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Wiener klinische Wochenschrift

, Volume 122, Issue 3–4, pp 65–74 | Cite as

Aldosteron und Hypertonie

  • Oliver Vonend
  • Ivo Quack
  • Lars Christian RumpEmail author
Review article

Zusammenfassung

Hyperaldosteronismus ist mit erhöhtem kardiovaskulärem Risiko verbunden. Bei Herzinsuffizienz konnte durch Blockade der Mineralokortikoid-Rezeptoren eine Reduktion in der Mortalität erreicht werden. Aber auch bei therapierefraktärer essentieller Hypertonie und metabolischem Syndrom scheint Aldosteron eine bedeutende Rolle zu spielen. Eine Therapie mit Mineralokortikoidrezeptor (MR)-Antagonisten ist bei Nachweis erhöhter Aldosteronspiegel insbesondere bei Patienten mit Aldosteron-Escape angebracht. Eine besondere Stellung nimmt der primäre Hyperaldosteronismus (PHA) ein. Er gilt als eine der häufigsten Ursachen einer sekundären Hypertonie. Da er klinisch meist normokaliäm verläuft, ist er unter Zuhilfenahme des Aldosteron-Renin Quotienten zu identifizieren. So sollten Patienten mit schwer einstellbarer Hypertonie , hypertensive jüngere Patienten und Patienten mit Inzidentalom ein PHA-Screening durchlaufen. Bei den Untersuchungen ist darauf zu achten, dass Medikamente, die mit dem Renin-Angiotensin-Aldosteron-System interagieren, abgesetzt beziehungsweise umgestellt werden. Nach dem Screening erfolgt ein Bestätigungstest (z.B. Kochsalzbelastungstest). Um zwischen idiopathischer bilateraler Nebennierenrinden-Hyperplasie und Aldosteron-produzierendem Adenom unterscheiden zu können, schließen sich CT und seitengetrennte Nebennierenvenenblutentnahme an. Bei einseitigem Adenom ist die unilaterale peritoneoskopische Adrenalektomie die Therapie der Wahl. Die bilaterale Nebennierenrinden-Hyperplasie wird medikamentös mit den MR-Antagonisten Spironolacton oder Eplerenon behandelt. Bei einer positiven Familienanamnese für primären Hyperaldosteronismus ist an familiären Hyperaldosteronismus (FH) zu denken. Derzeit werden FH Typ I, Typ II und Typ III unterschieden. Bei FH I liegt ein hybrides Gen aus CYP11B1 und CYP11B2 vor, welches eine ACTH-abhängig Aldosteron-Synthese vermittelt. Der Nachweis erfolgt zuverlässig durch PCR. Eine monogenetische Ursache für FH II und FH III konnte bislang nicht gefunden werden. Hyperaldosteronismus kann durch seine Wirkungen, die weit über die Wasser- und Salzregulation hinausgehen, negativen Einfluss auf kardiovaskuläre Ereignisse haben und sollte demnach einen festen Stellenwert in Diagnostik und Therapie der arteriellen Hypertonie erhalten.

Schlüsselwörter

Renin-Angiotensin-System Primärer Hyperaldosteronismus Seitengetrennte Nebennierenvenenblutentnahme Conn Mineralokortikoid-Rezeptor Antagonist 

The role of aldosterone in hypertension

Summary

Hyperaldosteronism is associated with elevated cardiovascular risk. Using mineralocorticoid receptor antagonists a significant reduction in mortality was archived in patients with heart failure. In addition, in refractory hypertension and in patients with metabolic syndrome aldosterone seems to play an important role. Therapy with mineralocorticoidreceptor (MR) antagonists is feasible when aldosterone levels are elevated, in particular in patients with aldosterone-escape. Of particular interest is primary aldosteronism (PA). PA is one of the major causes of secondary hypertension. Since most patients with PA present with normokalemia screening has to be performed using the aldosterone renin ratio, in particular patients with refractory hypertension, young hypertensive patients and patients with incidentaloma. One has to point out that drugs that interfere with the aldosterone-renin-aldosterone-system need to be discontinued or changed. After successful screening, confirmatory testing (e.g. i.v. salt suppression test) has to follow. In order to differentiate between unilateral and bilateral disease computed tomography and adrenal vein sampling are performed. While unilateral adenomas can be cured surgically, bilateral adrenal hyperplasia is treated with MR-antagonists. In case of positive family history for PA one should consider familiar hyperaldosteronism (FH). Three forms are currently defined – FH type I, type II and type III. A hybrid gene consisting of CYP11B1 and CYP11B2 that produces aldosterone in an ACTH dependant manner can be found in FH type I. Diagnosis is verified by long range PCR. No underlying monogenetic cause for FH II and FH II could be detected so far. Through mechanisms way more than water and salt regulation, hyperaldosteronism can negatively influence cardiovascular mortality and morbidity and should therefore play an important part in diagnosis and therapy of arterial hypertension.

Keywords

Renin-Angiotensin-Aldosterone-system Primary hyperaldosteronism Adrenal vein sampling Conn Mineralocorticoid receptor antagonist 

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Copyright information

© Springer-Verlag 2010

Authors and Affiliations

  1. 1.Klinik für NephrologieHeinrich Heine Universität DüsseldorfGermany

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