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”
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01307 Dresden
