence for major roles of PRA, circulatory volume and free peripheral catecholamines in the maintenance of benign essential hypertension. Low-PRA essential hypertension is usually not a hypervolemic state, but may reflect diminished adrenergic activity, factors associated with aging and effects of a high systemic pressure. High PRA in benign essential hypertension may be at least partly a consequence of hypovolemia resulting from high blood pressure-induced sodium diuresis.

Blood Pressure↗
PubMed1976

[Interrelations between blood pressure, blood volume, plasma renin and urinary catecholamines during beta-blockade in essential hypertension (author's transl)].

Studies in 55 patients with benign essential hypertension showed that the beta-blockers bufuralol (22 patients) and propranolol (33 patients) at a dose ratio of 1:4, possess comparable antihypertensive efficacy despite different properties regarding intrinsic sympathomimetic activity. Beta-blocker-monotherapy normalized blood pressure ( less than 140/90 mm Hg) in one fourth of the patients. Body weight and plasma and blood volumes remained unchanged during beta-blockade of four to six weeks duration, the mean plasma potassium was slightly increased. The inhibition of plasma renin activity (PRA) was more pronounced with propranolol (-69%) than with bufuralol (-47%). Wirth both beta-blockers decreases in blood pressure correlated inversely with pre-treatment PRA (p less than 0.05). Propranolol-induced changes in blood pressure correlated also with associated changes in PRA (p less than 0.005); in contrast, no such relationship was observed with bufuralol. The blood pressure effects of bufuralol, however, correlated significantly with changes in urinary noradrenaline excretion (r=0.41; p less than 0.05). Patient sub-groups with low, normal or high pre-treatment PRA in the average showed a comparable pattern of pre-treatment noradrenaline excretion and patients with normal renin levels exreted more adrenaline than those with low renin levels (p less than 0.001). These data are consistent with the concept that in untreated essential hypertension PRA may be an index of adrenergic activiity, the latter representing an important determinant of blood pressure response to beta-blockade. The blood pressure lowering effects of bufuralol in benign essential hypertension seem to be independent of renin and may be related, at least partly, to diminished free peripheral noradrenaline levels.

Adrenergic beta-Antagonists↗
PubMed1976

Hypertension in terminal renal failure.

Inverse interrelations between plasma renin activity and exchangeable sodium or blood volume were found in both normotensive (N = 23) and hypertensive (N =29) hemodialysis patients (r= 0.47; P less than 0.005); however, mean plasma renin for any given sodium/volume state was at least two-fold higher in hypertensive than in normotensive hemodialysis patients or normal subjects (N =31). In the hemodialysis patients, blood pressure correlated weakly but significantly with the products of circulating renin and exchangeable sodium (r=0.37; P less than 0.005) or blood volume (r = 0.29; P less than 0.05). Multiple regression analysis including duration of previous hypertension as the second independent variable increased these correlation coefficients to 0.44 and 0.42, respectively. This suggests that hypertension in endstage kidney disease is often associated with resetting of the body sodium/fluid=renin feedback mechanism. Inappropriately increased plasma renine activity relative to the body sodium/volume state as well as high blood pressure-induced vascular changes may play important complementary roles, but it appears evident that additional mechanisms are also operative in maintaining end-stage renal hypertension.

Adult↗
PubMed1976

Comparison of renal blood flow and transit times measured by means of 99mTc-labelled erythrocytes and Indocyanine Green in humans with normal and diseased kidneys.

