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Phosphat-Depletion

Phosphate-depletion

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Summary

The essential and critical role of inorganic phosphate has been known in veterinary medicine and experimental research on animals for decades. However, only recently has the phosphate depletion syndrome found widespread attention by clinicians. Hypophosphatemia is usually observed in the following clinical situations: chronic alcoholism, recovery phase of diabetic ketoacidosis, administration of phosphate-free solutions in parenteral nutrition, severe respiratory alkalosis, and infusion of fructose. Disturbed organ function in hypophosphatemia is the result of a depletion of inorganic phosphate in the cytoplasm of somatic cells. Such phosphate depletion may be due to either of the following mechanisms or a combination of both. (1) Negative external phosphate balance resulting from phosphate loss in urine or feces or (2) translocation of phosphate from the extracellular into the intracellular space with or without concomitant negative external phosphate balance. In principle, phosphate depletion interferes with the function of all somatic cells. In acute phosphate depletion, the clinically most important disturbances are observed in striated muscle (rhabdomyolysis with myoglobinuric acute renal failure), heart muscle (acute heart failure), and hematological systems (hemolysis, disturbed leukocyte and thrombocyte functions). In contrast, in chronic phosphate depletion skeletal abnormalities (osteomalacia) predominate. Organ disturbances are thought to result from diminished synthesis of ATP and other organic phosphate esters and/or from hypoxia secondary to changes in erythrocyte 2,3-DPG.

Zusammensetzung

Die kritische und lebenswichtige Rolle von anorganischem Phosphat ist in der Veterinärmedizin und der tierexperimentellen Forschung seit Jahrzehnten bekannt. Das Syndrom der Phosphat-Depletion fand in der Klinik jedoch erst seit kurzem stärkere Beachtung. Eine Hypophosphatämie wird bei folgenden Krankheitsbildern gehäuft beobachtet: chronischer Alkoholismus, Erholungsphase der diabetischen Ketoazidose, parenterale Ernährung mit Phosphat-freien Lösungen, schwere respiratorische Alkalose und Fruktose-Infusion. Die Organfunktionsstörungen bei Hypophosphatämie sind auf die Verarmung des Zytoplasmas an anorganischem Phosphat zurückzuführen. Eine derartige Phosphat-Verarmung kann (1) durch negative Phosphat-Bilanz des Gesamtorganismus als Folge renaler oder intestinaler Phosphat-Verluste oder (2) ohne negative äußere Phosphat-Bilanz durch Verschiebung von Phosphat aus dem extra- in den intrazellulären Raum auftreten. Die Phosphat-Depletion beeinträchtigt im Prinzip die Funktion aller Organe. Klinisch stehen bei der akuten Phosphat-Depletion Funktionsstörungen der Skelettmuskulatur (Rhabdomyolyse mit myoglobinurischem akutem Nierenversagen), Herzmuskulatur (akute Herzinsuffizienz) und des hämatologischen Systems (Hämolyse, gestörte Leukozyten- und Thrombozytenfunktion) im Vordergrund, während bei chronischer Phosphat-Depletion Skelettstörungen (Osteomalazie) vorherrschen. Die Organfunktionsstörungen sind wahrscheinlich auf verminderte Synthese von ATP und anderen organischen Phosphat-Metaboliten zurückzuführen. Verminderte 2,3-DPG-Spiegel in Erythrozyten und die hierdurch bedingte Hypoxie sind eine weitere mögliche Ursache von Organfunktionsstörungen.

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  1. Sektion Nephrologie, Medizinische Universitäts-Klinik, Bergheimer Straße 56a, D-6900, Heidelberg, Bundesrepublik Deutschland

    W. Kreusser, E. Ritz & R. Boland

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Stipendiat der Humboldt-Stiftung (Universidad Nacional del Sur Departamento de Ciencias Naturales, 8000 Bahia, Argentina)

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Kreusser, W., Ritz, E. & Boland, R. Phosphat-Depletion. Klin Wochenschr 58, 1–15 (1980). https://doi.org/10.1007/BF01477138

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