Zusammenfassung
Die Hyponatriämie stellt die häufigste Elektrolytstörung im klinischen Alltag dar
und ist auf Störungen der Osmoregulation zurückzuführen. Die Hyponatriämie weist somit
auf einen relativen Wasserüberschuss hin. Die Plasmaosmolalität unterliegt einer präzisen
Regulierung, die über ADH, den Durst, die Flüssigkeitszufuhr und die renale Wasserausscheidung
gewährleistet wird. Störungen der physiologischen Osmoregulation gehen daher im Prinzip
immer auf eine Veränderung der ADH-Sekretion, des Durstmechanismus, der adäquaten
Flüssigkeitszufuhr oder der renalen Wasserausscheidung zurück. Dabei ist die ADH-gesteuerte
renale Wasserausscheidung meist das für die Hyponatriämie entscheidende Regelglied.
Die pathologisch vermehrte ADH-Sekretion wird im klinischen Alltag vor allem bei Patienten
mit fortgeschrittener Herz- oder Leberinsuffizienz beobachtet sowie bei paraneoplastischen
Syndromen. In der erstgenannten Gruppe (Herz- und Leberinsuffizienz) ist das Signal
für die gesteigerte ADH-Sekretion barorezeptorvermittelt und entsprechend fallen diese
Patienten durch eher erhöhte Plasmakonzentrationen von Harnstoff und Kreatinin auf.
Bei paraneoplastischem Syndrom besteht hingegen eine ungeregelte ADH-Sekretion aus
Tumorzellen (z. B. kleinzelliges Bronchialkarzinom). Es liegen keine Kreislaufveränderungen
zugrunde. Dementsprechend ist diese Form der Hyponatriämie an auffallend niedrigen
Plasmakonzentrationen von Harnstoff, Kreatinin und Harnsäure, die sogar innerhalb
des Normbereiches liegen können, zu erkennen. Die Symptomatik der Hyponatriämie wird
im Wesentlichen von der Geschwindigkeit mit der sie sich entwickelt bestimmt (schneller
Eintritt der Störung → verstärkte Symptome). Im Vordergrund stehen dabei zerebrale
Symptome. In der Therapie der Hyponatriämie, bringt die Entwicklung der V2-Vasopressin-Rezeptorantagonisten
neue spezifische und viel versprechende Behandlungsmöglichkeiten mit sich.
Abstract
Hyponatraemia is the most frequent electrolyte disturbance in clinical practice. Hyponatraemia
is a disorder of the regulation of plasma osmolality and therefore represents an excess
of body water. Under physiological circumstances plasma osmolality is regulated by
ADH, thirst and renal water excretion. Therefore in hyponatraemia vasopressin, thirst
and/or renal water excretion will have to be dysregulated to bring about the hypoosmolality.
In clinical practice hyponatraemia is encountered in the advanced stages of congestive
heart failure (CHF), liver cirrhosis, and volume contraction as well as in the syndrome
of inappropriated antidiuretic hormone secretion (SIADH). In these disorders hyponatraemia
is caused by nonosmotic vasopressin and sustained fluid intake. Two types of hyponatraemia
are differentiated: a.) so-called nonosmotic related hyponatraemia (CHF, liver cirrhosis,
volume contraction) and b.) the SIADH-type hyponatraemia. The low arterial blood pressure
typically present in CHF, liver cirrhosis and volume contraction provides the stimulus
to baroreceptor activation, resulting in an increased vasopressin secretion. In SIADH-type
hyponatraemia the stimuli of nonosmotic vasopressin release are not precisely known.
These may originate either from tumour cells or from the hypothalamus. Hyponatraemic
patients may suffer from lethargy, difficulty to concentrate, disorientation muscular
cramps, grand mal seizures, and even coma. It is important to know that these symptoms
are mainly related to the rate of decrease of serum sodium concentration (rapid electrolyte
disturbance → symptoms). During the last few years pharmaceutical research has uncovered
novel agents that are effective oral V2 vasopressin receptor antagonists. Recently
these agents have yielded promising results in the treatment of experimental and clinical
hyponatraemia.
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Dr. med. Catrin Palm
Abteilung für Nephrologie · III. Med. Klinik · Universitätsklinik „Carl Gustav Carus”
Fetscherstraße 74
01307 Dresden