1. In nineteen patients with normal or diseased kidneys, renal blood flow, transit times and vascular volume were determined by means of an indicator-dilution method. Two different indicators, plasma-bound Indocyanine Green (IG) and 99mTc-labelled erythrocytes, were used simultaneously. 2. Comparison of the results indicates that IG slightly overestimates renal blood flow, appearance time, mean transit time and vascular volume, as the erythrocyte/IG ratios averaged 0.972, 0.903, 0.93, and 0.921 respectively. Overestimation of the mean transit time was less apparent when it was prolonged. In patients with reduced renal function, the average blood flow values obtained with the two indicators were in good agreement. 3. It is unlikely that axial streaming of erythrocytes accounts for their shorter mean transit time, because the individual erythrocyte/IG mean transit time ratios were independent of the rate of blood flow and the peripheral packed cell volume. 4. Since the erythrocyte/IG mean transit time ratios correlated significantly with the erythrocyte/IG ratios for appearance time and renal blood flow, the common mechanism leading to a depression of all erythrocyte/IG ratios is presumably extravascular circulation and delayed recovery of a small fraction of IG.

Acute Kidney Injury↗
PubMed1976

Blood pressure, circulating renin and the body sodium/volume state in patients with mild renal failure.

Hypertensive patients with various renal lesions and a mean plasma creatinine of 2mg/100ml showed increases (p is less than 0.05) in mean exchangeable sodium and plasma renin activity, while blood volume was not altered significantly. Patients with mild renal failure and normal blood pressure demonstrated no consistent abnormalities in these parameters. Blood pressure correlated significantly with exchangeable sodium and with the 'sodium-renin' and 'blood volume-renin' products; but not with circulating renin or volume individually. This suggests that subtle abnormalities in the physiological sodium/volume-renin feedback mechanism may occur already in the earliest stages of renal disease and may contribute to the hypertension in such patients.

Adult↗
PubMed1975

[Proceedings: Correlations between blood pressure, body sodium/blood volume state and plasma renin in patients with terminal kidney insufficiency].

Plasma renin activity was found to correlate inversely with exchangeable sodium or blood volume in both normotensive and hypertensive hemodialysis patients. However, in the hypertensive patients mean circulating renin for any given sodium/volume state was markedly higher than in normotensive patients or normal subjects. Blood pressure correlated more closely with the products of circulating renin and exchangeable sodium (r = 0.55; p less than 0.001) or blood volume (r = 0.43; p less than 0.001) than with the individual components (r less than or equal to 0.39); multiple regression analysis including duration of previous hypertension as a second independent variable further improved these correlations (r = 0.66 and r = 0.63 respectively). This suggests that the sodium/volume state, circulating renin and vascular changes resulting from previous hypertension may be important complementary determinants of blood pressure in hemodialysis patients.

Blood Pressure↗
PubMed1973

Renal distribution volumes of indocyanine green, ( 51 Cr)EDTA, and 24 Na in man during acute renal failure after shock. Implications for the pathogenesis of anuria.

The mechanism responsible for the anuria in acute renal failure after shock is still controversial. Suppressed glomerular filtration and/or tubular back-diffusion of the filtrate are major possible causes. In the present investigation, seven patients with acute anuria, three of these seven again in the polyuric phase, six patients with moderate renal impairment, four patients with chronic renal failure, and eight subjects with normal renal function were studied by a multiple indicator-dilution method in which the total renal blood flow and renal distribution volumes of indocyanine green, [(51)Cr]EDTA, and (24)Na were determined. In normal subjects the average values for one kidney were 582 ml/min, 42 ml, 92 ml, and 139 ml, respectively. The measurements in the patients with moderate renal impairment were similar to those in the normal subjects, but were decreased in chronic renal failure. In acute anuria, the average values were 269 ml/min, 40 ml, 101 ml, and 114 ml and the kidney volume, estimated radiographically, was increased by 40%. When expressed as milliliters per milliliters kidney, the average distribution volume of (24)Na was decreased from 0.64 to 0.38. This decrease is consistent with the hypothesis that suppressed filtration is largely responsible for the anuria and that back-diffusion is, at most, a contributory factor. The apparent contradiction between the relatively well-preserved total blood flow and the suppressed filtration may be due to a combination of afferent vasoconstriction and efferent vasodilatation. This view is supported by the observation that low filtration fractions were found in clearance measurements performed during the polyuric phase.

Anuria↗