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Studies on the activity of the renin-angiotensin-aldosterone system (RAAS) in patients with cirrhosis of the liver

Untersuchungen zur Aktivität des Renin-Angiotensin-Aldosteron Systems (RAAS) bei Patienten mit Lebercirrhose

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Zusammenfassung

Im Plasma von 77 Patienten mit Lebercirrhose [Gruppe I: unbehandelte Kranke mit Aszites (n=23); Gruppe II: dekompensierte Patienten während saluretischer Behandlung (n=32); Gruppe III: nach Aszitesausschwemmung, aber unter weiterer Spironolacton-Therapie (n=10); Gruppe IV: kompensierte, unbehandelte Cirrhosen (n=12)] wurden radioimmunologisch Reninaktivität (PRA) und Reninkonzentration (PRC), Angiotensinogen, Angiotensin II (AT II) und Aldosteron bestimmt. Abgesehen von einer Angiotensinogen-Verminderung zwischen 39% (Gruppe IV) und 73% (Gruppe III) in allen Gruppen waren bei unbehandelten Patienten in der Regel keine Veränderungen der übrigen Parameter des RAAS nachweisbar. Bei behandelten Kranken mit (Gruppe II) oder ohne (Gruppe III) Aszites fand sich eine hochsignifikante Zunahme der PRA, PRC, AT II- und Aldosteron-Plasmaspiegel. In der gesamten Cirrhosegruppe ergab sich eine enge, direkt proportionale Beziehung zwischen AT II und PRA, PRC sowie Aldosteron, was auf eine vorrangige Bedeutung von AT II für die Stimulierung der Aldosteronsekretion hindeutet. Die Plasma-Natriumkonzentration war invers zur PRA, PRC und zum AT II wie zum Aldosteron korreliert, jedoch konnte keine Beziehung zum Plasmakalium festgestellt werden.

Aus den erhobenen Befunden geht hervor, daß ein Hyperaldosteronismus bei Cirrhosekranken kaum als Ursache für die übersteigerte renale Natriumretention und die Aszitesbildung in Frage kommt. Überwiegend wird die Stimulierung des RAAS erst durch therapeutische Eingriffe und/oder durch ausgeprägte Störungen des Elektrolyt-Stoffwechsels hervorgerufen. Daher sind genau definierte Ausgangsbedingungen für die Untersuchung von Cirrhosepatienten unerläßlich, um therapiebedingte Aktivitätssteigerungen des RAAS ausschließen zu können.

Summary

Plasma renin activity (PRA), plasma renin concentration (PRC), angiotensinogen, angiotensin II (AT II) and plasma aldosterone were determined by radioimmunoassay in 77 patients with cirrhosis of the liver [group I: with ascites, untreated (n=23); group II: patients with ascites during treatment (n=32); group III: after removal of fluids, but under further spironolactone therapy (n=10); group IV: untreated subjects without ascites (n=12)]. With the exception of decreased angiotensinogen values in all groups ranging between 39% (group IV) and 73% (group III) no significant changes of the other parameters of the RAAS were found in untreated patients. A highly significant increase of PRA, PRC, AT II and plasma aldosterone was observed in treated cirrhotics with (group II) or without (group III) ascites. In the total series of patients AT II was closely related to PRA, PRC and aldosterone emphasizing again the predominant role of AT II to stimulate aldosterone secretion. Plasma sodium was inversely correlated to PRA, PRC, AT II and aldosterone, but no relationship was detected between these parameters of the RAAS and plasma potassium.

Our results indicate that hyperaldosteronism in cirrhosis appears unlikely to be the major determinant of avid renal sodium retention and ascites formation. An increased activity of the RAAS is most often initiated by therapeutic factors and/or markedly altered electrolyte metabolism. Therefore, basal conditions of the patients to be studied must be well defined to exclude any artificially induced stimulation of the RAAS.

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  1. Department of Internal Medicine, University of Würzburg, Germany

    H. Wernze, H. J. Spech & G. Müller

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Wernze, H., Spech, H.J. & Müller, G. Studies on the activity of the renin-angiotensin-aldosterone system (RAAS) in patients with cirrhosis of the liver. Klin Wochenschr 56, 389–397 (1978). https://doi.org/10.1007/BF01477293

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