1969
DOI: 10.1007/bf01487551
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Renin und Aldosteron bei idiopathischen �demen

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1969
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Cited by 7 publications
(4 citation statements)
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“…The observations that led to these conclusions included the finding of slightly subnormal concentration and pool size of circulating albumin, attributed to accelerated movement of albumin from the intravascular compartment to an enlarged extravascular pool. However, the plasma albumin concentrations in the patients reported were not low enough to constitute a mechanism for edema formation; the findings of hypoproteinemia have not been confirmed in other studies (Sims et al, 1965;Thorn, 1968;Veyrat et al, 1968;Werning et al, 1969;Kuchel et al, 1970;Streeten et aI., 1973;Oelkers et al, 1975;Edwards and Bayliss, 1976).…”
mentioning
confidence: 67%
See 1 more Smart Citation
“…The observations that led to these conclusions included the finding of slightly subnormal concentration and pool size of circulating albumin, attributed to accelerated movement of albumin from the intravascular compartment to an enlarged extravascular pool. However, the plasma albumin concentrations in the patients reported were not low enough to constitute a mechanism for edema formation; the findings of hypoproteinemia have not been confirmed in other studies (Sims et al, 1965;Thorn, 1968;Veyrat et al, 1968;Werning et al, 1969;Kuchel et al, 1970;Streeten et aI., 1973;Oelkers et al, 1975;Edwards and Bayliss, 1976).…”
mentioning
confidence: 67%
“…Our own data (Streeten et ai., 1973), obtained by bioassay (Boucher et al, 1964), failed to demonstrate excessive elevations in PRA in any of the edematous patients. Evidence published by other investigators has been conflicting, an excessive rise in PRA in patients with idiopathic edema being reported by some (Veyrat et ai., 1968;Kuchel et al, 1970), but being found only exceptionally or never by others (Werning et al, 1969;Oelkers et al, 1975;Katz, 1977;Mac-Gregor et ai., 1979;Sowers et al, 1982b). More studies are required to remove this uncertainty, as there is some evidence that restricted sodium intake may increase aldosterone secretion without raising plasma angiotensin II concentrations in man (Catt et al, 1971;Best et al, 1971;Boyd et al, 1972). c. Orthostatic Changes in Renal Blood Flow and Glomerular Filtration Rate.…”
Section: Findings In Patients With Edema and Orthostatic Sodium Retenmentioning
confidence: 85%
“…As underlying pathophysiological mechanisms, abnormalities in posture or in the function of ADH, atrial natriuretic factor (ANF), prolactin, and renal dopamine have been discussed, without convincing evidence . A change in capillary permeability with secondary involvement of the renin–angiotensin–aldosterone axis is sometimes assumed as the most probable, yet unproven, explanation . Mrs. B's periodic weight gain during manic phases is probably one aspect of such an idiopathic edema.…”
Section: Discussionmentioning
confidence: 99%
“…Auch die sogenannten idiopathischen Ödeme können, besonders in den dynamischen Phasen der Ödementstehung und -ausschwemmung, einen sekundären Hyperaldosteronismus bzw. eine Stimulation des Renin-Angiotensin-Aldosteron-Systems zeigen (3).…”
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